Evidence map›Paper›PMID 40555862›Full record

ArticleNeuroscience bulletin2025

Csde1 Mediates Neurogenesis via Post-transcriptional Regulation of the Cell Cycle.

Xiangbin Jia, Wenqi Xie, Bing Du, Mei He, Jia Chen, Meilin Chen, Ge Zhang, Ke Wang, Wanjing Xu, Yuxin Liao and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

21 authors.

Xiangbin JiaCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Wenqi XieCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Bing DuCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Mei HeCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Jia ChenCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Meilin ChenCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Ge ZhangCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Ke WangSchool of Medicine, Kunming University of Science and Technology, Kunming, 650500, China.
Wanjing XuHengyang Medical School, University of South China, Hengyang, 421001, China.
Yuxin LiaoCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Senwei TanCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Yongqing LyuCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Bin YuCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Zihang ZhengCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Xiaoyue SunCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Yang LiaoCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Zhengmao HuCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Ling YuanCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Jieqiong TanCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China.
Kun XiaCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China. xiakun@sklmg.edu.cn.ORCID http://orcid.org/0000-0002-1093-9236
Hui GuoCenter for Medical Genetics and Hunan Key Laboratory of Medical Genetics, MOE Key Laboratory of Rare Pediatric Disease, School of Life Sciences, Central South University, Changsha, 410078, China. guohui2@csu.edu.cn.ORCID http://orcid.org/0000-0002-1570-2545

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss-of-function variants in CSDE1 have been strongly linked to neuropsychiatric disorders, yet the precise role of CSDE1 in neurogenesis remains elusive. In this study, we demonstrate that knockout of Csde1 during cortical development in mice results in impaired neural progenitor proliferation, leading to abnormal cortical lamination and embryonic lethality. Transcriptomic analysis revealed that Csde1 upregulates the transcription of genes involved in the cell cycle network. Applying a dual thymidine-labelling approach, we further revealed prolonged cell cycle durations of neuronal progenitors in Csde1-knockout mice, with a notable extension of the G1 phase. Intersection with CLIP-seq data demonstrated that Csde1 binds to the 3' untranslated region (UTR) of mRNA transcripts encoding cell cycle genes. Particularly, we uncovered that Csde1 directly binds to the 3' UTR of mRNA transcripts encoding Cdk6, a pivotal gene in regulating the transition from the G1 to S phases of the cell cycle, thereby maintaining its stability. Collectively, this study elucidates Csde1 as a novel regulator of Cdk6, sheds new light on its critical roles in orchestrating brain development, and underscores how mutations in Csde1 may contribute to the pathogenesis of neuropsychiatric disorders.

Indexed as

Cell CycleDNA-Binding ProteinsNeurogenesis3' Untranslated RegionsAnimalsCell ProliferationCerebral CortexCyclin-Dependent Kinase 6MiceMice, Inbred C57BLMice, KnockoutNeural Stem CellsRNA-Binding Proteins3' Untranslated RegionsCdk6 protein, mouseCyclin-Dependent Kinase 6DNA-Binding ProteinsRNA-Binding ProteinsAutism spectrum disorderCdk6Cell cycleCsde1Neurogenesis

Identifiers

PMID40555862
PMCPMC12569293

What OpenQuestion holds

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Registered trials

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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.