scholarly journals The reduction of insulin gene transcription in HIT-T15 beta cells chronically exposed to high glucose concentration is associated with the loss of RIPE3b1 and STF-1 transcription factor expression.

1995 ◽  
Vol 9 (9) ◽  
pp. 1127-1134 ◽  
Author(s):  
A Sharma ◽  
L K Olson ◽  
R P Robertson ◽  
R Stein
Keyword(s):  
Transcription Factor ◽  
Beta Cells ◽  
Gene Transcription ◽  
High Glucose ◽  
Glucose Concentration ◽  
Insulin Gene ◽  
High Glucose Concentration ◽  
Factor Expression ◽  
Transcription Factor Expression ◽  
Insulin Gene Transcription

scholarly journals ATF3 expression is induced by low glucose in pancreatic ^|^alpha; and ^|^beta; cells and regulates glucagon but not insulin gene transcription

2014 ◽  
Vol 61 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Yong-Soo Lee ◽  
Masaki Kobayashi ◽  
Osamu Kikuchi ◽  
Tsutomu Sasaki ◽  
Hiromi Yokota-Hashimoto ◽  
...  
Keyword(s):  
Beta Cells ◽  
Gene Transcription ◽  
Insulin Gene ◽  
Low Glucose ◽  
Atf3 Expression ◽  
Insulin Gene Transcription

c-jun inhibits transcriptional activation by the insulin enhancer, and the insulin control element is the target of control

1994 ◽  
Vol 14 (1) ◽  
pp. 655-662
Author(s):  
E Henderson ◽  
R Stein
Keyword(s):  
Skeletal Muscle ◽  
Beta Cells ◽  
Gene Transcription ◽  
Transcriptional Activation ◽  
Pancreatic Beta Cells ◽  
Insulin Gene ◽  
Control Element ◽  
Basic Leucine Zipper ◽  
Insulin Control ◽  
Insulin Gene Transcription

Selective transcription of the insulin gene in pancreatic beta cells is regulated by its enhancer, located between nucleotides -340 and -91 relative to the transcription start site. One of the principal control elements within the enhancer is found between nucleotides -100 and -91 (GCCATCTGCT, referred to as the insulin control element [ICE]) and is regulated by both positive- and negative-acting transcription factors in the helix-loop-helix (HLH) family. It was previously shown that the c-jun proto-oncogene can repress insulin gene transcription. We have found that c-jun inhibits ICE-stimulated transcription. Inhibition of ICE-directed transcription is mediated by sequences within the carboxy-terminal region of the protein. These c-jun sequences span an activation domain and the basic leucine zipper DNA binding-dimerization region of the protein. Both regions of c-jun are conserved within the other members of the jun family: junB and junD. These proteins also suppress ICE-mediated transcription. The jun proteins do not appear to inhibit insulin gene transcription by binding directly to the ICE. c-jun and junB also block the trans-activation potential of two skeletal muscle-specific HLH proteins, MyoD and myogenin. These results suggests that the jun proteins may be common transcription control factors used in skeletal muscle and pancreatic beta cells to regulate HLH-mediated activity. We discuss the possible significance of these observations to insulin gene transcription in pancreatic beta cells.

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