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CDK7 Antibody (Center)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P50613 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 39038 Da |
| Gene ID | 1022 |
|---|---|
| Other Names | Cyclin-dependent kinase 7, 39 kDa protein kinase, p39 Mo15, CDK-activating kinase 1, Cell division protein kinase 7, Serine/threonine-protein kinase 1, TFIIH basal transcription factor complex kinase subunit, CDK7, CAK, CAK1, CDKN7, MO15, STK1 |
| Target/Specificity | This CDK7 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide selected from the Center region of Human CDK7. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | CDK7 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | CDK7 |
|---|---|
| Synonyms | CAK, CAK1, CDKN7, MO15, STK1 |
| Function | Serine/threonine kinase involved in cell cycle control and in RNA polymerase II-mediated RNA transcription. Cyclin-dependent kinases (CDKs) are activated by the binding to a cyclin and mediate the progression through the cell cycle. Each different complex controls a specific transition between 2 subsequent phases in the cell cycle. Required for both activation and complex formation of CDK1/cyclin-B during G2-M transition, and for activation of CDK2/cyclins during G1-S transition (but not complex formation). CDK7 is the catalytic subunit of the CDK-activating kinase (CAK) complex. Phosphorylates SPT5/SUPT5H, SF1/NR5A1, POLR2A, p53/TP53, CDK1, CDK2, CDK4, CDK6 and CDK11B/CDK11. CAK activates the cyclin-associated kinases CDK1, CDK2, CDK4 and CDK6 by threonine phosphorylation, thus regulating cell cycle progression. CAK complexed to the core-TFIIH basal transcription factor activates RNA polymerase II by serine phosphorylation of the repetitive C- terminal domain (CTD) of its large subunit (POLR2A), allowing its escape from the promoter and elongation of the transcripts (PubMed:9852112). Phosphorylation of POLR2A in complex with DNA promotes transcription initiation by triggering dissociation from DNA. Its expression and activity are constant throughout the cell cycle. Upon DNA damage, triggers p53/TP53 activation by phosphorylation, but is inactivated in turn by p53/TP53; this feedback loop may lead to an arrest of the cell cycle and of the transcription, helping in cell recovery, or to apoptosis. Required for DNA-bound peptides-mediated transcription and cellular growth inhibition. |
| Cellular Location | Nucleus. Cytoplasm. Cytoplasm, perinuclear region. Note=Colocalizes with PRKCI in the cytoplasm and nucleus (PubMed:15695176). Translocates from the nucleus to cytoplasm and perinuclear region in response to DNA-bound peptides (PubMed:19071173). |
| Tissue Location | Ubiquitous. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene is a member of the cyclin-dependent protein kinase (CDK) family. CDK family members are highly similar to the gene products of Saccharomyces cerevisiae cdc28, and Schizosaccharomyces pombe cdc2, and are known to be important regulators of cell cycle progression. This protein forms a trimeric complex with cyclin H and MAT1, which functions as a Cdk-activating kinase (CAK). It is an essential component of the transcription factor TFIIH, that is involved in transcription initiation and DNA repair. This protein is thought to serve as a direct link between the regulation of transcription and the cell cycle.
References
Zhou, M., et al., Proc. Natl. Acad. Sci. U.S.A. 100(22):12666-12671 (2003).
Kino, T., et al., Biochem. Biophys. Res. Commun. 298(1):17-23 (2002).
Schneider, E., et al., Oncogene 21(33):5031-5037 (2002).
Nekhai, S., et al., Virology 266(2):246-256 (2000).
Zhou, M., et al., Mol. Cell. Biol. 20(14):5077-5086 (2000).
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