Phospho-CDK5 (Tyr15) (E6C8N) Rabbit mAb #19051

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Supporting Data

REACTIVITY	H
SENSITIVITY	Endogenous
MW (kDa)	30
Source/Isotype	Rabbit IgG

Application Key:

WB-Western Blotting
IP-Immunoprecipitation

Species Cross-Reactivity Key:

H-Human

Product Information

Product Usage Information

Application	Dilution
Western Blotting	1:1000
Immunoprecipitation	1:50

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

Protocol

Specificity / Sensitivity

Phospho-CDK5 (Tyr15) (E6C8N) Rabbit mAb recognizes endogenous levels of CDK5 protein only when phosphorylated at Tyr15.

Species Reactivity:

Human

The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.

Species predicted to react based on 100% sequence homology:

Mouse, Rat

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr15 of human CDK5 protein.

Background

Cyclin-dependent kinases (CDKs) are serine/threonine kinases that are activated by cyclins and govern eukaryotic cell cycle progression. While CDK5 shares high sequence homology with its family members, it is thought mainly to function in postmitotic neurons to regulate the cytoarchitecture of these cells. Analogous to cyclins, the regulatory subunits p35 and p39 associate with and activate CDK5 despite the lack of sequence homology. CDK5 is ubiquitously expressed, with high levels of kinase activity detected primarily in the nervous system due to the narrow expression pattern of p35 and p39 in post-mitotic neurons. A large number of CDK5 substrates have been identified although no substrates have been specifically attributed to p35 or p39. Substrates of CDK5 include p35, PAK1, Src, β-catenin, tau, neurofilament-H, neurofilament-M, synapsin-1, APP, DARPP32, PP1-inhibitor, and Rb. p35 is rapidly degraded (T_1/2 <20 min) by the ubiquitin-proteasome pathway (1). However, p35 stability increases as CDK5 kinase activity decreases, likely as a result of decreased phosphorylation of p35 at Thr138 by CDK5 (2). Proteolytic cleavage of p35 by calpain produces p25 upon neurotoxic insult, resulting in prolonged activation of CDK5 by p25. Research studies have shown accumulation of p25 in neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS) (3,4).
Phosphorylation of CDK5 at Tyr15 has been shown to increase CDK5 activity in developing neurons and is thought to play a role in axon growth regulation among other associated functions (5).

Database Links

UniProt ID: Q00535

Entrez-Gene Id: 1020

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