|Positive WB detected in||HepG2 cells, mouse pancreas tissue, NIH/3T3 cells, mouse brain tissue|
|Positive IHC detected in||mouse kidney tissue, human renal cell carcinoma tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Positive IF detected in||NIH/3T3 cells|
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Immunofluorescence (IF)||IF : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
10430-1-AP targets CDK5 in WB, IHC, IF,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||CDK5 fusion protein Ag0686|
|Full Name||cyclin-dependent kinase 5|
|Calculated molecular weight||31 kDa, 33 kDa|
|Observed molecular weight||33 kDa|
|GenBank accession number||BC005115|
|Gene ID (NCBI)||1020|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Cyclin-dependent kinase 5 (CDK5), belongs to the cyclin-dependent kinase family, is a proline-directed serine/threonine-protein kinase that essential for neuronal cell cycle arrest and differentiation and may be involved in apoptotic cell death in neuronal diseases by triggering abortive cell cycle re-entry. CDK5 predominantly expressed in neurons where it phosphorylates both high molecular weight neurofilaments and microtubule-associated protein tau.
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Potent effects of dioscin against hepatocellular carcinoma through regulating TIGAR-mediated apoptosis, autophagy and DNA damage.
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Ginsenoside compound K ameliorates Alzheimer's disease in HT22 cells by adjusting energy metabolism.
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Nestin protects mouse podocytes against high glucose-induced apoptosis by a Cdk5-dependent mechanism.
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Hypoxia induces HT-22 neuronal cell death via Orai1/CDK5 pathway-mediated Tau hyperphosphorylation.
Inhibition of Cdk5 rejuvenates inhibitory circuits and restores experience-dependent plasticity in adult visual cortex.