Evidence map›Paper›PMID 30876848›Full record

ArticleNeuron2019

Nucleoporin Seh1 Interacts with Olig2/Brd7 to Promote Oligodendrocyte Differentiation and Myelination.

Zhixiong Liu, Minbiao Yan, Yaoji Liang, Min Liu, Kun Zhang, Dandan Shao, Rencai Jiang, Li Li, Chaomeng Wang, Daniel R Nussenzveig and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 85 citations in OpenAlex.

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  16. Nuclear transport proteins: structure, function, and disease relevance.Signal transduction and targeted therapy · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Zhixiong LiuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China; Cancer Research Center of Xiamen University, Xiamen, Fujian 361102, China.
Minbiao YanState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China; Cancer Research Center of Xiamen University, Xiamen, Fujian 361102, China.
Yaoji LiangSchool of Pharmaceutical Sciences, Xiamen University, Xiamen, Fujian 361102, China; XMU School of Pharmaceutical Sciences-Amogene Joint R&D Center for Genetic Diagnostics, Amogene Biotech, Xiamen, Fujian 361102, China; The First Affiliated Hospital, Medical College, Xiamen University, Xiamen, Fujian 361102, China.
Min LiuState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Kun ZhangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Dandan ShaoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Rencai JiangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Li LiState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Chaomeng WangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Daniel R NussenzveigDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9039, USA; Veterans Affairs North Texas Health Care System: Dallas VA Medical Center, Dallas, TX 75216, USA.
Kunkun ZhangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Shaoxuan ChenState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Chuanqi ZhongState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Wei MoState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China.
Beatriz M A FontouraDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9039, USA.
Liang ZhangState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian 361102, China; Cancer Research Center of Xiamen University, Xiamen, Fujian 361102, China. Electronic address: lzhangxmu@xmu.edu.cn.
Xiamen University · CNDallas VA Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

Crosstalk between human mRNA nuclear export and polyadenylation machineriesR01GM113874 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI CONRAD, NICHOLAS K, FONTOURA, BEATRIZ MA · 2015 to 2018
$1.8M
NIGMS NIH HHS R01 GM113874
6 · The paper itself

Abstract

Nucleoporins (Nups) are involved in neural development, and alterations in Nup genes are linked to human neurological diseases. However, physiological functions of specific Nups and the underlying mechanisms involved in these processes remain elusive. Here, we show that tissue-specific depletion of the nucleoporin Seh1 causes dramatic myelination defects in the CNS. Although proliferation is not altered in Seh1-deficient oligodendrocyte progenitor cells (OPCs), they fail to differentiate into mature oligodendrocytes, which impairs myelin production and remyelination after demyelinating injury. Genome-wide analyses show that Seh1 regulates a core myelinogenic regulatory network and establishes an accessible chromatin landscape. Mechanistically, Seh1 regulates OPCs differentiation by assembling Olig2 and Brd7 into a transcription complex at nuclear periphery. Together, our results reveal that Seh1 is required for oligodendrocyte differentiation and myelination by promoting assembly of an Olig2-dependent transcription complex and define a nucleoporin as a key player in the CNS.

Indexed as

AnimalsBromodomain Containing ProteinsCell DifferentiationChromosomal Proteins, Non-HistoneDemyelinating DiseasesMiceMyelin SheathNuclear PoreNuclear Pore Complex ProteinsOligodendrocyte Precursor CellsOligodendrocyte Transcription Factor 2RemyelinationBrd7 protein, mouseBromodomain Containing ProteinsChromosomal Proteins, Non-HistoneNuclear Pore Complex ProteinsOlig2 protein, mouseOligodendrocyte Transcription Factor 2Seh1l protein, mousedemyelinationdifferentiationmyelinnuclear pore complexnucleoporinoligodendrocyteSeh1

Identifiers

PMID30876848
PMCPMC6508993
OpenAlexW2920941152

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.