Disease relevance of Cdk5alpha

• Constitutive over-expression of dCdk5alpha in transgenic flies significantly prolongs their recovery time from 5 min to O(2) deprivation or anoxia in older flies (15 days) but not in young ones (4 days) [1].
• Baculovirus IAPs and P35, an inhibitor of aspartate-specific cysteine proteases, blocked Doom-induced apoptosis [2].
• In contrast, expression of P35 does not suppress norpA retinal degeneration, although a small delay in the rate of degeneration is observed in low light-low temperature conditions [3].

High impact information on Cdk5alpha

• Cell death, but not morphological changes, was blocked by the caspase inhibitor P35 [4].
• Expression of the antiapoptotic P35 protein suppresses this phenotype in the eye, suggesting that apoptosis is the major cellular defect caused by overexpression of K protein [5].
• The complex of Ckd5/Cdk5alpha is essential for neurite outgrowth during neuronal differentiation and possibly also for neuronal degeneration [1].
• Cyclin-dependent kinase 5 activator (Cdk5alpha) is an activator of Cdk5 kinase activity and its expression is restricted to neurons [1].
• We showed previously that ectopic expression of either rpr or hid triggers rapid PCD in adult photoreceptors, and this is completely suppressed by the coexpression of the baculoviral P35 caspase inhibitor [3].

Anatomical context of Cdk5alpha

• The anti-apoptotic baculoviral P35 protein acts downstream of hid activity to suppress the photoreceptor cell death driven by rpr and hid [6].

References