Multiple kinases regulate mafA expression in the pancreatic beta cell line MIN6

Nathan L. Vanderford, Jamie E.L. Cantrell, Gabriel J. Popa, Sabire Özcan

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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.

Original languageEnglish
Pages (from-to)138-142
Number of pages5
JournalArchives of Biochemistry and Biophysics
Issue number2
StatePublished - Dec 15 2008

Bibliographical note

Funding 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
  • CaMK
  • Diabetes
  • Glucose
  • Insulin
  • JNK
  • MafA
  • Transcription

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology


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