Evidence map›Paper›PMID 26159615›Full record

ArticleeLife2015

Slit2 as a β-catenin/Ctnnb1-dependent retrograde signal for presynaptic differentiation.

Haitao Wu, Arnab Barik, Yisheng Lu, Chengyong Shen, Andrew Bowman, Lei Li, Anupama Sathyamurthy, Thiri W Lin, Wen-Cheng Xiong, Lin Mei

Open access · goldAbstract read
In one paragraph

Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 60 citations in OpenAlex.

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  18. Postsynaptic CaScientific reports · 2019
    Article
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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

10 authors at 1 institution in 1 country.

Haitao WuDepartment of Neurobiology, Institute of Basic Medical Sciences, Beijing, China.
Arnab BarikDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.ORCID http://orcid.org/0000-0001-6850-0894
Yisheng LuDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Chengyong ShenDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Andrew BowmanDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Lei LiDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Anupama SathyamurthyDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Thiri W LinDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Wen-Cheng XiongDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Lin MeiDepartment of Neuroscience and Regenerative Medicine, Medical College of Georgia, Georgia Regents University, Augusta, United States.
Augusta University · US

Funding

Mechanisms of neuromuscular junction formationR01NS082007 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI XIONG, WEN-CHENG · 2013 to 2022
$5.2M
Retromer deficiency and Alzheimer's disease pathologyRF1AG045781 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI XIONG, WEN-CHENG · 2019 to 2019
$2.0M
Retromer deficiency and Alzheimer's disease pathologyR01AG045781 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI XIONG, WEN-CHENG · 2014 to 2017
$1.7M
Neuromuscular Junction FormationR01NS056415 · NINDS · AUGUSTA UNIVERSITY · PI MEI, LIN · 2008 to 2011
$1.4M
NIA NIH HHS AG045781NIA NIH HHS R01 AG045781NIA NIH HHS RF1 AG045781NINDS NIH HHS NS056415NINDS NIH HHS NS082007NINDS NIH HHS R01 NS056415NINDS NIH HHS R01 NS082007
6 · The paper itself

Abstract

Neuromuscular junction formation requires proper interaction between motoneurons and muscle cells. β-Catenin (Ctnnb1) in muscle is critical for motoneuron differentiation; however, little is known about the relevant retrograde signal. In this paper, we dissected which functions of muscle Ctnnb1 are critical by an in vivo transgenic approach. We show that Ctnnb1 mutant without the transactivation domain was unable to rescue presynaptic deficits of Ctnnb1 mutation, indicating the involvement of transcription regulation. On the other hand, the cell-adhesion function of Ctnnb1 is dispensable. We screened for proteins that may serve as a Ctnnb1-directed retrograde factor and identified Slit2. Transgenic expression of Slit2 specifically in the muscle was able to diminish presynaptic deficits by Ctnnb1 mutation in mice. Slit2 immobilized on beads was able to induce synaptophysin puncta in axons of spinal cord explants. Together, these observations suggest that Slit2 serves as a factor utilized by muscle Ctnnb1 to direct presynaptic differentiation.

Indexed as

Animalsbeta CateninIntercellular Signaling Peptides and ProteinsMice, KnockoutMice, TransgenicMuscle CellsMutant ProteinsNerve Tissue ProteinsNeuronsSlit Homolog 2 Proteinbeta CateninCTNNB1 protein, mouseIntercellular Signaling Peptides and ProteinsMutant ProteinsNerve Tissue ProteinsSlit Homolog 2 ProteinCtnnb1mouseneuroscienceNMJWnt

Identifiers

PMID26159615
PMCPMC4498096
OpenAlexW2139646760

What OpenQuestion holds

Textmetadata
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.