Evidence map›Paper›PMID 20308281›Full record

ArticleGenetics2010

Caenorhabditis elegans fibroblast growth factor receptor signaling can occur independently of the multi-substrate adaptor FRS2.

Te-Wen Lo, Daniel C Bennett, S Jay Goodman, Michael J Stern

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. The conserved fibroblast growth factor receptor-based signaling is required for dendrite regeneration.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Frontiers in immunology · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. Canonical RTK-Ras-ERK signaling and related alternative pathways.WormBook : the online review of C. elegans biology · 2013
    Review
  8. 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

4 authors at 1 institution in 1 country.

Te-Wen LoDepartment of Genetics, Yale University School of Medicine, New Haven, Connecticut 06520-8005, USA.
Daniel C Bennett
S Jay Goodman
Michael J Stern
Yale University · US

Funding

Skill Development for Diverse Scientific Careers: A New Course Predoctoral Program in Cellular and Molecular BiologyT32GM007223 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 1985 to 2019
$31.0M
SIGNALING GENES INVOLVED IN CELL MIGRATION IN C ELEGANSR01GM050504 · NIGMS · YALE UNIVERSITY · PI KOELLE, MICHAEL R · 1994 to 2007
$2.3M
TRANSPORT PROCESSES IN BIOLOGICAL SYSTEMST32DK007259 · NIDDK · YALE UNIVERSITY · PI BOULPAEP, EMILE L · 1986 to 2008
$963k
NIDDK NIH HHS T32 DK007259NIDDK NIH HHS T32 DK07259NIGMS NIH HHS GM50504NIGMS NIH HHS R01 GM050504NIGMS NIH HHS T32 GM007223NIGMS NIH HHS T32 GM07223
6 · The paper itself

Abstract

The components of receptor tyrosine kinase signaling complexes help to define the specificity of the effects of their activation. The Caenorhabditis elegans fibroblast growth factor receptor (FGFR), EGL-15, regulates a number of processes, including sex myoblast (SM) migration guidance and fluid homeostasis, both of which require a Grb2/Sos/Ras cassette of signaling components. Here we show that SEM-5/Grb2 can bind directly to EGL-15 to mediate SM chemoattraction. A yeast two-hybrid screen identified SEM-5 as able to interact with the carboxy-terminal domain (CTD) of EGL-15, a domain that is specifically required for SM chemoattraction. This interaction requires the SEM-5 SH2-binding motifs present in the CTD (Y(1009) and Y(1087)), and these sites are required for the CTD role of EGL-15 in SM chemoattraction. SEM-5, but not the SEM-5 binding sites located in the CTD, is required for the fluid homeostasis function of EGL-15, indicating that SEM-5 can link to EGL-15 through an alternative mechanism. The multi-substrate adaptor protein FRS2 serves to link vertebrate FGFRs to Grb2. In C. elegans, an FRS2-like gene, rog-1, functions upstream of a Ras/MAPK pathway for oocyte maturation but is not required for EGL-15 function. Thus, unlike the vertebrate FGFRs, which require the multi-substrate adaptor FRS2 to recruit Grb2, EGL-15 can recruit SEM-5/Grb2 directly.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBinding SitesCaenorhabditis elegansCell MovementGenesGRB2 Adaptor ProteinMembrane ProteinsProtein BindingProteinsReceptor Protein-Tyrosine KinasesReceptors, Fibroblast Growth FactorSignal TransductionAdaptor Proteins, Signal TransducingFRS2 protein, humanGRB2 Adaptor ProteinMembrane ProteinsProteinsReceptor Protein-Tyrosine KinasesReceptors, Fibroblast Growth Factor

Identifiers

PMID20308281
PMCPMC2881135
OpenAlexW2110586413

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.