Anti-Cyclin-dependent kinase 9 Cdk9 Antibody

Primary Antibodies

Store vial at -20°C prior to opening. Aliquot contents and freeze at -20°C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4°C as an undiluted liquid. Dilute only prior to immediate use. Expiration date is one (1) year from date of opening.

Liquid (sterile filtered)

This antibody has been tested for use in ELISA, immunoprecipitation, immunocytochemistry, and by western blot. Specific conditions for reactivity should be optimized by the end user. Expect a band at approximately 43 kDa corresponding to CDK9 (PITALRE) by western blotting in the appropriate cell lysate or extract. HeLa cells may be used as a positive control.

CDK9

CDK9 (PITALRE) (also known as cyclin-dependent kinase 9, Serine/threonine-protein kinase PITALRE, C-2K and Cell division cycle 2-like protein kinase 4) is a member of the cyclin-dependent protein kinase (CDK) family. CDK family members are highly similar to the gene products of S. cerevisiae cdc28, and S. pombe cdc2, and known as important cell cycle regulators. CDK9 (PITALRE) interacts with a conserved domain in the TRAF-C region of the tumor necrosis factor signal transducer TRAF2. This kinase also was found to be a component of the multiprotein complex TAK/P-TEFb, which is an elongation factor for RNA polymerase II-directed transcription and functions by phosphorylating the C-terminal domain of the largest subunit of RNA polymerase II. This protein forms a complex with and is regulated by its regulatory subunit cyclin T or cyclin K. HIV-1 Tat protein was found to interact with this protein and cyclin T, which suggested a possible involvement of this protein in AIDS. Tat stimulates human HIV-1 viral transcription elongation. This suggests that cyclin T1/cdk9(PITALRE) is one of the HIV-1 required host cellular cofactors generated during T cell activation. Cyclin T1/cdk9(PITALRE) is shown to interact with Tat to restore Tat activation in HeLa nuclear extracts depleted of P-TEFb. The cdk9(PITALRE) activity and cyclin T1 are essential for activation of transcription when tethered to the heterologous Rev response element RNA via the regulator of expression of virion Rev. CDK9 (PITALRE) is a ubiquitously expressed nuclear protein.

0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2, 0.01% (w/v) Sodium Azide

75 mg/mL by Refractometry

Protein kinase involved in the regulation of transcription. Member of the cyclin-dependent kinase pair (CDK9/cyclin-T) complex, also called positive transcription elongation factor b (P-TEFb), which facilitates the transition from abortive to productive elongation by phosphorylating the CTD (C-terminal domain) of the large subunit of RNA polymerase II (RNAP II) POLR2A, SUPT5H and RDBP. This complex is inactive when in the 7SK snRNP complex form. Phosphorylates EP300, MYOD1, RPB1/POLR2A and AR, and the negative elongation factors DSIF and NELF. Regulates cytokine inducible transcription networks by facilitating promoter recognition of target transcription factors (e.g. TNF-inducible RELA/p65 activation and IL-6-inducible STAT3 signaling). Promotes RNA synthesis in genetic programs for cell growth, differentiation and viral pathogenesis. P-TEFb is also involved in cotranscriptional histone modification, mRNA processing and mRNA export. Modulates a complex network of chromatin modifications including histone H2B monoubiquitination (H2Bub1), H3 lysine 4 trimethylation (H3K4me3) and H3K36me3; integrates phosphorylation during transcription with chromatin modifications to control co-transcriptional histone mRNA processing. The CDK9/cyclin-K complex has also a kinase activity towards CTD of RNAP II and can substitute for CDK9/cyclin-T P-TEFb in vitro. Replication stress response protein; the CDK9/cyclin-K complex is required for genome integrity maintenance, by promoting cell cycle recovery from replication arrest and limiting single- stranded DNA amount in response to replication stress, thus reducing the breakdown of stalled replication forks and avoiding DNA damage. In addition, probable function in DNA repair of isoform 2 via interaction with KU70/XRCC6. Promotes cardiac myocyte enlargement. RPB1/POLR2A phosphorylation on 'Ser-2' in CTD activates transcription. AR phosphorylation modulates AR transcription factor promoter selectivity and cell growth. DSIF and NELF phosphorylation promotes transcription by inhibiting their negative effect. The phosphorylation of MYOD1 enhances its transcriptional activity and thus promotes muscle differentiation.

Boster Bio Anti-Cyclin-dependent kinase 9 Cdk9 Antibody (Catalog # A00794). Tested in ELISA, IHC, IP, WB applications. This antibody reacts with Human, Mouse.

Ubiquitous.