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Quant-seq analysis to determine the effects of CDK12 and CDK13 inhibition by THZ531 in alternative polyadenylation

ABSTRACT: Quant-seq analysis to determine the effects of CDK12 and CDK13 inhibition by THZ531 in alternative polyadenylation

PROVIDER: PRJNA593226 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10582191.fastq.gz	Fastqsanger.gz
	SRR10582192.fastq.gz	Fastqsanger.gz
	SRR10582193.fastq.gz	Fastqsanger.gz

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Quant-seq analysis to determine the effects of CDK12 and CDK13 inhibition by THZ531 in alternative polyadenylation

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Quant-seq analysis of differential polyadenylation site usages in caused by different Pol II mutants with slow elongation rates in Flp-In-293 cells and dual inhibition of CDK12 and CDK13 by THZ531 HEK293T cells

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Covalent targeting of remote cysteine residues to develop CDK12 and CDK13 inhibitors [Affymetrix]

Project description:Cyclin-dependent kinases 12 and 13 (CDK12 and CDK13) play critical roles in the regulation of gene transcription. However, the absence of CDK12 and CDK13 inhibitors has hindered the ability to investigate the consequences of their inhibition in healthy cells and cancer cells. Here we describe the rational design of a first-in-class CDK12 and CDK13 covalent inhibitor, THZ531. Co-crystallization of THZ531 with CDK12–cyclin K indicates that THZ531 irreversibly targets a cysteine located outside the kinase domain. THZ531 causes a loss of gene expression with concurrent loss of elongating and hyperphosphorylated RNA polymerase II. In particular, THZ531 substantially decreases the expression of DNA damage response genes and key super-enhancer-associated transcription factor genes. Coincident with transcriptional perturbation, THZ531 dramatically induced apoptotic cell death. Small molecules capable of specifically targeting CDK12 and CDK13 may thus help identify cancer subtypes that are particularly dependent on their kinase activities.

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Project description:We performed Total RNA-seq on MV4;11 cells after 6 hours treatment of THZ531 to determine whether CDK12 and CDK13 inhibtion to cause splicing defects.

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Project description:We performed PRO-Seq to measure the Pol II elongation rate by measruing the distance of Pol II travels at viarous time points after relased from DRB induced pausing. We compared DMSO/DRB or THZ531/DRB co-treated sample to assess the effect of CDK12 and CDK13 inhibtion by THZ531 on transcriptional elongation rate.

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Quant-seq analysis of differential gene expression and polyadenylation site usages in caused by inhibition of CDK12 and CDK13 using THZ531 in THP-1 cells (3’ Quant-seq)

Project description:Quant-seq analysis of differential gene expression and polyadenylation site usages in caused by inhibition of CDK12 and CDK13 using THZ531 in THP-1 cells (3’ Quant-seq)

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Transcriptome wide analysis of differential gene expression and polyadenylation site usages caused by inhibition of CDK12 and/or CDK13 in MV4;11 cells (3’ Quant-seq)

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CDK13 cooperates with CDK12 to control global RNA polymerase II processivity

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