Evidence map›Paper›PMID 33938017›Full record

ArticleThe EMBO journal2021

Phf5a regulates DNA repair in class switch recombination via p400 and histone H2A variant deposition.

Nasim A Begum, Farazul Haque, Andre Stanlie, Afzal Husain, Samiran Mondal, Mikiyo Nakata, Takako Taniguchi, Hisaaki Taniguchi, Tasuku Honjo

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  5. Gene Expression Dysregulation in Whole Blood of Patients withInternational journal of molecular sciences · 2024
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  11. Review
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  14. Research progress and therapeutic prospect of PHF5A acting as a new target for malignant tumors.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022
    Review
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  17. Review
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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 4 institutions in 3 countries.

Nasim A BegumDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0001-7177-188X
Farazul HaqueDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Andre StanlieDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-4425-0250
Afzal HusainDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-6627-5520
Samiran MondalDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0003-4455-1202
Mikiyo NakataDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takako TaniguchiDivision of Disease Proteomics, Institute for Enzyme Research, University of Tokushima, Tokushima, Japan.
Hisaaki TaniguchiDivision of Disease Proteomics, Institute for Enzyme Research, University of Tokushima, Tokushima, Japan.
Tasuku HonjoDepartment of Immunology and Genomic Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0003-2300-3928
Kyoto University · JPTokushima University · JPAligarh Muslim University · INPfizer (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibody class switch recombination (CSR) is a locus-specific genomic rearrangement mediated by switch (S) region transcription, activation-induced cytidine deaminase (AID)-induced DNA breaks, and their resolution by non-homologous end joining (NHEJ)-mediated DNA repair. Due to the complex nature of the recombination process, numerous cofactors are intimately involved, making it important to identify rate-limiting factors that impact on DNA breaking and/or repair. Using an siRNA-based loss-of-function screen of genes predicted to encode PHD zinc-finger-motif proteins, we identify the splicing factor Phf5a/Sf3b14b as a novel modulator of the DNA repair step of CSR. Loss of Phf5a severely impairs AID-induced recombination, but does not perturb DNA breaks and somatic hypermutation. Phf5a regulates NHEJ-dependent DNA repair by preserving chromatin integrity to elicit optimal DNA damage response and subsequent recruitment of NHEJ factors at the S region. Phf5a stabilizes the p400 histone chaperone complex at the locus, which in turn promotes deposition of H2A variant such as H2AX and H2A.Z that are critical for the early DNA damage response and NHEJ, respectively. Depletion of Phf5a or p400 blocks the repair of both AID- and I-SceI-induced DNA double-strand breaks, supporting an important contribution of this axis to programmed as well as aberrant recombination.

Indexed as

DNA RepairAnimalsB-LymphocytesCell LineDNA-Binding ProteinsDNA HelicasesHistonesHumansImmunoglobulin Class SwitchingMiceMice, Inbred C57BLRecombination, GeneticRNA-Binding ProteinsRNA, Small InterferingTrans-ActivatorsDNA-Binding ProteinsDNA HelicasesEP400 protein, humanHistonesPHF5A protein, humanRNA-Binding ProteinsRNA, Small InterferingTrans-ActivatorsCSRgenomic instabilityH2A.ZNHEJPhf5a

Identifiers

PMID33938017
PMCPMC8204862
OpenAlexW3157477088

What OpenQuestion holds

Textmetadata
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.