Regulation of insulin gene transcription by nutrients

1996 ◽  
Vol 24 (2) ◽  
pp. 368-372 ◽  
Author(s):  
K. Docherty ◽  
W. M. Macfarlane ◽  
M. L. Read ◽  
S. B. Smith ◽  
M. E. Wilson ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Insulin Gene ◽  
Insulin Gene Transcription

Analysis of ∼700 Human Tissue Samples Identifies microRNAs That Are Associated with, Predictive of, and Necessary for Insulin Gene Transcription

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2160-P
Author(s):  
ANAND HARDIKAR ◽  
WILSON WONG ◽  
MUGDHA JOGLEKAR ◽  
LOUISE T. DALGAARD ◽  
ALICIA JENKINS ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Human Tissue ◽  
Insulin Gene ◽  
Tissue Samples ◽  
Insulin Gene Transcription

scholarly journals The Islet β Cell-enriched MafA Activator Is a Key Regulator of Insulin Gene Transcription

2005 ◽  
Vol 280 (12) ◽  
pp. 11887-11894 ◽  
Author(s):  
Li Zhao ◽  
Min Guo ◽  
Taka-aki Matsuoka ◽  
Derek K. Hagman ◽  
Susan D. Parazzoli ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Insulin Gene ◽  
Β Cell ◽  
Insulin Gene Transcription

scholarly journals PIASy is a SUMOylation-independent negative regulator of the insulin transactivator MafA

2019 ◽  
Vol 63 (4) ◽  
pp. 297-308
Author(s):  
Suzuka Onishi ◽  
Kohsuke Kataoka
Keyword(s):  
Transcription Factors ◽  
Gene Transcription ◽  
Gene Promoter ◽  
Terminal Region ◽  
Insulin Gene ◽  
Negative Regulator ◽  
Β Cell ◽  
E3 Ligases ◽  
Amino Terminal ◽  
Insulin Gene Transcription

Insulin plays a central role in glucose homeostasis and is produced exclusively by pancreatic islet β-cells. Insulin gene transcription is regulated by a set of β-cell-enriched transcription factors that bind to cis-regulatory elements within the promoter region, and regulation of the insulin gene promoter is closely linked to β-cell functionality. PIASy, a member of the PIAS family of SUMO E3 ligases, is thought to affect insulin gene transcription, but its mechanism of action is not fully understood. Here, we demonstrate that PIASy interacts with MafA and represses insulin gene promoter activity. MafA is a β-cell-restricted basic leucine-zipper transcriptional activator that binds to the C1 element of the insulin gene promoter. In line with previous studies showing the transactivator domain of MafA is SUMOylated, PIASy enhanced the SUMOylation of MafA. However, a SUMOylation-deficient mutant of MafA was still repressed by PIASy, indicating that this modification is dispensable for repression. Using a series of MafA and PIASy mutants, we found that the basic domain of MafA and the amino-terminal region of PIASy containing the SAP domain are necessary for their interaction. In addition, SUMO-interacting motif 1 (SIM1) at the carboxyl-terminal region of PIASy was required to repress the synergistic transactivation of MafA, Pdx1, and Beta2, transcription factors playing central roles in β-cell differentiation and function. The PINIT and SP-RING domains in the middle region of PIASy were dispensable. These findings suggest that PIASy binds to MafA through the SAP domain and negatively regulates the insulin gene promoter through a novel SIM1-dependent mechanism.

scholarly journals Glucose Regulation of Insulin Gene Transcription and Pre-mRNA Processing in Human Islets

Diabetes ◽  
2007 ◽  
Vol 56 (3) ◽  
pp. 827-835 ◽  
Author(s):  
C. Evans-Molina ◽  
J. C. Garmey ◽  
R. Ketchum ◽  
K. L. Brayman ◽  
S. Deng ◽  
...  
Keyword(s):  
Gene Transcription ◽  
Human Islets ◽  
Mrna Processing ◽  
Insulin Gene ◽  
Glucose Regulation ◽  
Insulin Gene Transcription

scholarly journals Repression of insulin gene expression by adenovirus type 5 E1a proteins.

1987 ◽  
Vol 7 (3) ◽  
pp. 1164-1170 ◽  
Author(s):  
R W Stein ◽  
E B Ziff
Keyword(s):  
Gene Transcription ◽  
Pancreatic Beta Cells ◽  
Adenovirus Type ◽  
Insulin Gene ◽  
Mrna Levels ◽  
Beta Cell Line ◽  
Element Activity ◽  
Relationship Of ◽  
Adenovirus Type 5 ◽  
Insulin Gene Transcription

Insulin gene transcription relies on enhancer and promoter elements which are active in pancreatic beta cells. We showed that adenovirus type 5 infection of HIT T-15 cells, a transformed hamster beta cell line, represses insulin gene transcription and mRNA levels. Using expression plasmids transiently introduced into HIT T-15 cells, we showed that adenovirus type 5 E1a transcription regulatory proteins repress insulin enhancer-promoter element activity as assayed with a surrogate xanthine-guanine phosphoribosyltransferase gene. We relate E1a repression of the insulin gene to other examples of repression of enhancer-dependent genes by E1a and discuss the possible relationship of this repression to insulin gene regulation.

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