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The Cyclin-dependent kinase 9 (CDK9) is critical for RNA Polymerase II (Pol II) transcription initiation, elongation, and termination in several key biological processes including development, differentiation, and cell fate responses.
Physical interaction between pRb and cdk9/cyclinT2 complex.
CDK7-mediated Ser-175 phosphorylation is a downstream nuclear event essential for facilitating CDK9 T-loop interactions with Tat
miR-613, as a tumour suppressor, involves in gastric cancer progression and metastasis by targeting CDK9
GRIP1 is phosphorylated at an N-terminal serine cluster by cyclin-dependent kinase-9 (CDK9), which is recruited into GC-induced GR:GRIP1:CDK9 hetero-complexes, producing distinct GRE-specific GRIP1 phospho-isoforms.
Recent studies have highlighted the importance of CDK9 in many relevant pathologic processes, like cancer, cardiovascular diseases, and viral replication.
This shows that CDK9 stimulates release of paused polymerase and activates transcription by increasing the number of transcribing polymerases and thus the amount of mRNA synthesized per time.
this study suggests that CDK2 and CDK9 are potential therapeutic targets in Neuroblastoma (NB) and that abrogating CDK2 and CDK9 activity by small molecules like dinaciclib is a promising strategy and a treatment option for NB patients
miR-206 is remarkably downregulated and is inversely correlated with CDK9 level in HCC cells. It is evident that miR-206 functions as a tumor suppressor through blocking CDK9-related pathway to induce apoptosis and inhibit HCC cell proliferation.
this study shows role of CDK9 in oncogenic processes of esophageal adenocarcinoma
CDK9, in addition to CDK1, has roles in mediating the growth inhibitory effect of dinaciclib on cyclin B1 in triple negative breast cancer
Cdk9 is a post-exposure drug target against human adenoviruses.
BRD4 and CDK9 have independent, coordinated roles in promoting the myofibroblast transition
RBPJ links MYC and transcriptional control through CDK9 in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH
Chemical degrader of BET bromodomain proteins, dBET6, led to the unexpected identification of BRD4 as master regulator of global transcription elongation in acute T-cell leukemia. BRD4 loss does not directly affect CDK9 localization.
H1 variant interphase phosphorylation is dynamically regulated in a site-specific and gene-specific fashion during pluripotent cell differentiation, and that enrichment of pS187-H1.4 at genes is positively related to their transcription. H1.4-S187 is likely to be a direct target of CDK9 during interphase, suggesting the possibility that this particular phosphorylation may contribute the release of paused RNA pol II
CDK9 is a player in the DNA damage response and is consistent with its participation in homology-directed recombination pathway by modulating BRCA1 response.
HSP90 downstream HSF1 gives positive feedback to the reactivation process through binding to cyclin-dependent kinase 9 (CDK9) and preventing it from undergoing degradation by the proteasome.
Quantitative measurement of the molecular interactions among Tat, CycT1 and CDK9 has showed that any third molecule enhances the binding between the other two molecules. These findings suggest that each component of the Tat:P-TEFb complex stabilizes the overall complex, thereby supporting the efficient transcriptional elongation during viral RNA synthesis.
We could conclude that there are many small molecules that bind to CDK9, but their lack of selectivity against other CDKs do not allow them to get to the clinical use
CDK9 clearly plays a fundamental role in early cellular growth and proliferation.
Pharmacological and genetic results present evidence that CDK9 is involved in the resolution of neutrophil-dependent inflammation.
The balance of Cdk9 and Larp7 plays a key role in cardiomyocyte proliferation and response to injury
cdk9 is essential for glia survival in adult Drosophila brain.
actin participates in transcription elongation by recruiting Cdk9,a catalytic subunit of P-TEFb, for phosphorylation of the Pol II C-terminal domain, and the actin-Cdk9 interaction promotes chromatin remodeling
Genetic transcription and RNA processing of PTefb kinase is coordinated on heat shock genes.
Cdk9 is required for heat shock gene expression, histone methylation and elongation factor recruitment.
SIRT2 deacetylates cyclin-dependent kinase 9 (CDK9) in a type I IFN-dependent manner and that the CDK9 deacetylation is essential for STAT1 phosphorylation at Ser-727.
Cdk9 plays a complex role in myocyte progenitor differentiation and apoptosis by regulating myogenic protein and muscle-specific microRNA expression.
findings revealed the crucial role of CDK9/Cyclin T1/Pol II pathway in promoting allorejection at multiple levels and may provide a new approach for transplantation tolerance induction through targeting CDK9
identified cyclin-dependent kinase 9 (Cdk9) as required for hepatocellular carcinoma disease maintenance
This study demonstrates that Ikaros directly interacts with GATA1, GATA2, and GATA3 as well as Cdk9/P-TEFb through specific protein domains.
Data show that the minimal 90-amino acid AF9 fragment in MLL-AF9 retains an ability to form higher order complexes with AF4*P-TEFb and with DOT1.
Data show that the CDK9 and cyclin T1 subunits of P-TEFb are present in mouse oocytes and preimplantation embryos, and that CDK9 is essential for embryonic genome activation in the mouse.
The present study examined whether Cdk9 forms a complex with GATA4 in mouse embryonic stem cells and is involved in their differentiation into cardiomyocytes.
Data report that a second cdk9 isoform, termed cdk9-55, plays a fundamental role in muscle regeneration and differentiation in vivo.
role in activating MyoD-dependent transcription
CDK9 has the intrinsic property to shuttle between nucleus and cytoplasm, and enhanced expression of cyclin T1 promotes its nuclear localization.
chronic activation of Cdk9 causes not only cardiomyocyte enlargement but also defective mitochondrial function, via diminished PGC-1 transcription, and a resulting susceptibility to apoptotic cardiomyopathy
PPARgamma-cdk9 interaction results in increased transcriptional activity of PPARgamma and therefore increased adipogenesis.
These data link the P-TEFb equilibrium to the intracellular transcriptional demand and proliferative/differentiated states of cells.
In mice with megakaryocytic GATA-1 deficiency, Cdk9 inhibition produced a fulminant but reversible megakaryoblastic disorder reminiscent of the transient myeloproliferative disorder of Down syndrome.
miR-1 and miR-133 may play significant roles in the myocardial differentiation of mouse ES cells, and Cdk9 may be involved in this process as a target of miR-1.
As receptor-activated Smads form transcriptional complexes, they are phosphorylated at an interdomain linker region by CDK8 and CDK9, which are components of transcriptional mediator and elongation complexes.
inhibition of CDK9 abrogated global transcriptional activity and rRNA production. Collectively, our data suggested that P-TEFb kinase activity is crucial for oocyte maturation, embryo development and regulation of RNA transcription in pig.
Full-length cDNA, morpholinos, and mutagenesis rescue constructs of cdk9L were used. Cdk9.S, Cdk9.L andCyclinT1 were expressed in the neural plate and neural plate border of neurula stage embryos and in the neural-crest-derived branchial arteries at the tailbud stage. Cdk9 knockdown causes an increase in RNA Pol II occupance and pausing of c-myc which regulates neural crest specification.
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.
, cell division cycle 2-like protein kinase 4
, cell division protein kinase 9
, serine/threonine protein kinase PITALRE
, serine/threonine-protein kinase PITALRE
, tat-associated kinase complex catalytic subunit
, cyclin-dependent kinase 9 (CDC2-related kinase)
, Cyclin-dependent kinase9 2.7
, p43 PITALRE
, positive transcription elongation factor b
, positive transcription elongation factor b, small subunit
, cyclin-dependent kinase 9
, cell division protein kinase 9-A
, cyclin-dependent kinase 9-A