Evidence map›Paper›PMID 35773249›Full record

ArticleCell death discovery2022

Transcription factor Sp9 is a negative regulator of D1-type MSN development.

Zhenmeiyu Li, Zicong Shang, Mengge Sun, Xin Jiang, Yu Tian, Lin Yang, Ziwu Wang, Zihao Su, Guoping Liu, Xiaosu Li and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Genes · 2025
    Article
  4. Review
  5. Article
  6. The transcription factorFrontiers in cell and developmental biology · 2022
    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

14 authors at 2 institutions in 1 country.

Zhenmeiyu Li *Institute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Zicong Shang *Institute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Mengge SunInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Xin JiangInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Yu TianInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Lin YangInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Ziwu WangInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Zihao SuInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Guoping LiuInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Xiaosu LiInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Yan YouInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Zhengang YangInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China.
Zhejun XuInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China. 14111520028@fudan.edu.cn.ORCID http://orcid.org/0000-0002-1933-6300
Zhuangzhi ZhangInstitute of Pediatrics, Children's Hospital of Fudan University, state Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, 200032, Shanghai, China. zz_zhang@fudan.edu.cn.ORCID http://orcid.org/0000-0002-9860-6689
Children's Hospital of Fudan University · CNFudan University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) NSFC 32070971National Natural Science Foundation of China (National Science Foundation of China) NSFC32100768Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 2018SHZDZX01
6 · The paper itself

Abstract

The striatum is the main input structure of the basal ganglia, receiving information from the cortex and the thalamus and consisting of D1- and D2- medium spiny neurons (MSNs). D1-MSNs and D2-MSNs are essential for motor control and cognitive behaviors and have implications in Parkinson's Disease. In the present study, we demonstrated that Sp9-positive progenitors produced both D1-MSNs and D2-MSNs and that Sp9 expression was rapidly downregulated in postmitotic D1-MSNs. Furthermore, we found that sustained Sp9 expression in lateral ganglionic eminence (LGE) progenitor cells and their descendants led to promoting D2-MSN identity and repressing D1-MSN identity during striatal development. As a result, sustained Sp9 expression resulted in an imbalance between D1-MSNs and D2-MSNs in the mouse striatum. In addition, the fate-changed D2-like MSNs survived normally in adulthood. Taken together, our findings supported that Sp9 was sufficient to promote D2-MSN identity and repress D1-MSN identity, and Sp9 was a negative regulator of D1-MSN fate.

Identifiers

PMID35773249
PMCPMC9247084
OpenAlexW4283737094

What OpenQuestion holds

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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.