Evidence map›Paper›PMID 39738787›Full record

ArticleCommunications biology2024

RBM4-mediated intron excision of Hsf1 induces BDNF for cerebellar foliation.

Chiu-Lun Shen, Yu-Young Tsai, Shen-Ju Chou, Yao-Ming Chang, Woan-Yuh Tarn

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

5 authors.

Chiu-Lun ShenInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Yu-Young TsaiInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0000-0002-3690-9609
Shen-Ju ChouInstitute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan.
Yao-Ming ChangInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
Woan-Yuh TarnInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan. wtarn@ibms.sinica.edu.tw.ORCID 0000-0001-6244-6639

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 112WIA0110115
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) plays important roles in brain development and neural function. Constitutive knockout of the splicing regulator RBM4 reduces BDNF expression in the developing brain and causes cerebellar hypoplasia, an autism-like feature. Here, we show that Rbm4 knockout induced intron 6 retention of Hsf1, leading to downregulation of HSF1 protein and its downstream target BDNF. RBM4-mediated Hsf1 intron excision regulated BDNF expression in cultured granule cells. Ectopic expression of HSF1 restored cerebellar foliation and motor learning of Rbm4-knockout mice, indicating a critical role for RBM4-HSF1-BDNF in cerebellar foliation. Moreover, N-methyl-D-aspartate receptor (NMDAR) signaling promoted the expression and nuclear translocation of RBM4, and hence increased the expression of both HSF and BDNF. A short CU-rich motif was responsible for NMDAR- and RBM4-mediated intron excision. Finally, RBM4 and polypyrimidine tract binding (PTB) proteins play antagonistic roles in intron excision, suggesting a role for splicing regulation in BDNF expression.

Indexed as

Brain-Derived Neurotrophic FactorCerebellumIntronsMice, KnockoutRNA-Binding ProteinsAnimalsHumansMiceMice, Inbred C57BLPolypyrimidine Tract-Binding ProteinReceptors, N-Methyl-D-AspartateBdnf protein, mouseBrain-Derived Neurotrophic FactorPolypyrimidine Tract-Binding ProteinReceptors, N-Methyl-D-AspartateRNA-Binding Proteins

Identifiers

PMID39738787
PMCPMC11685446

What OpenQuestion holds

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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.