CDK5 (D1F7M) Rabbit mAb #14145
- WB
- IP
- IF
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 30 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Simple Western™ | 1:10 - 1:50 |
| Immunoprecipitation | 1:50 |
| Immunofluorescence (Frozen) | 1:200 - 1:400 |
| Immunofluorescence (Immunocytochemistry) | 1:200 - 1:400 |
Storage
Protocol
Specificity / Sensitivity
CDK5 (D1F7M) Rabbit mAb recognizes endogenous levels of total CDK5 protein.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro253 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 (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).
Limited Uses
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