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By Nancy Y. Ip, Li-Huei Tsai

Cyclin established Kinase five offers a accomplished and updated number of experiences at the discovery, signaling mechanisms and features of Cdk5, in addition to the aptitude implication of Cdk5 within the remedy of neurodegenerative ailments. because the id of this distinct member of the Cdk kinfolk, Cdk5 has emerged as the most vital sign transduction mediators within the improvement, upkeep and fine-tuning of neuronal services and networking. extra reviews have published that Cdk5 can be linked to the legislation of neuronal survival in the course of improvement in addition to in neurodegenerative ailments. those observations point out that exact regulate of Cdk5 is vital for the legislation of neuronal survival. The pivotal function that Cdk5 seems to be to play in either the rules of neuronal survival and synaptic features therefore increases the attention-grabbing chance that Cdk5 inhibitors can have healing strength for the remedy of a few neurodegenerative diseases.

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J. Biol. Chem. 274, 4027 4035. P. (2001). Amphiphysin 1 binds the cyclin dependent kinase (cdk) 5 regulatory subunit p35 and is phosphorylated by cdk5 and cdc2. J. Biol. Chem. 276, 8104 8110. , and Takai, Y. (1996). Phosphorylation of Munc 18/n Sec1/rbSec1 by protein kinase C: its implication in regulating the interaction of Munc 18/n Sec1/rbSec1 with syntaxin. J. Biol. Chem. 271, 7265 7268. P. (1997). The SH3 domain of amphiphysin binds the proline rich domain of dynamin at a single site that defines a new SH3 binding consensus sequence.

2005). Kinetics of Src homology 3 domain association with the proline rich domain of dynamins: specificity, occlusion, and the effects of phosphorylation. J. Biol. Chem. 280, 23147 23156. B. (2005). Increased activity of cyclin dependent kinase 5 leads to attenuation of cocaine mediated dopamine signaling. Proc. Natl. Acad. Sci. A. 102, 1737 1742. J. (2003). Cdk5 is essential for synaptic vesicle endocytosis. Nat. Cell Biol. 5, 701 710. , and Matsui, H. (2002). Cdk5/p35 regulates neurotransmitter release through phosphorylation and down regulation of P/Q type voltage dependent calcium channel activity.

In (a), the cells were immunostained with anti  tubulin antibody. The localization of wild type CRMP1 EGFP showed filamentous structure, and this distribution pattern became diffusely distributed within the cytoplasm when co trans fected with Cdk5/p35 (b) (See Color Insert) embryonic brain, when compared to wild-type brain, thereby indicating that CRMP2 phosphorylated by Cdk5 reduced its affinity for tubulin in the embryonic mouse brain in vivo. To determine the role of GSK3b, we estimated the affinity of CRMP2 to tubulin in cell lysate of cortical neuron primary culture with or without LiCl, a GSK3b inhibitor.

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