Evidence map›Paper›PMID 23178491›Full record

ArticleOncogene2014

CHK2 kinase promotes pre-mRNA splicing via phosphorylating CDK11(p110).

H-H Choi, H-K Choi, S Y Jung, J Hyle, B-J Kim, K Yoon, E-J Cho, H-D Youn, J M Lahti, J Qin and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 30 citations in OpenAlex.

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  20. Targeting CDK11 in osteosarcoma cells using the CRISPR-Cas9 system.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2015
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

H-H ChoiDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea.
H-K ChoiDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea.
S Y JungCenter for Molecular Discovery, Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, USA.
J HyleDepartment of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN, USA.
B-J KimCenter for Molecular Discovery, Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, USA.
K YoonSchool of Life Science and Biotechnology, Sungkyunkwan University, Suwon, Republic of Korea.
E-J ChoSchool of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea.
H-D YounNational Research Laboratory for Metabolic Checkpoint, Departments of Biomedical Sciences and Biochemistry and Molecular Biology, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea.
J M LahtiDepartment of Genetics and Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN, USA.
J QinCenter for Molecular Discovery, Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, USA.
S-T KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Republic of Korea.
Sungkyunkwan University · KRBaylor College of Medicine · USSt. Jude Children's Research Hospital · USSamsung (South Korea) · KR

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
The Role of Caspase-8 in Neuroblastoma TumorigenesisR01CA067938 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI ZAMBETTI, GERARD PAUL · 1995 to 2013
$3.8M
NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA067938
6 · The paper itself

Abstract

Checkpoint kinase 2 (CHK2) kinase is a key mediator in many cellular responses to genotoxic stresses, including ionizing radiation (IR) and topoisomerase inhibitors. Upon IR, CHK2 is activated by ataxia telangiectasia mutated kinase and regulates the S-phase and G1-S checkpoints, apoptosis and DNA repair by phosphorylating downstream target proteins, such as p53 and Brca1. In addition, CHK2 is thought to be a multi-organ cancer susceptibility gene. In this study, we used a tandem affinity purification strategy to identify proteins that interact with CHK2 kinase. Cyclin-dependent kinase 11 (CDK11)(p110) kinase, implicated in pre-mRNA splicing and transcription, was identified as a CHK2-interacting protein. CHK2 kinase phosphorylated CDK11(p110) on serine 737 in vitro. Unexpectedly, CHK2 kinase constitutively phosphorylated CDK11(p110) in a DNA damage-independent manner. At a molecular level, CDK11(p110) phosphorylation was required for homodimerization without affecting its kinase activity. Overexpression of CHK2 promoted pre-mRNA splicing. Conversely, CHK2 depletion decreased endogenous splicing activity. Mutation of the phosphorylation site in CDK11(p110) to alanine abrogated its splicing-activating activity. These results provide the first evidence that CHK2 kinase promotes pre-mRNA splicing via phosphorylating CDK11(p110).

Indexed as

Amino Acid SequenceCheckpoint Kinase 2Cyclin-Dependent KinasesDNA DamageHEK293 CellsHT29 CellsHumansPhosphorylationProtein Interaction MappingProtein MultimerizationProtein Processing, Post-TranslationalRNA, MessengerRNA PrecursorsRNA SplicingCDK11a protein, humanCheckpoint Kinase 2CHEK2 protein, humanCyclin-Dependent KinasesRNA, MessengerRNA Precursors

Identifiers

PMID23178491
PMCPMC4131284
OpenAlexW2044629154

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.