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About Event
Cyclin-dependent kinases (CDKs) play a central role in regulating transcription by RNA polymerase II (RNAPII), coordinating the initiation, elongation, and termination of gene transcription. CDKs function in association with cyclins, which regulate their activity and substrate specificity. Several CDKs, including CDK7, CDK9, CDK11, CDK12, and CDK13, are directly involved in the transcription cycle. Through the phosphorylation of RNAPII and associated transcriptional regulators, CDKs ensure the precise control of gene expression in response to cellular needs and environmental signals.
Small-molecule CDK inhibitors are valuable tools for investigating these regulatory mechanisms because they allow rapid and reversible inhibition of kinase activity, enabling the analysis of transcriptional changes over time. The timing of inhibitor treatment is particularly important when distinguishing immediate transcriptional effects from secondary cellular responses. Short-term inhibition, typically assessed over minutes to a few hours, helps identify direct consequences of CDK inactivation, including changes in RNAPII phosphorylation, pausing, and transcriptional elongation. The timing of CDK11 inhibition is especially important because its effects on transcription and RNA processing can occur rapidly. Acute CDK11 inhibition can reveal immediate changes in RNAPII occupancy, nascent RNA synthesis, and SF3B1 phosphorylation. Longer treatments may additionally induce indirect effects, such as altered mRNA stability, changes in gene expression, cell-cycle arrest, and apoptosis.
