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>   home   >   Products   >   Primary Antibodies   >   Microbiology   >   CDK9 Antibody   

CDK9 Antibody

Rabbit Polyclonal Antibody

     
  • IHC - CDK9 Antibody ALS11315
    Anti-CDK9 antibody IHC of human skin.
  • ICC - CDK9 Antibody ALS11315
    Anti-cdk9 (PITALRE) Antibody - Immunocytochemical Staining.
  • SPECIFICATION
  • CITATIONS
  • PROTOCOLS
  • BACKGROUND
Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
WB, IHC-P, ICC, E, IP
Primary Accession P50750
Reactivity Human, Mouse, Rat
Host Rabbit
Clonality Polyclonal
Calculated MW 43kDa
Dilution ELISA (1:10000-1:50000), IHC-P (1:500), WB (1:500-1:3000)
Additional Information
Gene ID 1025
Other Names Cyclin-dependent kinase 9, 2.7.11.22, 2.7.11.23, C-2K, Cell division cycle 2-like protein kinase 4, Cell division protein kinase 9, Serine/threonine-protein kinase PITALRE, Tat-associated kinase complex catalytic subunit, CDK9, CDC2L4, TAK
Target/Specificity Multiple synthetic peptides corresponding to C-terminal and N-terminal domains of the protein coded by the human gene cdk9 (PITALRE).
Reconstitution & Storage Store vial at -20 C or below prior to opening. Dilute only prior to immediate use. Aliquot contents and freeze at -20 C or below. Avoid cycles of freezing and thawing.
PrecautionsCDK9 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name CDK9
Synonyms CDC2L4, TAK
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.
Cellular Location 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
Tissue Location Ubiquitous.
Research Areas
Citations (0)

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Background

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.

References

Grana X.,et al.Proc. Natl. Acad. Sci. U.S.A. 91:3834-3838(1994).
Best J.L.,et al.Biochem. Biophys. Res. Commun. 208:562-568(1995).
Liu H.,et al.Gene 252:51-59(2000).
Kalnine N.,et al.Submitted (OCT-2004) to the EMBL/GenBank/DDBJ databases.
Humphray S.J.,et al.Nature 429:369-374(2004).

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$ 395.00
Cat# ALS11315
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