Diabetes - Islet Patophysiology
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- 2010
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Mark
The interactions of thioredoxin and the complement system
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- Contribution to journal › Published meeting abstract
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Mark
Pyruvate dehydrogenase kinase 1 controls mitochondrial metabolism and insulin secretion in INS-1 832/13 clonal beta-cells
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- Contribution to journal › Article
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Mark
Complement inhibitor C4b-binding protein (C4BP) binding to islet amyloid polypeptide prevents complement activation and further fibril formation in the endocrine pancreas
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- Contribution to journal › Published meeting abstract
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Mark
ClC-3-A Granular Anion Transporter Involved in Insulin Secretion? Response
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- Contribution to journal › Letter
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Mark
Enhancement of glucagon secretion in mouse and human pancreatic alpha cells by protein kinase C (PKC) involves intracellular trafficking of PKCalpha and PKCdelta.
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- Contribution to journal › Article
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Mark
The role of wnt antagonists in impaired beta cell exocytosis
2010) 46th Annual Meeting of the European-Association-for-the- Study-of-Diabetes (EASD) In Diabetologia 53(Suppl. 1). p.91-91(
- Contribution to journal › Published meeting abstract
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Mark
TCF7L2-conferred apoptosis in pancreatic beta cells involves the p53 pathway
2010) 46th Annual Meeting of the European-Association-for-the- Study-of-Diabetes (EASD) In Diabetologia 53(Suppl. 1). p.298-298(
- Contribution to journal › Published meeting abstract
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Mark
Polymorphisms in CACNA1D affect insulin release and channel expression and associate with type 2 diabetes
2010) 46th Annual Meeting of the European-Association-for-the- Study-of-Diabetes (EASD) In Diabetologia 53(Suppl. 1). p.296-296(
- Contribution to journal › Published meeting abstract
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Mark
Complement receptor C5aR is expressed in pancreatic islets and affects glucose-induced insulin and glucagon secretion
2010) 46th Annual Meeting of the European-Association-for-the- Study-of-Diabetes (EASD) In Diabetologia 53(Suppl. 1). p.531-531(
- Contribution to journal › Published meeting abstract
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Mark
GLP-1 inhibits and adrenaline stimulates glucagon release by differential modulation of N- and L-type Ca2+ channel-dependent exocytosis.
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- Contribution to journal › Article