Ontology highlight
ABSTRACT:
PROVIDER: PRJNA165837 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Cdk11-Cyclin L controls the assembly of the RNA polymerase II Mediator [expression]
| PRJNA165855 | ENA
Project description:Cdk11-Cyclin L controls the assembly of the RNA polymerase II Mediator [ChIP-chip]
| PRJNA165857 | ENA
Project description:The L-Mediator is a general co-activator of RNA Polymerase II transcription and is formed by the reversible association of the S-Mediator and the kinase module harbouring Cdk8. We describe the Cdk11-Lcp1 complex and show that its inactivation alter the global expression profiles in a very similar way than mutations of the kinase module. Cdk11 is broadly distributed onto chromatin and phosphorylate the Med27 and Med4 Mediator subunits on conserved residues. The inactivation of either Cdk11 or the mutation of its target residues on the Mediator leads to a strongly decreased association of the kinase module and the S-Mediator. The results show that Cdk11-Lcp1 regulates that assembly of the L-Mediator complex.
2014-07-11 | GSE37961 | GEO
Project description:The L-Mediator is a general co-activator of RNA Polymerase II transcription and is formed by the reversible association of the S-Mediator and the kinase module harbouring Cdk8. We describe the Cdk11-Lcp1 complex and show that its inactivation alter the global expression profiles in a very similar way than mutations of the kinase module. Cdk11 is broadly distributed onto chromatin and phosphorylate the Med27 and Med4 Mediator subunits on conserved residues. The inactivation of either Cdk11 or the mutation of its target residues on the Mediator leads to a strongly decreased association of the kinase module and the S-Mediator. The results show that Cdk11-Lcp1 regulates that assembly of the L-Mediator complex. Total RNA was isolated from two biological replicates for all conditions, and each biological replicate was hybridized in duplicate on Agilent arrays (dye-swap).
2014-07-11 | E-GEOD-37960 | biostudies-arrayexpress
Project description:The L-Mediator is a general co-activator of RNA Polymerase II transcription and is formed by the reversible association of the S-Mediator and the kinase module harbouring Cdk8. We describe the Cdk11-Lcp1 complex and show that its inactivation alter the global expression profiles in a very similar way than mutations of the kinase module. Cdk11 is broadly distributed onto chromatin and phosphorylate the Med27 and Med4 Mediator subunits on conserved residues. The inactivation of either Cdk11 or the mutation of its target residues on the Mediator leads to a strongly decreased association of the kinase module and the S-Mediator. The results show that Cdk11-Lcp1 regulates that assembly of the L-Mediator complex. Two independent immunoprecipitations were done for HA-tagged Cdk11 and each biological replicate was hybridized in duplicate on Agilent arrays using input DNA as the reference channel.
2014-07-11 | E-GEOD-37961 | biostudies-arrayexpress
Project description:The L-Mediator is a general co-activator of RNA Polymerase II transcription and is formed by the reversible association of the S-Mediator and the kinase module harbouring Cdk8. We describe the Cdk11-Lcp1 complex and show that its inactivation alter the global expression profiles in a very similar way than mutations of the kinase module. Cdk11 is broadly distributed onto chromatin and phosphorylate the Med27 and Med4 Mediator subunits on conserved residues. The inactivation of either Cdk11 or the mutation of its target residues on the Mediator leads to a strongly decreased association of the kinase module and the S-Mediator. The results show that Cdk11-Lcp1 regulates that assembly of the L-Mediator complex.
2014-07-11 | GSE37960 | GEO
Project description:Controlled gene expression is achieved through the intricate regulation of RNA polymerase II (Pol II) progression through transcription-cycle checkpoints. The pausing checkpoint, where Pol II temporarily stalls prior to release into transcriptional elongation, is a key molecular mechanism that fine-tunes gene expression. While the critical contribution of cyclin-dependent-kinase 9 (CDK9) for Pol II pause-release is well established, the requirement for other CDKs has not been fully elucidated. Here we identify a new role for CDK11 in the Pol II pausing-to-elongation transition at a checkpoint that is distinct and independent from CDK9. Selective CDK11 inhibition results in genome-wide stalling of Pol II at transcription-start-site (TSS) proximal regions and acute RNA synthesis ablation near the beginning of transcriptional units. High-resolution chromatin-immunoprecipitation and precision-nuclear-run-on assays reveals spatial differences between CDK11- and CDK9-dependent Pol II pause sites, with CDK11 regulating Pol II closer to the TSS. Cancer cells exhibit profound reliance on functional CDK11, with selective CDK11 inhibition providing therapeutic efficacy in pre-clinical in vivo models of leukaemia and lymphoma, demonstrating the importance of CDK11-dependent Pol II regulation for aggressive haematological malignancies.
2025-08-25 | GSE280208 | GEO
Project description:Controlled gene expression is achieved through the intricate regulation of RNA polymerase II (Pol II) progression through transcription-cycle checkpoints. The pausing checkpoint, where Pol II temporarily stalls prior to release into transcriptional elongation, is a key molecular mechanism that fine-tunes gene expression. While the critical contribution of cyclin-dependent-kinase 9 (CDK9) for Pol II pause-release is well established, the requirement for other CDKs has not been fully elucidated. Here we identify a new role for CDK11 in the Pol II pausing-to-elongation transition at a checkpoint that is distinct and independent from CDK9. Selective CDK11 inhibition results in genome-wide stalling of Pol II at transcription-start-site (TSS) proximal regions and acute RNA synthesis ablation near the beginning of transcriptional units. High-resolution chromatin-immunoprecipitation and precision-nuclear-run-on assays reveals spatial differences between CDK11- and CDK9-dependent Pol II pause sites, with CDK11 regulating Pol II closer to the TSS. Cancer cells exhibit profound reliance on functional CDK11, with selective CDK11 inhibition providing therapeutic efficacy in pre-clinical in vivo models of leukaemia and lymphoma, demonstrating the importance of CDK11-dependent Pol II regulation for aggressive haematological malignancies.
2025-08-25 | GSE280103 | GEO
Project description:Controlled gene expression is achieved through the intricate regulation of RNA polymerase II (Pol II) progression through transcription-cycle checkpoints. The pausing checkpoint, where Pol II temporarily stalls prior to release into transcriptional elongation, is a key molecular mechanism that fine-tunes gene expression. While the critical contribution of cyclin-dependent-kinase 9 (CDK9) for Pol II pause-release is well established, the requirement for other CDKs has not been fully elucidated. Here we identify a new role for CDK11 in the Pol II pausing-to-elongation transition at a checkpoint that is distinct and independent from CDK9. Selective CDK11 inhibition results in genome-wide stalling of Pol II at transcription-start-site (TSS) proximal regions and acute RNA synthesis ablation near the beginning of transcriptional units. High-resolution chromatin-immunoprecipitation and precision-nuclear-run-on assays reveals spatial differences between CDK11- and CDK9-dependent Pol II pause sites, with CDK11 regulating Pol II closer to the TSS. Cancer cells exhibit profound reliance on functional CDK11, with selective CDK11 inhibition providing therapeutic efficacy in pre-clinical in vivo models of leukaemia and lymphoma, demonstrating the importance of CDK11-dependent Pol II regulation for aggressive haematological malignancies.
2025-08-25 | GSE280102 | GEO
Project description:CDK11 is an emerging druggable target for cancer therapy due to its prevalent roles in phosphorylating critical transcription and splicing factors and in facilitating cell cycle progression in cancer cells. Like other cyclin-dependent kinases, CDK11 requires its cognate cyclin, cyclin L1 or cyclin L2, for activation. However, little is known about how CDK11 activities might be modulated by other regulators. In this study, we show that CDK11 forms a tight complex with cyclins L1/L2 and SAP30BP, the latter of which is a poorly characterized factor. Acute degradation of SAP30BP mirrors that of CDK11 in causing widespread and strong defects in pre-mRNA splicing. Furthermore, we demonstrate that SAP30BP facilitates CDK11 kinase activities in vitro and in vivo, through ensuring the stabilities and the assembly of cyclins L1/L2 with CDK11. Together, these findings uncover SAP30BP as a critical CDK11 activator that regulates global pre-mRNA splicing.
2023-10-05 | GSE226804 | GEO