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International Journal of Endocrinology
Volume 2011 (2011), Article ID 530274, 10 pages
Review Article

Cyclin-Dependent Kinase 5/p35/p39: A Novel and Imminent Therapeutic Target for Diabetes Mellitus

1Department of Pharmaceutical Sciences, Faculty of Health, Medical Sciences, Indigenous and Alternative Systems of Medicine, Sam Higginbottom Institute of Agriculture, Technology & Sciences (SHIATS), Allahabad 211007, India
2Department of Pharmacology, Faculty of Pharmacy, Jamia Hamdard, New Delhi 110062, India

Received 16 July 2011; Accepted 10 August 2011

Academic Editor: A. L. Barkan

Copyright © 2011 Danish Ahmed and Manju Sharma. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Present therapies to minify hyperglycaemia and insulin resistance mainly target ATP-sensitive K+ channels ( K A T P ) of pancreatic cells and PPAR-γ to enhance the insulin secretion and potential for GLUT expression, respectively. These current approaches are frequently associated with the various side effects such as hypoglycaemia and cardiovascular adverse events. CDK5 is a serine/threonine protein kinase, which forms active complexes with p35 or p39 found principally in neurons and in pancreatic β cells. Pieces of evidence from recent studies recommend the vital role of CDK5 in physiological functions in nonneuronal cells such as glucose-stimulated insulin secretion in pancreatic cells. Inhibition of CDK5 averts the decrease of insulin gene expression through the inhibition of nuclear translocation of PDX-1 which is a transcription factor for the insulin gene. The present pieces of evidence designate that CDK5 might be a potential drug target for the regulation of glucose-stimulated insulin secretion in the treatment of diabetes mellitus.