Document Detail


Regulation of β-cell-specific and glucose-dependent MafA expression.
MedLine Citation:
PMID:  21278484     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
MafA, a basic-leucine zipper transcription factor that is important to pancreatic β-cell function, is regulated by several intricate mechanisms. MafA undergoes extensive posttranslational modification by phosphorylation, ubiquitination and sumoylation, and these modifications regulate the turnover, DNA binding and transactivation function of the protein. Regulation of MafA expression is equally complex. The initial characterization of the β-cell-specific MafA promoter identified six conserved sequence domains. One of these regions in particular contains consensus motifs and binding sites for several β-cell-enriched transcription factors which ultimately play critical roles in controlling the expression of the gene. Interestingly, in cell culture, acute high glucose stimulation induces the accumulation of MafA, and MafA, in turn, regulates β-cell function. However, under chronic high glucose conditions, which occurs in the context of the diabetic state, β-cell function and, coincidentally, MafA levels decline. Currently, the mechanisms controlling the glucose-dependent accumulation of MafA are not well understood. This commentary highlights a recent report that further defines the regulation of β-cell-specific MafA expression and confirms the longstanding assumption that MafA transcription is upregulated in β-cells acutely cultured in high glucose similar to what may occur in vivo under normoglycemic conditions.
Authors:
Nathan L Vanderford
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-1-01
Journal Detail:
Title:  Islets     Volume:  3     ISSN:  1938-2022     ISO Abbreviation:  -     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-1-31     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101495366     Medline TA:  Islets     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Markey Cancer Center; University of Kentucky; Lexington, Kentucky USA.
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