Evidence map›Paper›PMID 29615491›Full record

ArticleThe Journal of biological chemistry2018

Neuronal adaptor FE65 stimulates Rac1-mediated neurite outgrowth by recruiting and activating ELMO1.

Wen Li, Ka Ming Vincent Tam, Wai Wa Ray Chan, Alex Chun Koon, Jacky Chi Ki Ngo, Ho Yin Edwin Chan, Kwok-Fai Lau

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Targeting of ELMO2 by thebioRxiv : the preprint server for biology · 2026
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  11. Article
  12. BiallelicSmall GTPases · 2022
    Article
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  14. Review
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  18. Article
  19. Attenuation of amyloid-β generation by atypical protein kinase C-mediated phosphorylation of engulfment adaptor PTB domain containing 1 threonine 35.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. 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

7 authors at 1 institution in 1 country.

Wen LiFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong.
Ka Ming Vincent TamFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong.
Wai Wa Ray ChanFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong.
Alex Chun KoonFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong.
Jacky Chi Ki NgoFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong.
Ho Yin Edwin ChanFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong.
Kwok-Fai LauFrom the School of Life Sciences, Faculty of Science, Chinese University of Hong Kong, Shatin New Territories, Hong Kong kflau@cuhk.edu.hk.
Chinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurite outgrowth is a crucial process in developing neurons for neural network formation. Understanding the regulatory mechanisms of neurite outgrowth is essential for developing strategies to stimulate neurite regeneration after nerve injury and in neurodegenerative disorders. FE65 is a brain-enriched adaptor that stimulates Rac1-mediated neurite elongation. However, the precise mechanism by which FE65 promotes the process remains elusive. Here, we show that ELMO1, a subunit of ELMO1-DOCK180 bipartite Rac1 guanine nucleotide exchange factor (GEF), interacts with the FE65 N-terminal region. Overexpression of FE65 and/or ELMO1 enhances, whereas knockdown of FE65 or ELMO1 inhibits, neurite outgrowth and Rac1 activation. The effect of FE65 alone or together with ELMO1 is attenuated by an FE65 double mutation that disrupts FE65-ELMO1 interaction. Notably, FE65 is found to activate ELMO1 by diminishing ELMO1 intramolecular autoinhibitory interaction and to promote the targeting of ELMO1 to the plasma membrane, where Rac1 is activated. We also show that FE65, ELMO1, and DOCK180 form a tripartite complex. Knockdown of DOCK180 reduces the stimulatory effect of FE65-ELMO1 on Rac1 activation and neurite outgrowth. Thus, we identify a novel mechanism by which FE65 stimulates Rac1-mediated neurite outgrowth by recruiting and activating ELMO1.

Indexed as

NeurogenesisAdaptor Proteins, Signal TransducingAnimalsCell MovementCells, CulturedHumansNerve Tissue ProteinsNeuronal OutgrowthNeuronsNuclear Proteinsrac1 GTP-Binding ProteinRatsAdaptor Proteins, Signal TransducingAPBB1 protein, humanELMO1 protein, humanNerve Tissue ProteinsNuclear Proteinsrac1 GTP-Binding ProteinRAC1 protein, humanADP-ribosylation factor (ARF)amyloid precursor protein (APP)amyloid β A4 precursor protein-binding family B member 1ELMO1FE65guanine nucleotide exchange factor (GEF)neurite outgrowthRas-related C3 botulinum toxin substrate 1 (Rac1)

Identifiers

PMID29615491
PMCPMC5961050
OpenAlexW2795932837

What OpenQuestion holds

Textmetadata
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.