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

Figure 3

Choi et al. [1] show that PPARγ activity is controlled by the CDK5. Obesity leads to the various signals that cause the cleavage of p35 to p25 which will then translocates to the nucleus and forms a bond with CDK5 and activates it. CDK5 phosphorylates the PPARγ receptor on serine residue 273 averts the transcription of antiobesity effects, while the full activation of PPARγ by PPARγ agonists may probably responsible for the weight gain and Fluid retention.