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Genome-wide map of Pol II occupancy alterations on chromatin upon CDK12 and CDK13 inhibition (ChIP-Seq)

ABSTRACT: We performed ChIP-Seq on MV4;11 cells after 6 hours treatment of DMSO, 100nM and 200nM THZ531 to determine the location of Pol II occupancy

ORGANISM(S): Homo sapiens

PROVIDER: GSE141371 | GEO | 2020/04/29

REPOSITORIES: GEO

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Genome-wide map of Pol II occupancy alteration on chromatin upon CDK12 and CDK13 inhibition (ChIP-Seq)

Project description:We performed ChIP-Seq on MV4;11 cells after 6 hours treatment of DMSO, 100nM and 200nM THZ531 to determine the location of Pol II with phosphorylated Ser2 occupancy

2020-04-29 | GSE141369 | GEO

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

Project description:We performed 3' Quant-seq on MV4;11 cells after 6 hours treatment of THZ531 to determine whether CDK12 and CDK13 inhibtion cause alternative polyadenlation

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DRB-PRO-Seq for measuring Pol II transcriptional elongation rate alteration up on CDK12 and CDK13 inhibition by THZ531

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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Transcriptome wide alternative splicing analysis to determine the effect of CDK12 and CDK13 inhibition by THZ531 in alternative splicing (Total RNA-Seq)

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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Genome-wide map of Pol II and Ser2 phosphorylated Pol inoccupancy alteration on chromatin upon analog sensitive CDK12 and/or CDK13 inhibition (ChIP-Seq)

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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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Covalent targeting of remote cysteine residues to develop CDK12 and CDK13 inhibitors [ChIP-Seq]

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Investigating the effect of CDK inhibition in EML4-ALK cells by ChIP-seq for RNA polymerase II.

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Project description:We analyzed the 3' end of polyadenylated transcripts in Jurkat cells treated with either THZ531 (vs. DMSO) or the CDK12 degrader BSJ-4-116 (vs. BSJ-4-116NC).

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Transcriptome map of nascent RNA production alterations upon CDK9 and analog senstiveCDK12 and/or CDK13 inhibition (TT-Seq)

Project description:We performed TT-Seq on MV4;11 WT, CDK12AS/NULL, CDK13AS/AS, #1CDK12AS/NULL;CDK13AS/NULL and #2CDK12AS/NULL;CDK13AS/AS MV4;11 clones treated with 1-NM-PP1 or vehicle for 25 mintues to identify the effect of CDK12 and/or CDK13 on nasenct RNA production.

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