Evidence map›Paper›PMID 20697431›Full record

ArticleCell research2010

EphA3 functions are regulated by collaborating phosphotyrosine residues.

Guanfang Shi, Gang Yue, Renping Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  7. The EphB6 Receptor: Kinase-Dead but Very Much Alive.International journal of molecular sciences · 2021
    Review
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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

3 authors at 1 institution in 1 country.

Guanfang ShiDepartment of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854, USA.
Gang Yue
Renping Zhou
Rutgers, The State University of New Jersey · US

Funding

TITLE REGULATION OF NEURONAL MITOSISP01HD023315 · NICHD · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI DREYFUS, CHERYL F · 1987 to 2013
$17.5M
NICHD NIH HHS 5P01HD023315NICHD NIH HHS P01 HD023315
6 · The paper itself

Abstract

Ephrin ligands interact with Eph receptors to regulate a wide variety of biological and pathological processes. Recent studies have identified several downstream pathways that mediate the functions of these receptors. Activation of the receptors by ephrin binding results in the phosphorylation of the receptor tyrosine residues. These phosphorylated residues serve as docking sites for many of the downstream signaling pathways. However, the relative contributions of different phosphotyrosine residues remain undefined. In the present study, we mutated each individual tyrosine residues in the cytoplasmic domain of EphA3 receptor and studied the effects using cell migration, process retraction, and growth cone collapse assays. Stimulation of the EphA3 receptor with ephrin-A5 inhibits 293A cell migration, reduces NG108-15 cell neurite outgrowth, and induces growth cone collapse in hippocampal neurons. Mutation of either Y602 or Y779 alone partially decreases EphA3-induced responses. Full abrogation can only be achieved with mutations of both Y602 and Y779. These observations suggest a collaborative model of different downstream pathways.

Indexed as

Cell MovementEphrin-A5HEK293 CellsHippocampusHumansMutagenesis, Site-DirectedNeuritesNeuronsPhosphorylationPhosphotyrosineReceptor, EphA3Signal TransductionEphrin-A5PhosphotyrosineReceptor, EphA3

Identifiers

PMID20697431
PMCPMC2970634
OpenAlexW1977745736

What OpenQuestion holds

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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.