Evidence map›Paper›PMID 27452460›Full record

ArticleCell reports2016

The Zinc Finger Transcription Factor Sp9 Is Required for the Development of Striatopallidal Projection Neurons.

Qiangqiang Zhang, Yue Zhang, Chunyang Wang, Zhejun Xu, Qifei Liang, Lei An, Jiwen Li, Zhidong Liu, Yan You, Miao He and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

44 citing papers in PubMed, 76 citations in OpenAlex.

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  18. The transcription factorFrontiers in cell and developmental biology · 2022
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  20. DNA Methylation in Huntington's Disease.International journal of molecular sciences · 2021
    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

15 authors at 6 institutions in 2 countries.

Qiangqiang ZhangInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Yue ZhangInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Chunyang WangInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Zhejun XuInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Qifei LiangInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Lei AnInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Jiwen LiInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Zhidong LiuInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Yan YouInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Miao HeInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
Ying MaoInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China; Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, China.
Bin ChenDepartment of Molecular, Cell, and Developmental Biology, University of California Santa Cruz, Santa Cruz, CA 95064, USA.
Zhi-Qi XiongInstitute of Neuroscience, State Key Laboratory of Neuroscience, Chinese Academy of Sciences Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
John L RubensteinDepartment of Psychiatry, Neuroscience Program and Nina Ireland Laboratory of Developmental Neurobiology, University of California San Francisco, San Francisco, CA 94158, USA.
Zhengang YangInstitutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China; Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, China. Electronic address: yangz@fudan.edu.cn.
State Key Laboratory of Medical NeurobiologyFudan University · CNHuashan Hospital · CNShanghai Institutes for Biological Sciences · CNUniversity of California, San Francisco · USUniversity of California, Santa Cruz · US

Funding

Genetic Regulation of Telencephalon DevelopmentR37MH049428 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RUBENSTEIN, JOHN L. R. · 2008 to 2017
$5.9M
Transcriptional regulation of neuronal identity and connectivityR01MH094589 · NIMH · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI CHEN, BIN · 2011 to 2021
$3.7M
NIMH NIH HHS R01 MH094589NIMH NIH HHS R37 MH049428
6 · The paper itself

Abstract

Striatal medium-sized spiny neurons (MSNs), composed of striatonigral and striatopallidal neurons, are derived from the lateral ganglionic eminence (LGE). We find that the transcription factor Sp9 is expressed in LGE progenitors that generate nearly all striatal MSNs and that Sp9 expression is maintained in postmitotic striatopallidal MSNs. Sp9-null mice lose most striatopallidal MSNs because of decreased proliferation of striatopallidal MSN progenitors and increased Bax-dependent apoptosis, whereas the development of striatonigral neurons is largely unaffected. ChIP qPCR provides evidence that Ascl1 directly binds the Sp9 promoter. RNA-seq and in situ hybridization reveal that Sp9 promotes expression of Adora2a, P2ry1, Gpr6, and Grik3 in the LGE and striatum. Thus, Sp9 is crucial for the generation, differentiation, and survival of striatopallidal MSNs.

Indexed as

AnimalsApoptosisCell DifferentiationCell ProliferationCorpus StriatumGene ExpressionMiceMice, KnockoutNeuronsPromoter Regions, GeneticSubstantia NigraTranscription FactorsZinc FingersTranscription FactorsAdora2aAscl1Drd2LGESp9striatopallidal neuronstriatum

Identifiers

PMID27452460
PMCPMC4972643
OpenAlexW2493234177

What OpenQuestion holds

Textmetadata
LicenceTDM
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.