CDK8 (P455) Antibody #4106
Filter:
- WB
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 53 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
CDK8 (P455) Antibody detects endogenous levels of total CDK8 protein.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro455 of human CDK8. Antibodies are purified using protein A and peptide affinity chromatography.
Background
The mammalian Mediator Complex is a multi-subunit protein complex that couples specific transcriptional regulators to RNA polymerase II (Pol II) and the basal transcription machinery. Interactions between distinct Mediator subunits and transcription factors allow for specific gene regulation (reviewed in 1).
Mediator complex interactions control various biological processes, including insulin signaling (2), NF-κB-dependent signaling (3), stem cell pluripotency and self renewal (4,5), and proliferation of colon cancer cells (6,7).
CDK8/Cyclin C, along with Med12 and Med13, constitute a subcomplex within the Mediator Complex thought to act as a molecular switch, inhibiting Pol II recruitment and transcription initiation (8,9). Expression of CDK8 abrogates E2F-1-dependent inhibition of β-catenin activity in colon cancer cells (9). High levels of CDK8 coincide with high β-catenin-dependent transcription in colon cancer cells, and their proliferation can be inhibited by suppressing CDK8 expression (8).
CDK8 can phosphorylate Ser727 on STAT1, which reduces natural killer (NK) cell toxicity (10,11). As such, inhibitors are being pursued as potential therapeutics to enhance NK cell activity and combat a variety of cancer types (12,13).
Mediator complex interactions control various biological processes, including insulin signaling (2), NF-κB-dependent signaling (3), stem cell pluripotency and self renewal (4,5), and proliferation of colon cancer cells (6,7).
CDK8/Cyclin C, along with Med12 and Med13, constitute a subcomplex within the Mediator Complex thought to act as a molecular switch, inhibiting Pol II recruitment and transcription initiation (8,9). Expression of CDK8 abrogates E2F-1-dependent inhibition of β-catenin activity in colon cancer cells (9). High levels of CDK8 coincide with high β-catenin-dependent transcription in colon cancer cells, and their proliferation can be inhibited by suppressing CDK8 expression (8).
CDK8 can phosphorylate Ser727 on STAT1, which reduces natural killer (NK) cell toxicity (10,11). As such, inhibitors are being pursued as potential therapeutics to enhance NK cell activity and combat a variety of cancer types (12,13).
- Malik, S. and Roeder, R.G. (2005) Trends Biochem Sci 30, 256-63.
- Wang, W. et al. (2009) Dev Cell 16, 764-71.
- van Essen, D. et al. (2009) PLoS Biol 7, e73.
- Tutter, A.V. et al. (2009) J Biol Chem 284, 3709-18.
- Varelas, X. et al. (2008) Nat Cell Biol 10, 837-48.
- Firestein, R. et al. (2008) Nature 455, 547-51.
- Morris, E.J. et al. (2008) Nature 455, 552-6.
- Knuesel, M.T. et al. (2009) Mol Cell Biol 29, 650-61.
- Knuesel, M.T. et al. (2009) Genes Dev 23, 439-51.
- Bancerek, J. et al. (2013) Immunity 38, 250-62.
- Putz, E.M. et al. (2013) Cell Rep 4, 437-44.
- Dale, T. et al. (2015) Nat Chem Biol 11, 973-80.
- Rzymski, T. et al. (2017) Oncotarget , .
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