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Rabbit Anti-CDK9 Antibody (CSB-PA005079ESR1HU)
Supplier: CUSABIO BIOTECH CO.
C-2K Antibody,Cell division cycle 2-like protein kinase 4 Antibody,Cell division protein kinase 9 Antibody,Serine/threonine-protein kinase PITALRE Antibody,Tat-associated kinase complex catalytic subunit Antibody,CDK9 Antibody,CDC2L4 Antibody, TAK AntibodyMore alternative names for the antibody
C-2K antibody|CDC2L4 antibody|Cdk 9 antibody|Cdk9 antibody|CDK9_HUMAN antibody|Cell division cycle 2-like protein kinase 4 antibody|Cell division protein kinase 9 antibody|CTK1 antibody|Cyclin dependent kinase 9 antibody|Cyclin-dependent kinase 9 antibody|PITALRE antibody|Serine/threonine-protein kinase PITALRE antibody|TAK antibody|Tat associated kinase complex catalytic subunit antibody
Anti-Cdk9 antibody (ab6544)
Anti-Cdk9 antibody (ab6544)
Recommended applications: ELISA, IHC
Recommended dilution: Recommended dilution:IHC:1:20-1:200
Recommended protocols: check protocols
|Catalogue No.|| |
Recombinant human Cyclin-dependent kinase 9 protein (153-372AA)
|Recommended dilution|| |
|Molecular weight|| |
Antigen Affinity Purified
Shipped at 4 Celcius Degree. Upon delivery aliquot and store at -20 Celcius Degree or -80 Celcius Degree. Avoid repeated freeze.
|Database links|| |
Entrez Gene:1025( Human), Entrez Gene:107951( Mouse), Entrez Gene:362110( Rat), Omim:603251( Human), SwissProt:P50750( Human), SwissProt:Q99J95( Mouse), SwissProt:Q641Z4( Rat), Unigene:150423( Human), Unigene:706809( Human), Unigene:27557( Mouse), Unigene:98228( Rat)
|Protein function|| |
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. .
|Protein tissue specificity|| |
|Involvement in disease|| |
Note=Chronic activation of CDK9 causes cardiac myocyte enlargement leading to cardiac hypertrophy, and confers predisposition to heart failure.
|Protein sequence and domain|| |
Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily.
|Protein post-translational modifications|| |
Autophosphorylation at Thr-186, Ser-347, Thr-350, Ser-353, Thr-354 and Ser-357 triggers kinase activity by promoting cyclin and substrate binding (e.g. HIV TAT) upon conformational changes. Thr-186 phosphorylation requires the calcium Ca(2+) signaling pathway, including CaMK1D and calmodulin. This inhibition is relieved by Thr-29 dephosphorylation. However, phosphorylation at Thr-29 is inhibitory within the HIV transcription initiation complex. Phosphorylation at Ser-175 inhibits kinase activity. Can be phosphorylated on either Thr-362 or Thr-363 but not on both simultaneously (PubMed:18566585). .; Dephosphorylation of Thr-186 by PPM1A and PPM1B blocks CDK9 activity and may lead to CDK9 proteasomal degradation. However, PPP1CA-mediated Thr-186 dephosphorylation is required to release P-TEFb from its inactive P-TEFb/7SK snRNP complex. Dephosphorylation of C-terminus Thr and Ser residues by protein phosphatase-1 (PP1) triggers CDK9 activity, contributing to the activation of HIV-1 transcription.; N6-acetylation of Lys-44 by CBP/p300 promotes kinase activity, whereas acetylation of both Lys-44 and Lys-48 mediated by PCAF/KAT2B and GCN5/KAT2A reduces kinase activity. The acetylated form associates with PML bodies in the nuclear matrix and with the transcriptionally silent HIV-1 genome; deacetylated upon transcription stimulation. .; Polyubiquitinated and thus activated by UBR5. This ubiquitination is promoted by TFIIS/TCEA1 and favors ‘Ser-2’ phosphorylation of RPB1/POLR2A CTD. .
|Protein cellular localization|| |
Nucleus. Cytoplasm. Nucleus, PML body. Note=Accumulates on chromatin in response to replication stress. Complexed with CCNT1 in nuclear speckles, but uncomplexed form in the cytoplasm. The translocation from nucleus to cytoplasm is XPO1/CRM1-dependent. Associates with PML body when acetylated.
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|Product type|| |
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