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miR (show MLXIP Proteins)-613, as a tumour suppressor, involves in gastric cancer progression and metastasis by targeting CDK9
GRIP1 (show NCOA2 Proteins) 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 (show NCOA2 Proteins) 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 (show CDK2 Proteins) and CDK9 are potential therapeutic targets in Neuroblastoma (show ARHGEF16 Proteins) (NB) and that abrogating CDK2 (show CDK2 Proteins) and CDK9 activity by small molecules like dinaciclib is a promising strategy and a treatment option for NB patients
miR (show MLXIP Proteins)-206 is remarkably downregulated and is inversely correlated with CDK9 level in HCC (show FAM126A Proteins) cells. It is evident that miR (show MLXIP Proteins)-206 functions as a tumor suppressor through blocking CDK9-related pathway to induce apoptosis and inhibit HCC (show FAM126A Proteins) cell proliferation.
this study shows role of CDK9 in oncogenic processes of esophageal adenocarcinoma
CDK9, in addition to CDK1 (show CDK1 Proteins), has roles in mediating the growth inhibitory effect of dinaciclib on cyclin B1 (show CCNB1 Proteins) in triple negative breast cancer
Cdk9 is a post-exposure drug target against human adenoviruses.
BRD4 (show BRD4 Proteins) and CDK9 have independent, coordinated roles in promoting the myofibroblast transition
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 Proteins) plays a key role in cardiomyocyte proliferation and response to injury
actin (show ACTB Proteins) 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 Proteins)-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 Proteins) recruitment.
Cdk9 plays a complex role in myocyte progenitor differentiation and apoptosis by regulating myogenic protein and muscle-specific (show EIF3K Proteins) microRNA expression.
findings revealed the crucial role of CDK9/Cyclin T1 (show CCNT1 Proteins)/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 Proteins) directly interacts with GATA1 (show GATA1 Proteins), GATA2 (show GATA2 Proteins), and GATA3 (show GATA3 Proteins) as well as Cdk9/P-TEFb through specific protein domains.
Data show that the minimal 90-amino acid AF9 (show MLLT3 Proteins) fragment in MLL (show MLL Proteins)-AF9 (show MLLT3 Proteins) retains an ability to form higher order complexes with AF4*P-TEFb (show CCNT1 Proteins) and with DOT1 (show DOT1L Proteins).
Data show that the CDK9 and cyclin T1 (show CCNT1 Proteins) subunits of P-TEFb (show CCNT1 Proteins) 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 Proteins) 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 Proteins)-dependent transcription
inhibition of CDK9 abrogated global transcriptional activity and rRNA production. Collectively, our data suggested that P-TEFb (show CCNT1 Proteins) 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 Proteins) 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