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Validated All-in-One™ qPCR Primer for CDK9(NM_001261.3) Search again
Product ID:
HQP000321
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
C-2k, CDC2L4, CTK1, PITALRE, TAK
Gene Description:
cyclin dependent kinase 9
Target Gene Accession:
NM_001261.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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 S. cerevisiae cdc28, and S. pombe cdc2, and known as important cell cycle regulators. This kinase 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. [provided by RefSeq].
Gene References into function
- The transcription elongation factor P-TEFb interacts with and phosphorylates Tat-SF1
- CDK9 may play an antiapoptotic role during monocyte differentiation
- NF-kappaB binds P-TEFb to stimulate transcriptional elongation by RNA polymerase II
- phosphorylates hSpt5
- P-TEFb containing cyclin K and Cdk9 can activate transcription via RNA.
- interaction with pRb
- CDK9 has the intrinsic property to shuttle between nucleus and cytoplasm, and enhanced expression of cyclin T1 promotes its nuclear localization.
- The interaction of cdk9 with the NF-kappaB factors can control HIV-1 transcription.
- chimeras between kinase-inactive mutant Cdk9 and truncated cyclin T1 proteins efficiently inhibit Tat transactivation and human immunodeficiency virus gene expression
- interaction with gp130
- Positive transcription elongation factor b (P-TEFb) comprises a cyclin (T1 or T2) and a kinase, cyclin-dependent kinase 9 (CDK9), which phosphorylates the carboxyl-terminal domain of RNA polymerase II
- CDK9 is constitutively expressed throughout the cell cycle, and its steady-state expression is independent of SKP2
- Fusion of the PML coiled-coil domain to Cdk9 forms high MW complexes to which cyclin T1 is recruited. The CC-Cdk9 chimera effectively inhibits HIV-1 Tat activation. Expression of CC-Cdk9 inhibits cell proliferation, as shown by colony-formation assay.
- major portion of nuclear P-TEFb is sequestered and inactivated by the coordinated actions of the 7SK snRNA
- RNAi-mediated gene silencing of P-TEFb in HeLa cells was not lethal and inhibited Tat transactivation and HIV-1 replication in host cells
- review of work indicating under some circumstances TAK/P-TEFb is likely to be limiting for HIV replication in CD4+ T cells and macrophages; review of mechanisms of regulation of the TAK/P-TEFb subunits in these cell types
- Cdk9 is a component of the elongation factor P-TEFb, in the STAT3-mediated expression of p21waf1.
- functional differences between the 42k and 55k isoforms of Cdk9 are likely to depend on access to substrates based on their differential subcellular localization and expression patterns
- Review. Cdk9 has dual transcriptional roles in hypertrophic growth and mitochondrial dysfunction in cardiac myocytes.
- CDK9 mediates TNF-alpha-induced MMP-9 transcription
- role in regulation of HIV-1 transcription elongation and histone methylation.
- HEXIM1 and HEXIM2 maintain the balance between active and inactive forms of P-TEFb, a heterodimeric complex composed of cyclin-dependent kinase 9 and cyclin T.
- Cdk9/Cyclin T1 complex is required for neuron differentiation induced by retinoic acid; in neuroblastoma and primary neuroectodermal tumor tumor Cdk9 is more expressed the more differentiated the tumor is.
- requirement of ICP22 and the U(L)13 protein kinase of HSV-1 in the posttranslational modification of RNA POL II
- Analysis of T-loop phosphorylation in Cdk9 indicated that phosphorylation of Thr(186), but not Ser(175), was essential for kinase activity.
- Existence of a feedback-loop between p53 and cdk9, pinpointing a novel mechanism by which p53 regulates the basal transcriptional machinery.
- The results establish that cdk9/cyclin T2a-mediated coactivation of MyoD depends on serine 37 phosphorylation.
- These data link the P-TEFb equilibrium to the intracellular transcriptional demand and proliferative/differentiated states of cells.
- Our data suggest that Tat-C/EBPbeta association is mediated through cdk9, and that phosphorylated C/EBPbeta may influence AIDS progression by increasing expression of HIV-1 genes.
- Cdk9/Cyclin T1 complex may be important in the activation/differentiation program of lymphoid cells and that its upregulation may contribute to malignant transformation.
- These results suggest that acetylation of CDK9 is an important posttranslational modification that is involved in regulating P-TEFb transcriptional elongation function.
- Upon induction of NF-kappaB, a subset of target genes is regulated differentially by either P-TEFb or DSIF.[P-TEFb, DSIF]
- K-cyclin/Cdk9 interaction greatly enhanced the kinase activity of Cdk9 toward p53.
- an IL-6-inducible STAT3 and CDK9 binding to the proximal gamma-FBG promoter as well as increased loading of RNA Pol II
- Parvin-beta might influence breast cancer progression
- while the P-TEFb level remains constant, the Brd4-P-TEFb interaction increases dramatically in cells progressing from late mitosis to early G(1).
- This data suggests an active role for the Cdk9/Cyclin T1 complex during lymphoid differentiation through germinal center reaction.
- TATA-box element mediates the assembly of processive transcription complexes responsive to CDK9 and that specific combinations of upstream activation binding sites contribute to the recruitment of these complexes
- GCN5 & P/CAF regulate CDK9 function by specifically acetylating the catalytic core of the enzyme especially a Lys needed for ATP coordination & the phosphotransfer reaction. Acetylation markedly reduces both the kinase function & transcriptional activity
- PP2B and PP1alpha cooperatively disrupt 7SK snRNP to release P-TEFb for transcription in response to Ca2+ signaling.
- Study shows that CDK9/CycT1 autophosphorylates on Thr186 in the activation segment and three C-terminal phosphorylation sites; autophosphorylation on all sites occurs in cis.
- The authors conclude that cdk9 plays a critical role in the optimization of expression of genes regulated by ICP22 and that one function of cdk9 in HSV-1-infected cells may be to bring ICP22 into the RNA Pol II transcriptional complex.
- contribution of Cdk9 activity to megakaryocytic differentiation
- Overexpression of PPM1A and the related PPM1B greatly reduced Cdk9 T-loop phosphorylation
- The authors provide evidence that Brd4 regulates P-TEFb kinase activity by inducing a negative pathway via phosphorylation of CDK9 at threonine 29 (T29) in the HIV transcription initiation complex, inhibiting CDK9 kinase activity.