Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26. - Wikidata - wikimedia - TriplyDB

Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

http://www.wikidata.org/entity/Q35809679

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Role of a propeller loop in the quaternary structure and enzymatic activity of prolyl dipeptidases DPP-IV and DPP9 One site mutation disrupts dimer formation in human DPP-IV proteins Dipeptidyl peptidase IV activity and/or structure homologs: contributing factors in the pathogenesis of rheumatoid arthritis?Dipeptidyl Peptidase-4 Regulation of SDF-1/CXCR4 Axis: Implications for Cardiovascular Disease DPP4 in Diabetes Potential role of dipeptidyl peptidase IV in the pathophysiology of heart failure GLP-1-based strategies: a physiological analysis of differential mode of action Dipeptidyl-peptidase 4 inhibition: linking metabolic control to cardiovascular protection Recent Advances in Dipeptidyl-Peptidase-4 Inhibition Therapy: Lessons from the Bench and Clinical Trials Proteolysis controls endogenous substance P levels Deletion of PREPl causes growth impairment and hypotonia in mice Circulating CD26 is negatively associated with inflammation in human and experimental arthritis.Vildagliptin: an inhibitor of dipeptidyl peptidase-4 with antidiabetic properties.Genetic ablation or pharmacological blockade of dipeptidyl peptidase IV does not impact T cell-dependent immune responses.Glucagon-like peptide-1 receptor signalling reduces microvascular thrombosis, nitro-oxidative stress and platelet activation in endotoxaemic mice.Glucagon-like peptide 1 receptor plays a critical role in geniposide-regulated insulin secretion in INS-1 cells GIP and GLP-1, the two incretin hormones: Similarities and differences Expanding the dipeptidyl peptidase 4-regulated peptidome via an optimized peptidomics platform.Genetic deletion or pharmacological inhibition of dipeptidyl peptidase-4 improves cardiovascular outcomes after myocardial infarction in mice.Adipocyte Accumulation in the Bone Marrow during Obesity and Aging Impairs Stem Cell-Based Hematopoietic and Bone Regeneration The incretin system and cardiometabolic disease Kinetic study of the processing by dipeptidyl-peptidase IV/CD26 of neuropeptides involved in pancreatic insulin secretion.Analysis of the proteolysis of bioactive peptides using a peptidomics approach.Peptidomics approach to elucidate the proteolytic regulation of bioactive peptides.Peptidomics of the prolyl peptidases Emerging gliptins for type 2 diabetes.Proglucagon-derived peptides: mechanisms of action and therapeutic potential.Inhibition of circulating dipeptidyl peptidase 4 activity in patients with metastatic prostate cancer.Endoplasmic reticulum chaperon tauroursodeoxycholic acid alleviates obesity-induced myocardial contractile dysfunction A novel consensus motif in fibronectin mediates dipeptidyl peptidase IV adhesion and metastasis.Sitagliptin: a dipeptidyl peptidase IV inhibitor for the treatment of type 2 diabetes.Dipeptidyl peptidase IV (DPP IV) inhibitors: A newly emerging drug class for the treatment of type 2 diabetes.Effective mobilization of hematopoietic progenitor cells in G-CSF mobilization defective CD26-/- mice through AMD3100-induced disruption of the CXCL12-CXCR4 axis.Therapeutic potential of dipeptidyl peptidase IV inhibitors for the treatment of type 2 diabetes.Identification and validation of novel contraction-regulated myokines released from primary human skeletal muscle cells A peptidomics strategy to elucidate the proteolytic pathways that inactivate peptide hormones.Differential effects of PPAR-{gamma} activation versus chemical or genetic reduction of DPP-4 activity on bone quality in mice.The role of incretins in glucose homeostasis and diabetes treatment.Targeted inactivation of dipeptidyl peptidase 9 enzymatic activity causes mouse neonate lethality.Extracellular proteases as targets for drug development

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P2860

Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

http://www.wikidata.org/entity/Q35809679

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2000 nî lūn-bûn

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name

Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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Proceedings of the National Academy of Sciences of the United States of America

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Enhanced insulin secretion and improved glucose tolerance in mice lacking CD26.

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A M Bernard

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D J Drucker

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D Marguet

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L Baggio

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M Pierres

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N Wagtmann

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P F Nielsen

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T Kobayashi

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T Watanabe

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U Ribel

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P2860

Cloning and characterization of a novel peptidase from rat and human ileum

Attractin (DPPT-L), a member of the CUB family of cell adhesion and guidance proteins, is secreted by activated human T lymphocytes and modulates immune cell interactions

Mouse fibroblast-activation protein--conserved Fap gene organization and biochemical function as a serine protease

Direct association of adenosine deaminase with a T cell activation antigen, CD26

Dipeptidyl-peptidase IV hydrolyses gastric inhibitory polypeptide, glucagon-like peptide-1(7-36)amide, peptide histidine methionine and is responsible for their degradation in human serum

Glucose intolerance caused by a defect in the entero-insular axis: a study in gastric inhibitory polypeptide receptor knockout mice

The enteroinsular axis in dipeptidyl peptidase IV-negative rats

Improved glucose tolerance in Zucker fatty rats by oral administration of the dipeptidyl peptidase IV inhibitor isoleucine thiazolidide.

CD26, let it cut or cut it down.

Dipeptidyl-peptidase IV (CD26)--role in the inactivation of regulatory peptides.

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6874-6879

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10.1073/PNAS.120069197

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97

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10823914

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18768

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