PubMed:19463742 JSONTXT

{"project":"LitCoin-sentences","denotations":[{"id":"T1","span":{"begin":0,"end":108},"obj":"Sentence"},{"id":"T2","span":{"begin":109,"end":180},"obj":"Sentence"},{"id":"T3","span":{"begin":181,"end":294},"obj":"Sentence"},{"id":"T4","span":{"begin":295,"end":476},"obj":"Sentence"},{"id":"T5","span":{"begin":477,"end":622},"obj":"Sentence"},{"id":"T6","span":{"begin":623,"end":689},"obj":"Sentence"},{"id":"T7","span":{"begin":690,"end":809},"obj":"Sentence"},{"id":"T8","span":{"begin":810,"end":890},"obj":"Sentence"},{"id":"T9","span":{"begin":891,"end":1016},"obj":"Sentence"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

{"project":"LitCoin-entities-OrganismTaxon-PD","denotations":[{"id":"T1","span":{"begin":406,"end":411},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":784,"end":787},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"NCBItxid:10116"},{"id":"A3","pred":"db_id","subj":"T2","obj":"NCBItxid:10114"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

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receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

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{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":320,"end":323},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":477,"end":480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":522,"end":525},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":623,"end":626},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":810,"end":813},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0010691"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0010691"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0100185"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0010691"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0010691"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

{"project":"LitCoin_CellLine","denotations":[{"id":"T1","span":{"begin":371,"end":377},"obj":"CellLine"},{"id":"T2","span":{"begin":878,"end":883},"obj":"CellLine"}],"attributes":[{"id":"A1","pred":"cellosaurus_accession_id","subj":"T1","obj":"CVCL_0045"},{"id":"A2","pred":"cellosaurus_accession_id","subj":"T2","obj":"CVCL_6236"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":406,"end":411},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":784,"end":787},"obj":"OrganismTaxon"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T1","span":{"begin":320,"end":327},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":477,"end":484},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":623,"end":630},"obj":"ChemicalEntity"},{"id":"T4","span":{"begin":715,"end":727},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":810,"end":817},"obj":"ChemicalEntity"},{"id":"T6","span":{"begin":847,"end":854},"obj":"ChemicalEntity"}],"attributes":[{"id":"A1","pred":"ID:","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A2","pred":"ID:","subj":"T2","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A4","pred":"ID:","subj":"T4","obj":"ChemicalEntity"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D005947"},{"id":"A7","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_4167"},{"id":"A8","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_17234"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

{"project":"LitCoin-training-merged","denotations":[{"id":"T2","span":{"begin":878,"end":883},"obj":"CellLine"},{"id":"T1","span":{"begin":371,"end":377},"obj":"CellLine"},{"id":"T6","span":{"begin":847,"end":854},"obj":"ChemicalEntity"},{"id":"T5","span":{"begin":810,"end":817},"obj":"ChemicalEntity"},{"id":"T4","span":{"begin":715,"end":727},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":623,"end":630},"obj":"ChemicalEntity"},{"id":"T96262","span":{"begin":477,"end":484},"obj":"ChemicalEntity"},{"id":"T74640","span":{"begin":320,"end":327},"obj":"ChemicalEntity"},{"id":"T14","span":{"begin":878,"end":881},"obj":"GeneOrGeneProduct"},{"id":"T13","span":{"begin":814,"end":817},"obj":"GeneOrGeneProduct"},{"id":"T12","span":{"begin":627,"end":630},"obj":"GeneOrGeneProduct"},{"id":"T11","span":{"begin":589,"end":610},"obj":"GeneOrGeneProduct"},{"id":"T10","span":{"begin":522,"end":527},"obj":"GeneOrGeneProduct"},{"id":"T9","span":{"begin":481,"end":484},"obj":"GeneOrGeneProduct"},{"id":"T8","span":{"begin":443,"end":464},"obj":"GeneOrGeneProduct"},{"id":"T7","span":{"begin":412,"end":416},"obj":"GeneOrGeneProduct"},{"id":"T29245","span":{"begin":324,"end":327},"obj":"GeneOrGeneProduct"},{"id":"T4465","span":{"begin":264,"end":287},"obj":"GeneOrGeneProduct"},{"id":"T28790","span":{"begin":215,"end":219},"obj":"GeneOrGeneProduct"},{"id":"T73467","span":{"begin":185,"end":213},"obj":"GeneOrGeneProduct"},{"id":"T99498","span":{"begin":44,"end":67},"obj":"GeneOrGeneProduct"},{"id":"T7398","span":{"begin":0,"end":23},"obj":"GeneOrGeneProduct"},{"id":"T8216","span":{"begin":784,"end":787},"obj":"OrganismTaxon"},{"id":"T29152","span":{"begin":406,"end":411},"obj":"OrganismTaxon"}],"attributes":[{"id":"A2","pred":"cellosaurus_accession_id","subj":"T2","obj":"CVCL_6236"},{"id":"A1","pred":"cellosaurus_accession_id","subj":"T1","obj":"CVCL_0045"},{"id":"A8","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_17234"},{"id":"A7","pred":"ID:","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_4167"},{"id":"A6","pred":"ID:","subj":"T6","obj":"D005947"},{"id":"A5","pred":"ID:","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A4","pred":"ID:","subj":"T4","obj":"ChemicalEntity"},{"id":"A3","pred":"ID:","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A81782","pred":"ID:","subj":"T96262","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"},{"id":"A98520","pred":"ID:","subj":"T74640","obj":"http://purl.obolibrary.org/obo/CHEBI_136034"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}

{"project":"PMID_GLOBAL","denotations":[{"id":"T1","span":{"begin":320,"end":323},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":477,"end":480},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":522,"end":525},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":623,"end":626},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":810,"end":813},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0010691"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0010691"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0100185"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0010691"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0010691"}],"text":"Melanocortin-4 receptor activation inhibits c-Jun N-terminal kinase activity and promotes insulin signaling.\nThe melanocortin system is crucial to regulation of energy homeostasis. The melanocortin receptor type 4 (MC4R) modulates insulin signaling via effects on c-Jun N-terminal kinase (JNK). The melanocortin agonist NDP-MSH dose-dependently inhibited JNK activity in HEK293 cells stably expressing the human MC4R; effects were reversed by melanocortin receptor antagonist. NDP-MSH time- and dose-dependently inhibited IRS-1(ser307) phosphorylation, effects also reversed by a specific melanocortin receptor antagonist. NDP-MSH augmented insulin-stimulated AKT phosphorylation in vitro. The melanocortin agonist melanotan II increased insulin-stimulated AKT phosphorylation in the rat hypothalamus in vivo. NDP-MSH increased insulin-stimulated glucose uptake in hypothalamic GT1-1 cells. The current study shows that the melanocortinergic system interacts with insulin signaling via novel effects on JNK activity."}