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Cyclin dependent kinase 5 (CDK5): a possible link between neuropathologies and diabetes
Author(s) -
Stevens Jessica,
Aguanno Ann
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.492.2
Subject(s) - cyclin dependent kinase 5 , kinase , biology , phenotype , insulin , microbiology and biotechnology , cyclin dependent kinase 2 , endocrinology , neuroscience , medicine , protein kinase a , biochemistry , gene
We study the role of CDK5 in mammalian development. Although a member of the cyclin dependent kinase family, CDK5 has been shown to influence differentiation of non‐dividing nervous tissues. Previously, our lab has used PC12 cells to study CDK5's role in neuronal development. Experiments involving growth factor‐induced (NGF, FGF) differentiation of PC12 cells in the presence of CDK5 inhibitors resulted in drastic morphological changes. Recent reports suggest CDK5 may also play an extra neuronal role. Here we report the impact of CDK5 manipulation in pancreatic tissue using the acinar cell line AR42J. The transdiffereniation of these cells from non‐insulin producing (acinar) to insulin producing (beta‐like) cells was induced by the administration of the chemical exendin‐4. Cells were assayed for the insulin phenotype, with a primary rat islet cell line used as a positive control. To asses the role of CDK5 in the pathway to this phenotype, insulin levels were quantified following simultaneous treatment of these cells with both exendin‐4 and the CDK5 specific inhibitor, olomoucine. Results suggest a role for CDK5 in the acquisition of this insulin phenotype. This data, coupled with the neurological role of CDK5, suggests a correlation between pathologies such as Alzheimer's disease and Type 2 Diabetes.