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Authors show that, after UV irradiation, the cyclin-dependent kinase 9 (CDK9)/cyclin T1 kinase unit is specifically released from the HEXIM1 complex and that this released fraction is degraded in the absence of the Cockayne syndrome group B protein (CSB).
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The CDK9 inhibitor FIT-039 showed potent anti-HPV activity without significant toxicity in preclinical studies. Thus, FIT-039 is expected to be a novel therapeutic for cervical intraepithelial neoplasia (CIN) to prevent cervical cancer.
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high expression associated with poorer patient prognosis in synovial sarcoma
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interfering with the axis of RBM7 and P-TEFb provokes cellular hypersensitivity to DNA-damage-inducing agents due to activation of apoptosis. Our work uncovers the importance of stress-dependent stimulation of Pol II pause release, which enables a pro-survival transcriptional response that is crucial for cell fate upon genotoxic insult.
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SUMO and MYC mediate opposite effects upon global transcription by controlling the level of CDK9 sumoylation.
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our study implied that MALAT1/miR-206/CDK9 axis can provide novel insights into the biological mechanism of osteosarcoma progression.
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Study demonstrated that the level of CDK9 expression is associated with the clinical prognosis of patients with osteosarcoma. Its inhibition decreases osteosarcoma cell growth and proliferation by preventing RNAPII phosphorylation. These findings suggest that CDK9 may be a potential novel molecular biomarker for the early detection of disease.
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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.
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Physical interaction between pRb and cdk9/cyclinT2 complex.
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CDK7-mediated Ser-175 phosphorylation is a downstream nuclear event essential for facilitating CDK9 T-loop interactions with Tat
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miR-613, as a tumour suppressor, involves in gastric cancer progression and metastasis by targeting CDK9
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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.
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Recent studies have highlighted the importance of CDK9 in many relevant pathologic processes, like cancer, cardiovascular diseases, and viral replication.
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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.
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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
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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.
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this study shows role of CDK9 in oncogenic processes of esophageal adenocarcinoma
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CDK9, in addition to CDK1, has roles in mediating the growth inhibitory effect of dinaciclib on cyclin B1 in triple negative breast cancer
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Cdk9 is a post-exposure drug target against human adenoviruses.
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BRD4 and CDK9 have independent, coordinated roles in promoting the myofibroblast transition