Evidence map›Paper›PMID 37993446›Full record

ArticleNature communications2023

A dual role of RBM42 in modulating splicing and translation of CDKN1A/p21 during DNA damage response.

Bella M Ben-Oz, Feras E Machour, Marian Nicola, Amir Argoetti, Galia Polyak, Rawad Hanna, Oded Kleifeld, Yael Mandel-Gutfreund, Nabieh Ayoub

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  17. Key molecular DNA damage responses of human cells to radiation.Frontiers in cell and developmental biology · 2024
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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

9 authors at 1 institution in 1 country.

Bella M Ben-OzDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.
Feras E MachourDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.
Marian NicolaDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.
Amir ArgoettiDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.ORCID 0000-0002-0412-003X
Galia PolyakDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.ORCID 0009-0007-5580-8807
Rawad HannaDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.
Oded KleifeldDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.ORCID 0000-0003-3091-7154
Yael Mandel-GutfreundDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel.
Nabieh AyoubDepartment of Biology, Technion - Israel Institute of Technology, Haifa, 3200003, Israel. ayoubn@technion.ac.il.ORCID 0000-0002-9549-9929
Technion – Israel Institute of Technology · IL

Funding

Israel Cancer Association (ICA) 20200080Israel Science Foundation (ISF) 2511/18Israel Science Foundation (ISF) 2511/19
6 · The paper itself

Abstract

p53-mediated cell cycle arrest during DNA damage is dependent on the induction of p21 protein, encoded by the CDKN1A gene. p21 inhibits cyclin-dependent kinases required for cell cycle progression to guarantee accurate repair of DNA lesions. Hence, fine-tuning of p21 levels is crucial to preserve genomic stability. Currently, the multilayered regulation of p21 levels during DNA damage is not fully understood. Herein, we identify the human RNA binding motif protein 42 (RBM42) as a regulator of p21 levels during DNA damage. Genome-wide transcriptome and interactome analysis reveals that RBM42 alters the expression of p53-regulated genes during DNA damage. Specifically, we demonstrate that RBM42 facilitates CDKN1A splicing by counteracting the splicing inhibitory effect of RBM4 protein. Unexpectedly, we also show that RBM42, underpins translation of various splicing targets, including CDKN1A. Concordantly, transcriptome-wide mapping of RBM42-RNA interactions using eCLIP further substantiates the dual function of RBM42 in regulating splicing and translation of its target genes, including CDKN1A. Collectively, our data show that RBM42 couples splicing and translation machineries to fine-tune gene expression during DNA damage response.

Indexed as

Genes, cdcTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21DNA DamageHumansRNA-Binding ProteinsRNA SplicingCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21RBM4 protein, humanRNA-Binding ProteinsTumor Suppressor Protein p53

Identifiers

PMID37993446
PMCPMC10665399
OpenAlexW4388900933

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.