PubMed:9294109 JSONTXT

{"project":"NCBI-Disease-Corpus-GPT5-withguidelines","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"Modifier"},{"id":"T2","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T4","span":{"begin":158,"end":175},"obj":"DiseaseClass"},{"id":"T5","span":{"begin":261,"end":263},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-GPT5-noguidelines","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":143,"end":157},"obj":"Modifier"},{"id":"T3","span":{"begin":158,"end":175},"obj":"DiseaseClass"},{"id":"T4","span":{"begin":176,"end":185},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-GPT5-guidelineprompt","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":158,"end":175},"obj":"DiseaseClass"},{"id":"T4","span":{"begin":261,"end":263},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-Moderated1","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"Modifier"},{"id":"T2","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T4","span":{"begin":158,"end":175},"obj":"DiseaseClass"},{"id":"T5","span":{"begin":261,"end":263},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T1","span":{"begin":646,"end":650},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:10095"},{"id":"A2","pred":"db_id","subj":"T1","obj":"NCBItxid:10088"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":113},"obj":"Sentence"},{"id":"T2","span":{"begin":114,"end":347},"obj":"Sentence"},{"id":"T3","span":{"begin":348,"end":651},"obj":"Sentence"},{"id":"T4","span":{"begin":652,"end":844},"obj":"Sentence"},{"id":"T5","span":{"begin":845,"end":960},"obj":"Sentence"},{"id":"T6","span":{"begin":961,"end":1099},"obj":"Sentence"},{"id":"T7","span":{"begin":1100,"end":1222},"obj":"Sentence"},{"id":"T8","span":{"begin":1223,"end":1364},"obj":"Sentence"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-entities","denotations":[{"id":"202","span":{"begin":0,"end":33},"obj":"GeneOrGeneProduct"},{"id":"203","span":{"begin":71,"end":75},"obj":"ChemicalEntity"},{"id":"204","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"},{"id":"205","span":{"begin":134,"end":136},"obj":"DiseaseOrPhenotypicFeature"},{"id":"206","span":{"begin":158,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"207","span":{"begin":261,"end":278},"obj":"GeneOrGeneProduct"},{"id":"208","span":{"begin":280,"end":284},"obj":"GeneOrGeneProduct"},{"id":"209","span":{"begin":397,"end":401},"obj":"GeneOrGeneProduct"},{"id":"210","span":{"begin":461,"end":465},"obj":"ChemicalEntity"},{"id":"211","span":{"begin":519,"end":523},"obj":"ChemicalEntity"},{"id":"212","span":{"begin":555,"end":558},"obj":"ChemicalEntity"},{"id":"213","span":{"begin":627,"end":631},"obj":"GeneOrGeneProduct"},{"id":"214","span":{"begin":646,"end":650},"obj":"OrganismTaxon"},{"id":"215","span":{"begin":676,"end":680},"obj":"GeneOrGeneProduct"},{"id":"216","span":{"begin":721,"end":725},"obj":"ChemicalEntity"},{"id":"217","span":{"begin":822,"end":826},"obj":"ChemicalEntity"},{"id":"218","span":{"begin":831,"end":834},"obj":"ChemicalEntity"},{"id":"219","span":{"begin":892,"end":896},"obj":"ChemicalEntity"},{"id":"220","span":{"begin":926,"end":939},"obj":"ChemicalEntity"},{"id":"221","span":{"begin":957,"end":959},"obj":"ChemicalEntity"},{"id":"222","span":{"begin":997,"end":1001},"obj":"ChemicalEntity"},{"id":"223","span":{"begin":1062,"end":1066},"obj":"ChemicalEntity"},{"id":"224","span":{"begin":1086,"end":1090},"obj":"ChemicalEntity"},{"id":"225","span":{"begin":1140,"end":1153},"obj":"ChemicalEntity"},{"id":"226","span":{"begin":1158,"end":1192},"obj":"ChemicalEntity"},{"id":"227","span":{"begin":1209,"end":1213},"obj":"GeneOrGeneProduct"},{"id":"228","span":{"begin":1260,"end":1264},"obj":"GeneOrGeneProduct"}],"attributes":[{"id":"A7","pred":"db_id","subj":"208","obj":"NCBIGene:13400"},{"id":"A14","pred":"db_id","subj":"215","obj":"NCBIGene:13400"},{"id":"A15","pred":"db_id","subj":"216","obj":"MESH:D002118"},{"id":"A20","pred":"db_id","subj":"221","obj":"MESH:D011188"},{"id":"A5","pred":"db_id","subj":"206","obj":"MESH:D009135"},{"id":"A17","pred":"db_id","subj":"218","obj":"MESH:D012964"},{"id":"A23","pred":"db_id","subj":"224","obj":"MESH:D002118"},{"id":"A1","pred":"db_id","subj":"202","obj":"NCBIGene:13400"},{"id":"A12","pred":"db_id","subj":"213","obj":"NCBIGene:13400"},{"id":"A25","pred":"db_id","subj":"227","obj":"NCBIGene:13400"},{"id":"A10","pred":"db_id","subj":"211","obj":"MESH:D002118"},{"id":"A24","pred":"db_id","subj":"226","obj":"MESH:D053498"},{"id":"A9","pred":"db_id","subj":"210","obj":"MESH:D002118"},{"id":"A13","pred":"db_id","subj":"214","obj":"NCBITaxon:10090"},{"id":"A3","pred":"db_id","subj":"204","obj":"MESH:D009223"},{"id":"A2","pred":"db_id","subj":"203","obj":"MESH:D002118"},{"id":"A11","pred":"db_id","subj":"212","obj":"MESH:D000255"},{"id":"A16","pred":"db_id","subj":"217","obj":"MESH:D002118"},{"id":"A18","pred":"db_id","subj":"219","obj":"MESH:D002118"},{"id":"A6","pred":"db_id","subj":"207","obj":"NCBIGene:13400"},{"id":"A19","pred":"db_id","subj":"220","obj":"MESH:D000109"},{"id":"A26","pred":"db_id","subj":"228","obj":"NCBIGene:13400"},{"id":"A4","pred":"db_id","subj":"205","obj":"MESH:D009223"},{"id":"A21","pred":"db_id","subj":"222","obj":"MESH:D002118"},{"id":"A8","pred":"db_id","subj":"209","obj":"NCBIGene:13400"},{"id":"A22","pred":"db_id","subj":"223","obj":"MESH:D002118"}],"namespaces":[{"prefix":"_base","uri":"https://w3id.org/biolink/vocab/"},{"prefix":"MESH","uri":"http://id.nlm.nih.gov/mesh/"},{"prefix":"NCBITaxon","uri":"https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id="},{"prefix":"NCBIGene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"OMIM","uri":"https://www.omim.org/entry/"},{"prefix":"DBSNP","uri":"https://www.ncbi.nlm.nih.gov/snp/"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin_Mondo","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0016107"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0016107"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-GeneOrGeneProduct-v0","denotations":[{"id":"T1","span":{"begin":19,"end":33},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":71,"end":74},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":91,"end":106},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":107,"end":112},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":214,"end":223},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":245,"end":259},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":261,"end":278},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":280,"end":284},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":397,"end":401},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":452,"end":459},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":461,"end":464},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":511,"end":518},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":519,"end":522},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":555,"end":558},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":570,"end":575},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":588,"end":603},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":604,"end":609},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":627,"end":631},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":637,"end":645},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":646,"end":650},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":676,"end":680},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":712,"end":719},"obj":"GeneOrGeneProduct"},{"id":"T23","span":{"begin":721,"end":724},"obj":"GeneOrGeneProduct"},{"id":"T24","span":{"begin":777,"end":781},"obj":"GeneOrGeneProduct"},{"id":"T25","span":{"begin":782,"end":793},"obj":"GeneOrGeneProduct"},{"id":"T26","span":{"begin":822,"end":825},"obj":"GeneOrGeneProduct"},{"id":"T27","span":{"begin":831,"end":843},"obj":"GeneOrGeneProduct"},{"id":"T28","span":{"begin":849,"end":855},"obj":"GeneOrGeneProduct"},{"id":"T29","span":{"begin":873,"end":880},"obj":"GeneOrGeneProduct"},{"id":"T30","span":{"begin":892,"end":895},"obj":"GeneOrGeneProduct"},{"id":"T31","span":{"begin":943,"end":947},"obj":"GeneOrGeneProduct"},{"id":"T32","span":{"begin":997,"end":1000},"obj":"GeneOrGeneProduct"},{"id":"T33","span":{"begin":1048,"end":1061},"obj":"GeneOrGeneProduct"},{"id":"T34","span":{"begin":1062,"end":1065},"obj":"GeneOrGeneProduct"},{"id":"T35","span":{"begin":1086,"end":1098},"obj":"GeneOrGeneProduct"},{"id":"T36","span":{"begin":1128,"end":1136},"obj":"GeneOrGeneProduct"},{"id":"T37","span":{"begin":1140,"end":1153},"obj":"GeneOrGeneProduct"},{"id":"T38","span":{"begin":1181,"end":1192},"obj":"GeneOrGeneProduct"},{"id":"T39","span":{"begin":1209,"end":1213},"obj":"GeneOrGeneProduct"},{"id":"T40","span":{"begin":1260,"end":1264},"obj":"GeneOrGeneProduct"},{"id":"T41","span":{"begin":1295,"end":1302},"obj":"GeneOrGeneProduct"},{"id":"T42","span":{"begin":1348,"end":1363},"obj":"GeneOrGeneProduct"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-GeneOrGeneProduct-v2","denotations":[{"id":"T1","span":{"begin":19,"end":33},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":91,"end":106},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":214,"end":223},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":245,"end":259},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":261,"end":278},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":280,"end":284},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":397,"end":401},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":588,"end":603},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":627,"end":631},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":637,"end":645},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":676,"end":680},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":831,"end":843},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":849,"end":855},"obj":"GeneOrGeneProduct"},{"id":"T14","span":{"begin":873,"end":880},"obj":"GeneOrGeneProduct"},{"id":"T15","span":{"begin":943,"end":947},"obj":"GeneOrGeneProduct"},{"id":"T16","span":{"begin":1048,"end":1061},"obj":"GeneOrGeneProduct"},{"id":"T17","span":{"begin":1086,"end":1098},"obj":"GeneOrGeneProduct"},{"id":"T18","span":{"begin":1140,"end":1153},"obj":"GeneOrGeneProduct"},{"id":"T19","span":{"begin":1181,"end":1192},"obj":"GeneOrGeneProduct"},{"id":"T20","span":{"begin":1209,"end":1213},"obj":"GeneOrGeneProduct"},{"id":"T21","span":{"begin":1260,"end":1264},"obj":"GeneOrGeneProduct"},{"id":"T22","span":{"begin":1348,"end":1363},"obj":"GeneOrGeneProduct"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"originalLabel","subj":"T1","obj":"D009223"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"D009223"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-GeneOrGeneProduct-v3","denotations":[{"id":"T1","span":{"begin":0,"end":33},"obj":"GeneOrGeneProduct"},{"id":"T2","span":{"begin":214,"end":223},"obj":"GeneOrGeneProduct"},{"id":"T3","span":{"begin":243,"end":252},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":261,"end":278},"obj":"GeneOrGeneProduct"},{"id":"T5","span":{"begin":280,"end":284},"obj":"GeneOrGeneProduct"},{"id":"T6","span":{"begin":397,"end":401},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":627,"end":631},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":676,"end":680},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":831,"end":843},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1140,"end":1153},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1181,"end":1192},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":1209,"end":1213},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":1260,"end":1264},"obj":"GeneOrGeneProduct"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":134,"end":136},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":261,"end":263},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":331,"end":334},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":414,"end":417},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":566,"end":569},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0044688"},{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0016107"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0016367"},{"id":"A6","pred":"mondo_id","subj":"T5","obj":"0005015"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0016107"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"0044688"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0016367"},{"id":"A4","pred":"mondo_id","subj":"T3","obj":"0005015"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"0044688"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":134,"end":136},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":158,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":261,"end":263},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A2","pred":"ID:","subj":"T2","obj":"D009223"},{"id":"A4","pred":"ID:","subj":"T4","obj":"DISEASE"},{"id":"A5","pred":"ID:","subj":"T5","obj":"DISEASE"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D009223"},{"id":"A3","pred":"ID:","subj":"T3","obj":"DISEASE"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":134,"end":136},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":158,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":261,"end":263},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A4","pred":"#label","subj":"T4","obj":"DISEASE"},{"id":"A1","pred":"#label","subj":"T1","obj":"D009223"},{"id":"A2","pred":"#label","subj":"T2","obj":"D009223"},{"id":"A5","pred":"#label","subj":"T5","obj":"DISEASE"},{"id":"A3","pred":"#label","subj":"T3","obj":"DISEASE"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T1","span":{"begin":331,"end":334},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":414,"end":417},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":555,"end":558},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":566,"end":569},"obj":"ChemicalEntity"},{"id":"T6","span":{"begin":926,"end":939},"obj":"ChemicalEntity"},{"id":"T8","span":{"begin":1140,"end":1153},"obj":"ChemicalEntity"},{"id":"T9","span":{"begin":1158,"end":1192},"obj":"ChemicalEntity"}],"attributes":[{"id":"A2","pred":"ID:","subj":"T2","obj":"http://purl.obolibrary.org/obo/CHEBI_24870"},{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_30616"},{"id":"A4","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_15422"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_24870"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D000109"},{"id":"A7","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_15355"},{"id":"A1","pred":"ID:","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_24870"},{"id":"A9","pred":"ID:","subj":"T9","obj":"ChemicalEntity"},{"id":"A8","pred":"ID:","subj":"T8","obj":"ChemicalEntity"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":646,"end":650},"obj":"OrganismTaxon"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"LitCoin-training-merged","denotations":[{"id":"T9","span":{"begin":1158,"end":1192},"obj":"ChemicalEntity"},{"id":"T8","span":{"begin":1140,"end":1153},"obj":"ChemicalEntity"},{"id":"T6","span":{"begin":926,"end":939},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":566,"end":569},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":555,"end":558},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":414,"end":417},"obj":"ChemicalEntity"},{"id":"T1","span":{"begin":331,"end":334},"obj":"ChemicalEntity"},{"id":"T13","span":{"begin":1260,"end":1264},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":1209,"end":1213},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":1181,"end":1192},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":1140,"end":1153},"obj":"GeneOrGeneProduct"},{"id":"T46831","span":{"begin":831,"end":843},"obj":"GeneOrGeneProduct"},{"id":"T80422","span":{"begin":676,"end":680},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":627,"end":631},"obj":"GeneOrGeneProduct"},{"id":"T59818","span":{"begin":397,"end":401},"obj":"GeneOrGeneProduct"},{"id":"T61827","span":{"begin":280,"end":284},"obj":"GeneOrGeneProduct"},{"id":"T4","span":{"begin":261,"end":278},"obj":"GeneOrGeneProduct"},{"id":"T43756","span":{"begin":243,"end":252},"obj":"GeneOrGeneProduct"},{"id":"T54116","span":{"begin":214,"end":223},"obj":"GeneOrGeneProduct"},{"id":"T20744","span":{"begin":0,"end":33},"obj":"GeneOrGeneProduct"},{"id":"T43458","span":{"begin":261,"end":263},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T40387","span":{"begin":158,"end":175},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T23231","span":{"begin":134,"end":136},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T98445","span":{"begin":114,"end":132},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T69515","span":{"begin":0,"end":18},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12830","span":{"begin":646,"end":650},"obj":"OrganismTaxon"}],"attributes":[{"id":"A15132","pred":"#label","subj":"T23231","obj":"DISEASE"},{"id":"A9","pred":"ID:","subj":"T9","obj":"ChemicalEntity"},{"id":"A38487","pred":"#label","subj":"T43458","obj":"DISEASE"},{"id":"A1","pred":"ID:","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_24870"},{"id":"A85949","pred":"#label","subj":"T98445","obj":"D009223"},{"id":"A4","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_15422"},{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_30616"},{"id":"A91886","pred":"#label","subj":"T69515","obj":"D009223"},{"id":"A7","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_15355"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D000109"},{"id":"A2","pred":"ID:","subj":"T2","obj":"http://purl.obolibrary.org/obo/CHEBI_24870"},{"id":"A64845","pred":"#label","subj":"T40387","obj":"DISEASE"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_24870"},{"id":"A8","pred":"ID:","subj":"T8","obj":"ChemicalEntity"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBIDiseaseCorpus","denotations":[{"id":"T1","span":{"begin":0,"end":18},"obj":"Modifier:D009223"},{"id":"T2","span":{"begin":114,"end":132},"obj":"SpecificDisease:D009223"},{"id":"T3","span":{"begin":134,"end":136},"obj":"SpecificDisease:D009223"},{"id":"T4","span":{"begin":158,"end":175},"obj":"DiseaseClass:D009135"},{"id":"T5","span":{"begin":261,"end":263},"obj":"Modifier:D009223"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Test","denotations":[{"id":"T472","span":{"begin":0,"end":18},"obj":"Modifier"},{"id":"T473","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T474","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T475","span":{"begin":158,"end":175},"obj":"DiseaseClass"},{"id":"T476","span":{"begin":261,"end":263},"obj":"Modifier"}],"attributes":[{"id":"A472","pred":"database_id","subj":"T472","obj":"D009223"},{"id":"A473","pred":"database_id","subj":"T473","obj":"D009223"},{"id":"A474","pred":"database_id","subj":"T474","obj":"D009223"},{"id":"A475","pred":"database_id","subj":"T475","obj":"D009135"},{"id":"A476","pred":"database_id","subj":"T476","obj":"D009223"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Test-Assistant-Knowledge","denotations":[{"id":"T1","span":{"begin":114,"end":137},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":158,"end":175},"obj":"DiseaseClass"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Test-4o-NoGuidelineInPrompt","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":158,"end":175},"obj":"DiseaseClass"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-o3-2","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-high-o3-1","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-high-o3-2","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Test-4o-GuidelineInPrompt","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-UpdatedGuideline","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-humanintheloop","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":261,"end":263},"obj":"Modifier"},{"id":"T4","span":{"begin":280,"end":284},"obj":"Modifier"},{"id":"T5","span":{"begin":397,"end":401},"obj":"Modifier"},{"id":"T6","span":{"begin":627,"end":631},"obj":"Modifier"},{"id":"T7","span":{"begin":676,"end":680},"obj":"Modifier"},{"id":"T8","span":{"begin":1209,"end":1213},"obj":"Modifier"},{"id":"T9","span":{"begin":1260,"end":1264},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-rezarta1","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-All","denotations":[{"id":"T472","span":{"begin":0,"end":18},"obj":"Modifier"},{"id":"T473","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T474","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T475","span":{"begin":158,"end":175},"obj":"DiseaseClass"},{"id":"T476","span":{"begin":261,"end":263},"obj":"Modifier"}],"attributes":[{"id":"A472","pred":"database_id","subj":"T472","obj":"D009223"},{"id":"A473","pred":"database_id","subj":"T473","obj":"D009223"},{"id":"A474","pred":"database_id","subj":"T474","obj":"D009223"},{"id":"A475","pred":"database_id","subj":"T475","obj":"D009135"},{"id":"A476","pred":"database_id","subj":"T476","obj":"D009223"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-2stage-All","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":261,"end":263},"obj":"Modifier"},{"id":"T4","span":{"begin":397,"end":401},"obj":"Modifier"},{"id":"T5","span":{"begin":627,"end":631},"obj":"Modifier"},{"id":"T6","span":{"begin":676,"end":680},"obj":"Modifier"},{"id":"T7","span":{"begin":1209,"end":1213},"obj":"Modifier"},{"id":"T8","span":{"begin":1260,"end":1264},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-rezarta-All","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-4oGuideline-All","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"NCBI-Disease-Corpus-Simple-All","denotations":[{"id":"T1","span":{"begin":9,"end":18},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":123,"end":132},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":158,"end":175},"obj":"DiseaseClass"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"123456","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"SpecificDisease"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"},{"id":"T3","span":{"begin":261,"end":263},"obj":"Modifier"},{"id":"T4","span":{"begin":280,"end":284},"obj":"Modifier"},{"id":"T5","span":{"begin":397,"end":401},"obj":"Modifier"},{"id":"T6","span":{"begin":627,"end":631},"obj":"Modifier"},{"id":"T7","span":{"begin":676,"end":680},"obj":"Modifier"},{"id":"T8","span":{"begin":1209,"end":1213},"obj":"Modifier"},{"id":"T9","span":{"begin":1260,"end":1264},"obj":"Modifier"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}

{"project":"12345","denotations":[{"id":"T1","span":{"begin":114,"end":132},"obj":"Modifier"},{"id":"T2","span":{"begin":134,"end":136},"obj":"SpecificDisease"}],"text":"Myotonic dystrophy protein kinase is involved in the modulation of the Ca2+ homeostasis in skeletal muscle cells.\nMyotonic dystrophy (DM), the most prevalent muscular disorder in adults, is caused by (CTG)n-repeat expansion in a gene encoding a protein kinase (DM protein kinase; DMPK) and involves changes in cytoarchitecture and ion homeostasis. To obtain clues to the normal biological role of DMPK in cellular ion homeostasis, we have compared the resting [Ca2+]i, the amplitude and shape of depolarization-induced Ca2+ transients, and the content of ATP-driven ion pumps in cultured skeletal muscle cells of wild-type and DMPK[-/-] knockout mice. In vitro-differentiated DMPK[-/-] myotubes exhibit a higher resting [Ca2+]i than do wild-type myotubes because of an altered open probability of voltage-dependent l-type Ca2+ and Na+ channels. The mutant myotubes exhibit smaller and slower Ca2+ responses upon triggering by acetylcholine or high external K+. In addition, we observed that these Ca2+ transients partially result from an influx of extracellular Ca2+ through the l-type Ca2+ channel. Neither the content nor the activity of Na+/K+ ATPase and sarcoplasmic reticulum Ca2+-ATPase are affected by DMPK absence. In conclusion, our data suggest that DMPK is involved in modulating the initial events of excitation-contraction coupling in skeletal muscle."}