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@article{2437577,
author = {Hluchý, Milan and Blažek, Dalibor},
doi = {http://dx.doi.org/10.1016/j.tcb.2024.08.004},
keywords = {constitutive splicing; OTS964; histone transcription; C-terminal domain of RNA polymerase II; ULM–UHM interaction; cell cycle progression},
language = {eng},
issn = {0962-8924},
journal = {Trends in Cell Biology},
title = {CDK11, a splicing-associated kinase regulating gene expression},
url = {https://www.sciencedirect.com/science/article/pii/S0962892424001612?via%3Dihub},
year = {2024}
}
TY - JOUR
ID - 2437577
AU - Hluchý, Milan - Blažek, Dalibor
PY - 2024
TI - CDK11, a splicing-associated kinase regulating gene expression
JF - Trends in Cell Biology
PB - Cell Press
SN - 09628924
KW - constitutive splicing
KW - OTS964
KW - histone transcription
KW - C-terminal domain of RNA polymerase II
KW - ULM–UHM interaction
KW - cell cycle progression
UR - https://www.sciencedirect.com/science/article/pii/S0962892424001612?via%3Dihub
N2 - The ability of a cell to properly express its genes depends on optimal transcription and splicing. RNA polymerase II (RNAPII) transcribes protein-coding genes and produces pre-mRNAs, which undergo, largely co-transcriptionally, intron excision by the spliceosome complex. Spliceosome activation is a major control step, leading to a catalytically active complex. Recent work has showed that cyclin-dependent kinase (CDK)11 regulates spliceosome activation via the phosphorylation of SF3B1, a core spliceosome component. Thus, CDK11 arises as a major coordinator of gene expression in metazoans due to its role in the rate-limiting step of pre-mRNA splicing. This review outlines the evolution of CDK11 and SF3B1 and their emerging roles in splicing regulation. It also discusses how CDK11 and its inhibition affect transcription and cell cycle progression.
ER -
HLUCHÝ, Milan a Dalibor BLAŽEK. CDK11, a splicing-associated kinase regulating gene expression. \textit{Trends in Cell Biology}. Cell Press, 2024. ISSN~0962-8924. Dostupné z: https://dx.doi.org/10.1016/j.tcb.2024.08.004.
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