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Cdk9 is a post-exposure drug target against human adenoviruses.
BRD4 (show BRD4 ELISA Kits) and CDK9 have independent, coordinated roles in promoting the myofibroblast transition
RBPJ (show RBPJ ELISA Kits) links MYC (show MYC ELISA Kits) and transcriptional control through CDK9 in brain tumors, providing potential nodes of fragility for therapeutic intervention, potentially distinct from NOTCH (show NOTCH1 ELISA Kits)
Chemical degrader of BET bromodomain proteins, dBET6, led to the unexpected identification of BRD4 (show BRD4 ELISA Kits) as master regulator of global transcription elongation in acute T-cell leukemia. BRD4 (show BRD4 ELISA Kits) 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 (show HSP90 ELISA Kits) downstream HSF1 (show HSF1 ELISA Kits) 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 (show TAT ELISA Kits), CycT1 (show CCNT1 ELISA Kits) 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 (show TEF ELISA Kits) 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
Findings indicate that cyclin-dependent kinase 9 (CDK9) represent an important role for inflammation in the pathogenesis of atherosclerosis.
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 (show LARP7 ELISA Kits) plays a key role in cardiomyocyte proliferation and response to injury
actin (show ACTB ELISA Kits) 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 (show ACTB ELISA Kits)-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 (show TSFM ELISA Kits) recruitment.
findings revealed the crucial role of CDK9/Cyclin T1 (show CCNT1 ELISA Kits)/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 (show IKZF1 ELISA Kits) directly interacts with GATA1 (show GATA1 ELISA Kits), GATA2 (show GATA2 ELISA Kits), and GATA3 (show GATA3 ELISA Kits) as well as Cdk9/P-TEFb through specific protein domains.
Data show that the minimal 90-amino acid AF9 (show MLLT3 ELISA Kits) fragment in MLL (show MLL ELISA Kits)-AF9 (show MLLT3 ELISA Kits) retains an ability to form higher order complexes with AF4*P-TEFb (show CCNT1 ELISA Kits) and with DOT1 (show DOT1L ELISA Kits).
Data show that the CDK9 and cyclin T1 (show CCNT1 ELISA Kits) subunits of P-TEFb (show CCNT1 ELISA Kits) 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 (show GATA4 ELISA Kits) 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 (show MYOD1 ELISA Kits)-dependent transcription
CDK9 has the intrinsic property to shuttle between nucleus and cytoplasm, and enhanced expression of cyclin T1 (show CCNT1 ELISA Kits) promotes its nuclear localization.
chronic activation of Cdk9 causes not only cardiomyocyte enlargement but also defective mitochondrial function, via diminished PGC-1 (show PPARGC1A ELISA Kits) transcription, and a resulting susceptibility to apoptotic cardiomyopathy
inhibition of CDK9 abrogated global transcriptional activity and rRNA production. Collectively, our data suggested that P-TEFb (show CCNT1 ELISA Kits) 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 (show MYC ELISA Kits) 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