Evidence map›Paper›PMID 22899245›Full record

ArticleArchives of dermatological research2013

The candidate tumor suppressor gene Ecrg4 as a wound terminating factor in cutaneous injury.

Ashkaun Shaterian, Steven Kao, Lin Chen, Luisa A DiPietro, Raul Coimbra, Brian P Eliceiri, Andrew Baird

Abstract read
In one paragraph

Article in Archives of dermatological research, 2013. 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
1.3field-weighted citation impact, top 21% 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, 29 citations in OpenAlex.

  1. Cancer as an evolutionary reversal-time for a paradigm shift.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026
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  12. ECRG4 as a novel tumor suppressor gene inhibits colorectal cancer cell growth in vitro and in vivo.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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  17. Esophageal cancer-related gene-4 (ECRG4) interactions with the innate immunity receptor complex.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
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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

7 authors at 2 institutions in 1 country.

Ashkaun ShaterianDivision of Trauma, Surgical Critical Care and Burns, Department of Surgery, University of California San Diego School of Medicine, 212 Dickinson Street, San Diego, CA 92103, USA. ashaterian@ucsd.edu
Steven Kao
Lin Chen
Luisa A DiPietro
Raul Coimbra
Brian P Eliceiri
Andrew Baird
University of California, San Diego · USUniversity of Illinois Chicago · US

Funding

ANGIOGENESIS IN WOUND REPAIRR01GM050875 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DIPIETRO, LUISA A · 1999 to 2020
$6.6M
Role of Src family kinases in endothelial cell biologyR01HL073396 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ELICEIRI, BRIAN P · 2002 to 2011
$3.5M
A Combinatorial Approach to Wound Healing for Protein, Gene and Cell TherapeuticsP20GM078421 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BAIRD, ANDREW · 2006 to 2009
$3.4M
Epithelial-connective tissue interactions: Influence on scar formationP20GM078426 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DIPIETRO, LUISA A · 2006 to 2009
$3.0M
Vascular mechanisms regulating breast cancer brain metastasisR01CA170140 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ELICEIRI, BRIAN P, FELDING, BRUNIE H. · 2012 to 2016
$1.8M
Targeting the choroid plexus for drug translocation into CSFR21EY018479 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BAIRD, ANDREW · 2007 to 2010
$606k
Biotechnology and Biological Sciences Research Council BB/C50466X/1NCI NIH HHS R01 CA170140NCRR NIH HHS 1TL1RR03197NEI NIH HHS EY018479NEI NIH HHS R21 EY018479NHLBI NIH HHS HL73396NHLBI NIH HHS R01 HL073396NIGMS NIH HHS GM078421NIGMS NIH HHS GM078426NIGMS NIH HHS P20 GM078421NIGMS NIH HHS P20 GM078426NIGMS NIH HHS R01 GM050875
6 · The paper itself

Abstract

The Esophageal cancer-related gene-4 (Ecrg4) is a candidate tumor suppressor gene whose secreted protein product has been implicated in the development and progression of epithelial cancers, neuroprogenitor cell activation after central nervous system injury, cell senescence in neurodegeneration, and the survival of hematopoietic stem cells. Here, we investigated the temporal and spatial localization of Ecrg4 expression in healthy and injured mouse skin, and evaluated the biological activity of Ecrg4 using viral-mediated gene delivery in cutaneous wound healing models. Using in situ hybridization and immunohistochemistry, we found both Ecrg4 mRNA and its protein product localized to the epidermis, dermis, and hair follicles of healthy mouse skin. Upon cutaneous injury, Ecrg4 redistributed to the wound margins where gene microarray and quantitative RT-PCR showed an increased gene expression 5-10 days post-injury as a late phase injury response gene. Ecrg4 over-expression inhibited the directional migration of fibroblasts in modified Boyden chambers in vitro, but had no effect on rates of fibroblast proliferation. Ecrg4 over-expression in vivo at the wound margins delayed the rate of wound closure at 1 and 2 days after full-thickness punch injury. These findings point to the candidate tumor suppressor gene Ecrg4 as a novel, biologically active, constituent of skin and skin injury. The possibility that Ecrg4 serves as a wound termination factor during wound resolution is discussed.

Indexed as

AnimalsCell MovementCells, CulturedDisease Models, AnimalFibroblastsGenes, Tumor SuppressorGenetic VectorsHumansMiceMice, Inbred BALB CNeoplasm ProteinsSkinTransgenesTumor Suppressor ProteinsWound HealingECRG4 protein, humanNeoplasm ProteinsTumor Suppressor Proteins

Identifiers

PMID22899245
PMCPMC3510341
OpenAlexW1999602576

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.