Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll PDX-1 and MafA play a crucial role in pancreatic beta-cell differentiation and maintenance of mature beta-cell function Kaneto H; Miyatsuka T; Kawamori D; Yamamoto K; Kato K; Shiraiwa T; Katakami N; Yamasaki Y; Matsuhisa M; Matsuoka TAEndocr J 2008[May]; 55 (2): 235-52Pancreatic and duodenal homeobox factor-1 (PDX-1) plays a crucial role in pancreas development, beta-cell differentiation, and maintenance of mature beta-cell function. PDX-1 expression is maintained in pancreatic precursor cells during pancreas development but becomes restricted to beta-cells in mature pancreas. In mature beta-cells, PDX-1 transactivates the insulin and other genes involved in glucose sensing and metabolism such as GLUT2 and glucokinase. MafA is a recently isolated beta-cell-specific transcription factor which functions as a potent activator of insulin gene transcription. Furthermore, these transcription factors play an important role in induction of insulin-producing cells in various non-beta-cells and thus could be therapeutic targets for diabetes. On the other hand, under diabetic conditions, expression and/or activities of PDX-1 and MafA in beta-cells are reduced, which leads to suppression of insulin biosynthesis and secretion. It is likely that alteration of such transcription factors explains, at least in part, the molecular mechanism for beta-cell glucose toxicity found in diabetes.|Animals[MESH]|Cell Differentiation/physiology[MESH]|Diabetes Mellitus, Type 2/etiology/metabolism/physiopathology[MESH]|Disease Models, Animal[MESH]|Glucose/metabolism[MESH]|Homeodomain Proteins/*physiology[MESH]|Humans[MESH]|Insulin-Secreting Cells/cytology/*physiology[MESH]|Insulin/metabolism[MESH]|Maf Transcription Factors, Large/*physiology[MESH]|Mice[MESH]|Rats[MESH]|Trans-Activators/*physiology[MESH] |