MafA is a basic leucine zipper transcription factor expressed within the beta cells of the pancreas and is required to maintain normal glucose homeostasis as it is involved in various aspects of beta cell biology. MafA protein levels are known to increase in response to high glucose through mechanisms that have yet to be fully characterized. We investigated whether discrete intracellular signaling events control mafA expression. We found that the general kinase inhibitor staurosporine induces mafA expression without altering the stability of the protein. Inhibition of the MAP-kinase JNK mimics the effects of staurosporine on the expression of mafA. Calmodulin kinase and calcium signaling are also important in stimulating mafA expression by high glucose. However, staurosporine, JNK, and calmodulin kinase have different effects on the induction of insulin expression. These data reveal that MafA levels are tightly controlled by the coordinated action of multiple kinase pathways.
|Number of pages||5|
|Journal||Archives of Biochemistry and Biophysics|
|State||Published - Dec 15 2008|
Bibliographical noteFunding Information:
This work was supported by NIH/NIDDK Grant 5R01DK067581 and the National Center for Research Resources Grant P20 RR20171 and a Pre-doctoral Fellowship from the American Heart Association, Great Rivers Affiliate, to N.L.V.
- Beta cells
ASJC Scopus subject areas
- Molecular Biology