Cell Signaling Technology

Product Pathways - Neuroscience

CDK5 Antibody #2506

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R Endogenous 30 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

CDK5 Antibody detects endogenous levels of total CDK5 protein, recombinant CDK5 but not recombinant CDK1-4 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the sequence of human CDK5. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from PC12 and Jurkat cells, using CDK5 Antibody.

Western Blotting

Western Blotting

Western blot analysis of recombinant CDK1-5, using CDK5 Antibody (top) and GST Antibody #2622 (bottom).

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 (T1/2 <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).

  1. Dhavan, R. and Tsai, L.H. (2001) Nat Rev Mol Cell Biol 2, 749-59.
  2. Patrick, G.N. et al. (1998) J Biol Chem 273, 24057-64.
  3. Lee, M.S. et al. (2000) Nature 405, 360-4.
  4. Kusakawa, G. et al. (2000) J Biol Chem 275, 17166-72.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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