Evidence map›Paper›PMID 36997512›Full record

ArticleNature communications2023

The RNA-binding protein hnRNP F is required for the germinal center B cell response.

Hengjun Huang, Yuxing Li, Gaopu Zhang, Gui-Xin Ruan, Zhijian Zhu, Wenjing Chen, Jia Zou, Rui Zhang, Jing Wang, Yu Ouyang and 2 more

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
2.1field-weighted citation impact, top 13% 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, 13 citations in OpenAlex.

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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

12 authors at 3 institutions in 2 countries.

Hengjun HuangSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.ORCID 0000-0001-9842-9312
Yuxing LiSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Gaopu ZhangSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Gui-Xin RuanMedical School, Taizhou University, Taizhou, 318000, China.
Zhijian ZhuSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Wenjing ChenSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Jia ZouDepartment of Computer Science and Engineering, College of Engineering, Southern University of Science and Technology, Shenzhen, 518055, China.
Rui ZhangSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Jing WangSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Yu OuyangSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China.
Shengli XuSingapore Immunology Network, Agency for Science, Technology and Research, Singapore, 138648, Singapore. xu_shengli@immunol.a-star.edu.sg.ORCID 0000-0002-2541-3608
Xijun OuSchool of Life Sciences, Southern University of Science and Technology, Shenzhen, 518055, China. ouxj@sustech.edu.cn.ORCID 0000-0002-4525-5205
Southern University of Science and Technology · CNAgency for Science, Technology and Research · SGTaizhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The T cell-dependent (TD) antibody response involves the generation of high affinity, immunoglobulin heavy chain class-switched antibodies that are generated through germinal center (GC) response. This process is controlled by coordinated transcriptional and post-transcriptional gene regulatory mechanisms. RNA-binding proteins (RBPs) have emerged as critical players in post-transcriptional gene regulation. Here we demonstrate that B cell-specific deletion of RBP hnRNP F leads to diminished production of class-switched antibodies with high affinities in response to a TD antigen challenge. B cells deficient in hnRNP F are characterized by defective proliferation and c-Myc upregulation upon antigenic stimulation. Mechanistically, hnRNP F directly binds to the G-tracts of Cd40 pre-mRNA to promote the inclusion of Cd40 exon 6 that encodes its transmembrane domain, thus enabling appropriate CD40 cell surface expression. Furthermore, we find that hnRNP A1 and A2B1 can bind to the same region of Cd40 pre-mRNA but suppress exon 6 inclusion, suggesting that these hnRNPs and hnRNP F might antagonize each-other's effects on Cd40 splicing. In summary, our study uncovers an important posttranscriptional mechanism regulating the GC response.

Indexed as

Heterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear Ribonucleoprotein Group F-HBase SequenceB-LymphocytesGerminal CenterHeterogeneous-Nuclear RibonucleoproteinsIntronsRNA PrecursorsHeterogeneous-Nuclear Ribonucleoprotein Group A-BHeterogeneous-Nuclear Ribonucleoprotein Group F-HHeterogeneous-Nuclear RibonucleoproteinsRNA Precursors

Identifiers

PMID36997512
PMCPMC10063658
OpenAlexW4361274097

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.