PubMed:21835783 JSONTXT

{"project":"Glycan-Motif","denotations":[{"id":"T1","span":{"begin":367,"end":374},"obj":"https://glytoucan.org/Structures/Glycans/G70323CJ"},{"id":"T2","span":{"begin":376,"end":382},"obj":"https://glytoucan.org/Structures/Glycans/G82576YO"},{"id":"T3","span":{"begin":387,"end":406},"obj":"https://glytoucan.org/Structures/Glycans/G64581RP"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GlyCosmos6-Glycan-Motif-Image","denotations":[{"id":"T1","span":{"begin":367,"end":374},"obj":"Glycan_Motif"},{"id":"T2","span":{"begin":376,"end":382},"obj":"Glycan_Motif"},{"id":"T3","span":{"begin":387,"end":406},"obj":"Glycan_Motif"}],"attributes":[{"id":"A1","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G70323CJ"},{"id":"A2","pred":"image","subj":"T2","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G82576YO"},{"id":"A3","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G64581RP"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GlyCosmos6-Glycan-Motif-Structure","denotations":[{"id":"T1","span":{"begin":367,"end":374},"obj":"https://glytoucan.org/Structures/Glycans/G70323CJ"},{"id":"T2","span":{"begin":376,"end":382},"obj":"https://glytoucan.org/Structures/Glycans/G82576YO"},{"id":"T3","span":{"begin":387,"end":406},"obj":"https://glytoucan.org/Structures/Glycans/G64581RP"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

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{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":144,"end":150},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T2","span":{"begin":638,"end":644},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T3","span":{"begin":645,"end":653},"obj":"http://purl.obolibrary.org/obo/MAT_0000491"},{"id":"T4","span":{"begin":692,"end":698},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T5","span":{"begin":892,"end":898},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T6","span":{"begin":899,"end":907},"obj":"http://purl.obolibrary.org/obo/MAT_0000491"},{"id":"T7","span":{"begin":1115,"end":1121},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T8","span":{"begin":1202,"end":1208},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T9","span":{"begin":1512,"end":1518},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":23,"end":45},"obj":"gene:4153"},{"id":"T1","span":{"begin":107,"end":115},"obj":"disease:C0022116"},{"id":"T2","span":{"begin":318,"end":321},"obj":"gene:4153"},{"id":"T3","span":{"begin":471,"end":490},"obj":"disease:C0022660"},{"id":"T4","span":{"begin":294,"end":316},"obj":"gene:4153"},{"id":"T5","span":{"begin":471,"end":490},"obj":"disease:C0022660"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

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{"project":"uniprot-human","denotations":[{"id":"T1","span":{"begin":23,"end":45},"obj":"http://www.uniprot.org/uniprot/Q96TF8"},{"id":"T2","span":{"begin":294,"end":316},"obj":"http://www.uniprot.org/uniprot/Q96TF8"},{"id":"T3","span":{"begin":318,"end":321},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T4","span":{"begin":492,"end":495},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T5","span":{"begin":537,"end":540},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T6","span":{"begin":930,"end":933},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T7","span":{"begin":997,"end":1000},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T8","span":{"begin":1004,"end":1007},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T9","span":{"begin":1125,"end":1128},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T10","span":{"begin":1383,"end":1386},"obj":"http://www.uniprot.org/uniprot/P13727"},{"id":"T11","span":{"begin":318,"end":321},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T12","span":{"begin":492,"end":495},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T13","span":{"begin":537,"end":540},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T14","span":{"begin":930,"end":933},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T15","span":{"begin":997,"end":1000},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T16","span":{"begin":1004,"end":1007},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T17","span":{"begin":1125,"end":1128},"obj":"http://www.uniprot.org/uniprot/Q6FI04"},{"id":"T18","span":{"begin":1383,"end":1386},"obj":"http://www.uniprot.org/uniprot/Q6FI04"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"uniprot-mouse","denotations":[{"id":"T1","span":{"begin":23,"end":45},"obj":"http://www.uniprot.org/uniprot/P39039"},{"id":"T2","span":{"begin":294,"end":316},"obj":"http://www.uniprot.org/uniprot/P39039"},{"id":"T3","span":{"begin":23,"end":45},"obj":"http://www.uniprot.org/uniprot/P41317"},{"id":"T4","span":{"begin":294,"end":316},"obj":"http://www.uniprot.org/uniprot/P41317"},{"id":"T5","span":{"begin":318,"end":321},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T6","span":{"begin":492,"end":495},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T7","span":{"begin":537,"end":540},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T8","span":{"begin":930,"end":933},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T9","span":{"begin":997,"end":1000},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T10","span":{"begin":1004,"end":1007},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T11","span":{"begin":1125,"end":1128},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T12","span":{"begin":1383,"end":1386},"obj":"http://www.uniprot.org/uniprot/Q61878"},{"id":"T13","span":{"begin":318,"end":321},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T14","span":{"begin":492,"end":495},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T15","span":{"begin":537,"end":540},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T16","span":{"begin":930,"end":933},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T17","span":{"begin":997,"end":1000},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T18","span":{"begin":1004,"end":1007},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T19","span":{"begin":1125,"end":1128},"obj":"http://www.uniprot.org/uniprot/P04370"},{"id":"T20","span":{"begin":1383,"end":1386},"obj":"http://www.uniprot.org/uniprot/P04370"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GlycoBiology-NCBITAXON","denotations":[{"id":"T1","span":{"begin":1022,"end":1024},"obj":"http://purl.bioontology.org/ontology/NCBITAXON/13893"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GO-BP","denotations":[{"id":"T1","span":{"begin":82,"end":103},"obj":"http://purl.obolibrary.org/obo/GO_0006956"},{"id":"T2","span":{"begin":503,"end":524},"obj":"http://purl.obolibrary.org/obo/GO_0006956"},{"id":"T3","span":{"begin":733,"end":754},"obj":"http://purl.obolibrary.org/obo/GO_0006956"},{"id":"T4","span":{"begin":1239,"end":1260},"obj":"http://purl.obolibrary.org/obo/GO_0006956"},{"id":"T5","span":{"begin":1411,"end":1432},"obj":"http://purl.obolibrary.org/obo/GO_0006956"},{"id":"T6","span":{"begin":446,"end":458},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T7","span":{"begin":744,"end":758},"obj":"http://purl.obolibrary.org/obo/GO_0050501"},{"id":"T8","span":{"begin":843,"end":855},"obj":"http://purl.obolibrary.org/obo/GO_0070085"},{"id":"T9","span":{"begin":879,"end":888},"obj":"http://purl.obolibrary.org/obo/GO_0051179"},{"id":"T10","span":{"begin":1025,"end":1034},"obj":"http://purl.obolibrary.org/obo/GO_0051179"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GO-MF","denotations":[{"id":"T1","span":{"begin":23,"end":37},"obj":"http://purl.obolibrary.org/obo/GO_2001065"},{"id":"T2","span":{"begin":294,"end":308},"obj":"http://purl.obolibrary.org/obo/GO_2001065"},{"id":"T3","span":{"begin":30,"end":37},"obj":"http://purl.obolibrary.org/obo/GO_0070026"},{"id":"T4","span":{"begin":301,"end":308},"obj":"http://purl.obolibrary.org/obo/GO_0070026"},{"id":"T5","span":{"begin":1370,"end":1377},"obj":"http://purl.obolibrary.org/obo/GO_0070026"},{"id":"T6","span":{"begin":30,"end":37},"obj":"http://purl.obolibrary.org/obo/GO_0003680"},{"id":"T7","span":{"begin":301,"end":308},"obj":"http://purl.obolibrary.org/obo/GO_0003680"},{"id":"T8","span":{"begin":1370,"end":1377},"obj":"http://purl.obolibrary.org/obo/GO_0003680"},{"id":"T9","span":{"begin":30,"end":37},"obj":"http://purl.obolibrary.org/obo/GO_0017091"},{"id":"T10","span":{"begin":301,"end":308},"obj":"http://purl.obolibrary.org/obo/GO_0017091"},{"id":"T11","span":{"begin":1370,"end":1377},"obj":"http://purl.obolibrary.org/obo/GO_0017091"},{"id":"T12","span":{"begin":30,"end":37},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T13","span":{"begin":301,"end":308},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T14","span":{"begin":1370,"end":1377},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T15","span":{"begin":30,"end":45},"obj":"http://purl.obolibrary.org/obo/GO_0005515"},{"id":"T16","span":{"begin":301,"end":316},"obj":"http://purl.obolibrary.org/obo/GO_0005515"},{"id":"T17","span":{"begin":934,"end":941},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GO-CC","denotations":[{"id":"T1","span":{"begin":621,"end":634},"obj":"http://purl.obolibrary.org/obo/GO_0005903"},{"id":"T2","span":{"begin":654,"end":661},"obj":"http://purl.obolibrary.org/obo/GO_0097649"},{"id":"T3","span":{"begin":908,"end":915},"obj":"http://purl.obolibrary.org/obo/GO_0097649"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"UBERON-AE","denotations":[{"id":"T1","span":{"begin":144,"end":150},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T2","span":{"begin":638,"end":644},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T3","span":{"begin":692,"end":698},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T4","span":{"begin":892,"end":898},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T5","span":{"begin":1115,"end":1121},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T6","span":{"begin":1202,"end":1208},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T7","span":{"begin":1512,"end":1518},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"T8","span":{"begin":342,"end":347},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"T9","span":{"begin":986,"end":991},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"T10","span":{"begin":645,"end":661},"obj":"http://purl.obolibrary.org/obo/UBERON_0004134"},{"id":"T11","span":{"begin":899,"end":915},"obj":"http://purl.obolibrary.org/obo/UBERON_0004134"},{"id":"T12","span":{"begin":776,"end":787},"obj":"http://purl.obolibrary.org/obo/UBERON_2000106"},{"id":"T13","span":{"begin":1060,"end":1066},"obj":"http://purl.obolibrary.org/obo/UBERON_0001851"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"Allie","denotations":[{"id":"SS1_21835783_1_0","span":{"begin":152,"end":172},"obj":"expanded"},{"id":"SS2_21835783_1_0","span":{"begin":174,"end":177},"obj":"abbr"},{"id":"SS1_21835783_2_0","span":{"begin":294,"end":316},"obj":"expanded"},{"id":"SS2_21835783_2_0","span":{"begin":318,"end":321},"obj":"abbr"},{"id":"SS1_21835783_6_0","span":{"begin":986,"end":1000},"obj":"expanded"},{"id":"SS2_21835783_6_0","span":{"begin":1002,"end":1007},"obj":"abbr"}],"relations":[{"id":"AE1_21835783_1_0","pred":"abbreviatedTo","subj":"SS1_21835783_1_0","obj":"SS2_21835783_1_0"},{"id":"AE1_21835783_2_0","pred":"abbreviatedTo","subj":"SS1_21835783_2_0","obj":"SS2_21835783_2_0"},{"id":"AE1_21835783_6_0","pred":"abbreviatedTo","subj":"SS1_21835783_6_0","obj":"SS2_21835783_6_0"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"EDAM-topics","denotations":[{"id":"T1","span":{"begin":8,"end":19},"obj":"http://edamontology.org/topic_0602"},{"id":"T2","span":{"begin":38,"end":45},"obj":"http://edamontology.org/topic_0078"},{"id":"T3","span":{"begin":232,"end":239},"obj":"http://edamontology.org/topic_3678"},{"id":"T4","span":{"begin":309,"end":316},"obj":"http://edamontology.org/topic_0078"},{"id":"T5","span":{"begin":548,"end":555},"obj":"http://edamontology.org/topic_0602"},{"id":"T6","span":{"begin":768,"end":775},"obj":"http://edamontology.org/topic_3678"},{"id":"T7","span":{"begin":958,"end":963},"obj":"http://edamontology.org/topic_3678"},{"id":"T8","span":{"begin":1146,"end":1154},"obj":"http://edamontology.org/topic_0602"},{"id":"T9","span":{"begin":1273,"end":1284},"obj":"http://edamontology.org/topic_0602"},{"id":"T10","span":{"begin":1336,"end":1341},"obj":"http://edamontology.org/topic_3678"},{"id":"T11","span":{"begin":1452,"end":1459},"obj":"http://edamontology.org/topic_0602"},{"id":"T12","span":{"begin":1519,"end":1534},"obj":"http://edamontology.org/topic_3421"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"EDAM-DFO","denotations":[{"id":"T1","span":{"begin":38,"end":45},"obj":"http://edamontology.org/format_1208"},{"id":"T2","span":{"begin":38,"end":45},"obj":"http://edamontology.org/data_1467"},{"id":"T3","span":{"begin":309,"end":316},"obj":"http://edamontology.org/data_1467"},{"id":"T4","span":{"begin":309,"end":316},"obj":"http://edamontology.org/format_1208"},{"id":"T5","span":{"begin":407,"end":415},"obj":"http://edamontology.org/data_1756"},{"id":"T6","span":{"begin":548,"end":555},"obj":"http://edamontology.org/data_2600"},{"id":"T7","span":{"begin":803,"end":813},"obj":"http://edamontology.org/data_0842"},{"id":"T8","span":{"begin":803,"end":813},"obj":"http://edamontology.org/data_2611"},{"id":"T9","span":{"begin":968,"end":980},"obj":"http://edamontology.org/operation_2246"},{"id":"T10","span":{"begin":1452,"end":1459},"obj":"http://edamontology.org/data_2600"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"21835783-2#69#91#gene4153","span":{"begin":294,"end":316},"obj":"gene4153"},{"id":"21835783-2#93#96#gene4153","span":{"begin":318,"end":321},"obj":"gene4153"},{"id":"21835783-2#246#265#diseaseC0022660","span":{"begin":471,"end":490},"obj":"diseaseC0022660"},{"id":"21835783-2#246#265#diseaseC3854173","span":{"begin":471,"end":490},"obj":"diseaseC3854173"},{"id":"21835783-2#246#265#diseaseC0022660","span":{"begin":471,"end":490},"obj":"diseaseC0022660"},{"id":"21835783-2#246#265#diseaseC3854173","span":{"begin":471,"end":490},"obj":"diseaseC3854173"}],"relations":[{"id":"69#91#gene4153246#265#diseaseC0022660","pred":"associated_with","subj":"21835783-2#69#91#gene4153","obj":"21835783-2#246#265#diseaseC0022660"},{"id":"69#91#gene4153246#265#diseaseC3854173","pred":"associated_with","subj":"21835783-2#69#91#gene4153","obj":"21835783-2#246#265#diseaseC3854173"},{"id":"69#91#gene4153246#265#diseaseC0022660","pred":"associated_with","subj":"21835783-2#69#91#gene4153","obj":"21835783-2#246#265#diseaseC0022660"},{"id":"69#91#gene4153246#265#diseaseC3854173","pred":"associated_with","subj":"21835783-2#69#91#gene4153","obj":"21835783-2#246#265#diseaseC3854173"},{"id":"93#96#gene4153246#265#diseaseC0022660","pred":"associated_with","subj":"21835783-2#93#96#gene4153","obj":"21835783-2#246#265#diseaseC0022660"},{"id":"93#96#gene4153246#265#diseaseC3854173","pred":"associated_with","subj":"21835783-2#93#96#gene4153","obj":"21835783-2#246#265#diseaseC3854173"},{"id":"93#96#gene4153246#265#diseaseC0022660","pred":"associated_with","subj":"21835783-2#93#96#gene4153","obj":"21835783-2#246#265#diseaseC0022660"},{"id":"93#96#gene4153246#265#diseaseC3854173","pred":"associated_with","subj":"21835783-2#93#96#gene4153","obj":"21835783-2#246#265#diseaseC3854173"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"GlycoBiology-MAT","denotations":[{"id":"T1","span":{"begin":144,"end":150},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T2","span":{"begin":638,"end":644},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T3","span":{"begin":645,"end":653},"obj":"http://purl.obolibrary.org/obo/MAT_0000491"},{"id":"T4","span":{"begin":692,"end":698},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T5","span":{"begin":892,"end":898},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T6","span":{"begin":899,"end":907},"obj":"http://purl.obolibrary.org/obo/MAT_0000491"},{"id":"T7","span":{"begin":1115,"end":1121},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T8","span":{"begin":1202,"end":1208},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"T9","span":{"begin":1512,"end":1518},"obj":"http://purl.obolibrary.org/obo/MAT_0000119"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"Lectin","denotations":[{"id":"Lectin_T1","span":{"begin":23,"end":45},"obj":"https://acgg.asia/db/lfdb/LfDB0016"},{"id":"Lectin_T2","span":{"begin":294,"end":316},"obj":"https://acgg.asia/db/lfdb/LfDB0016"},{"id":"Lectin_T3","span":{"begin":23,"end":45},"obj":"https://acgg.asia/db/lfdb/LfDB0042"},{"id":"Lectin_T4","span":{"begin":294,"end":316},"obj":"https://acgg.asia/db/lfdb/LfDB0042"},{"id":"Lectin_T5","span":{"begin":318,"end":321},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T6","span":{"begin":492,"end":495},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T7","span":{"begin":537,"end":540},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T8","span":{"begin":930,"end":933},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T9","span":{"begin":997,"end":1000},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T10","span":{"begin":1004,"end":1007},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T11","span":{"begin":1125,"end":1128},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T12","span":{"begin":1383,"end":1386},"obj":"https://acgg.asia/db/lfdb/LfDB0015"},{"id":"Lectin_T13","span":{"begin":318,"end":321},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T14","span":{"begin":492,"end":495},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T15","span":{"begin":537,"end":540},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T16","span":{"begin":930,"end":933},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T17","span":{"begin":997,"end":1000},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T18","span":{"begin":1004,"end":1007},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T19","span":{"begin":1125,"end":1128},"obj":"https://acgg.asia/db/lfdb/LfDB0041"},{"id":"Lectin_T20","span":{"begin":1383,"end":1386},"obj":"https://acgg.asia/db/lfdb/LfDB0041"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":342,"end":347},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":986,"end":991},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":144,"end":150},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":638,"end":644},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":692,"end":698},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":892,"end":898},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":1115,"end":1121},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":1202,"end":1208},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1512,"end":1518},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":776,"end":787},"obj":"http://purl.obolibrary.org/obo/UBERON_2000106"},{"id":"PD-UBERON-AE-B_T11","span":{"begin":645,"end":661},"obj":"http://purl.obolibrary.org/obo/UBERON_0004134"},{"id":"PD-UBERON-AE-B_T12","span":{"begin":899,"end":915},"obj":"http://purl.obolibrary.org/obo/UBERON_0004134"},{"id":"PD-UBERON-AE-B_T13","span":{"begin":1060,"end":1066},"obj":"http://purl.obolibrary.org/obo/UBERON_0001851"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":204,"end":223},"obj":"Phenotype"},{"id":"T2","span":{"begin":471,"end":490},"obj":"Phenotype"},{"id":"T3","span":{"begin":1478,"end":1497},"obj":"Phenotype"},{"id":"T4","span":{"begin":1551,"end":1556},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0001919"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0001919"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0001919"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"HP:0031273"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":107,"end":134},"obj":"Disease"},{"id":"T2","span":{"begin":152,"end":160},"obj":"Disease"},{"id":"T3","span":{"begin":204,"end":223},"obj":"Disease"},{"id":"T4","span":{"begin":471,"end":490},"obj":"Disease"},{"id":"T5","span":{"begin":1478,"end":1497},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005203"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0005053"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0002492"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0002492"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0002492"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"Lectin-Jamboree-Sentence","blocks":[{"id":"T1","span":{"begin":0,"end":151},"obj":"Sentence"},{"id":"T2","span":{"begin":152,"end":224},"obj":"Sentence"},{"id":"T3","span":{"begin":225,"end":491},"obj":"Sentence"},{"id":"T4","span":{"begin":492,"end":699},"obj":"Sentence"},{"id":"T5","span":{"begin":700,"end":788},"obj":"Sentence"},{"id":"T6","span":{"begin":789,"end":942},"obj":"Sentence"},{"id":"T7","span":{"begin":943,"end":1122},"obj":"Sentence"},{"id":"T8","span":{"begin":1123,"end":1307},"obj":"Sentence"},{"id":"T9","span":{"begin":1308,"end":1557},"obj":"Sentence"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":138,"end":143},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":686,"end":691},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":1109,"end":1114},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":1196,"end":1201},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"10088"},{"id":"A2","pred":"db_id","subj":"T1","obj":"10090"},{"id":"A3","pred":"db_id","subj":"T3","obj":"10088"},{"id":"A4","pred":"db_id","subj":"T3","obj":"10090"},{"id":"A5","pred":"db_id","subj":"T5","obj":"10088"},{"id":"A6","pred":"db_id","subj":"T5","obj":"10090"},{"id":"A7","pred":"db_id","subj":"T7","obj":"10088"},{"id":"A8","pred":"db_id","subj":"T7","obj":"10090"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":144,"end":150},"obj":"Body_part"},{"id":"T2","span":{"begin":621,"end":634},"obj":"Body_part"},{"id":"T3","span":{"begin":638,"end":661},"obj":"Body_part"},{"id":"T4","span":{"begin":692,"end":698},"obj":"Body_part"},{"id":"T5","span":{"begin":892,"end":915},"obj":"Body_part"},{"id":"T6","span":{"begin":1060,"end":1066},"obj":"Body_part"},{"id":"T7","span":{"begin":1075,"end":1082},"obj":"Body_part"},{"id":"T9","span":{"begin":1115,"end":1121},"obj":"Body_part"},{"id":"T10","span":{"begin":1202,"end":1208},"obj":"Body_part"},{"id":"T11","span":{"begin":1512,"end":1518},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/UBERON_0012424"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0004134"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/UBERON_0004134"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0001851"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0000958"},{"id":"A8","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0001896"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"A11","pred":"uberon_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/UBERON_0002113"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":144,"end":150},"obj":"Body_part"},{"id":"T2","span":{"begin":638,"end":644},"obj":"Body_part"},{"id":"T3","span":{"begin":645,"end":653},"obj":"Body_part"},{"id":"T4","span":{"begin":692,"end":698},"obj":"Body_part"},{"id":"T5","span":{"begin":892,"end":898},"obj":"Body_part"},{"id":"T6","span":{"begin":899,"end":907},"obj":"Body_part"},{"id":"T7","span":{"begin":1115,"end":1121},"obj":"Body_part"},{"id":"T8","span":{"begin":1202,"end":1208},"obj":"Body_part"},{"id":"T9","span":{"begin":1512,"end":1518},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"A2","pred":"mat_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"A3","pred":"mat_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MAT_0000491"},{"id":"A4","pred":"mat_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"A5","pred":"mat_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"A6","pred":"mat_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/MAT_0000491"},{"id":"A7","pred":"mat_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"A8","pred":"mat_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/MAT_0000119"},{"id":"A9","pred":"mat_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MAT_0000119"}],"text":"Role of interaction of mannan-binding protein with meprins at the initial step of complement activation in ischemia/reperfusion injury to mouse kidney.\nIschemia/reperfusion (I/R) is an important cause of acute renal failure. Recent studies have shown that the complement system mediated by the mannan-binding protein (MBP), which is a C-type serum lectin recognizing mannose, fucose and N-acetylglucosamine residues, plays a critical role in the pathogenesis of ischemic acute renal failure. MBP causes complement activation through the MBP lectin pathway and a resulting complement component, C3b, is accumulated on the brush borders of kidney proximal tubules in a renal I/R-operated mouse kidney. However, the initial step of the complement activation has not been studied extensively. We previously identified both meprins α and β, highly glycosylated zinc metalloproteases, localized on kidney proximal tubules as endogenous MBP ligands. In the present study, we demonstrated that serum-type MBP (S-MBP) and C3b were co-localized with meprins on both the cortex and the medulla in the renal I/R-operated mouse kidney. S-MBP was indicated to interact with meprins in vivo in the I/R-operated mouse kidney and was shown to initiate the complement activation through the interaction with meprins in vitro. Taken together, the present study strongly suggested that the binding of S-MBP to meprins triggers the complement activation through the lectin pathway and may cause the acute renal failure due to I/R on kidney transplantation and hemorrhagic shock."}