Evidence map›Paper›PMID 24409221›Full record

ArticlePloS one2013

Functional consequences of the macrophage stimulating protein 689C inflammatory bowel disease risk allele.

Steven E Kauder, Lydia Santell, Elaine Mai, Lilyan Y Wright, Elizabeth Luis, Elsa N N'Diaye, Jeff Lutman, Navneet Ratti, Susan M Sa, Henry R Maun and 10 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. A network map of macrophage-stimulating protein (MSP) signaling.Journal of cell communication and signaling · 2023
    Article
  5. Review
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  9. Review
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  16. Ron receptor signaling is protective against DSS-induced colitis in mice.American journal of physiology. Gastrointestinal and liver physiology · 2014
    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

20 authors at 2 institutions in 1 country.

Steven E KauderDiscovery Immunology, Genentech Inc., South San Francisco, California, United States of America.
Lydia SantellEarly Discovery Biochemistry, Genentech Inc., South San Francisco, California, United States of America.
Elaine MaiBiochemical and Cellular Pharmacology, Genentech Inc., South San Francisco, California, United States of America.
Lilyan Y WrightImmunology, Tissue Growth and Repair- Diagnostics Discovery, Genentech Inc., South San Francisco, California, United States of America.
Elizabeth LuisProtein Chemistry, Genentech Inc., South San Francisco, California, United States of America.
Elsa N N'DiayeDiscovery Immunology, Genentech Inc., South San Francisco, California, United States of America.
Jeff LutmanPharmacokinetics and Pharmacodynamics, Genentech Inc., South San Francisco, California, United States of America.
Navneet RattiPathology, Genentech Inc., South San Francisco, California, United States of America.
Susan M SaPathology, Genentech Inc., South San Francisco, California, United States of America.
Henry R MaunEarly Discovery Biochemistry, Genentech Inc., South San Francisco, California, United States of America.
Eric StefanichPharmacokinetics and Pharmacodynamics, Genentech Inc., South San Francisco, California, United States of America.
Lino C GonzalezProtein Chemistry, Genentech Inc., South San Francisco, California, United States of America.
Robert R GrahamImmunology, Tissue Growth and Repair -Human Genetics, Genentech Inc., South San Francisco, California, United States of America.
Lauri DiehlPathology, Genentech Inc., South San Francisco, California, United States of America.
William A FaubionDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, United States of America.
Mary E KeirImmunology, Tissue Growth and Repair- Diagnostics Discovery, Genentech Inc., South San Francisco, California, United States of America.
Judy YoungBiochemical and Cellular Pharmacology, Genentech Inc., South San Francisco, California, United States of America.
Amitabha ChaudhuriMolecular Oncology, Genentech Inc., South San Francisco, California, United States of America.
Robert A LazarusEarly Discovery Biochemistry, Genentech Inc., South San Francisco, California, United States of America.
Jackson G EgenDiscovery Immunology, Genentech Inc., South San Francisco, California, United States of America.
Mayo Clinic · USMolecular Oncology (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMacrophage stimulating protein (MSP) is a serum growth factor that binds to and activates the receptor tyrosine kinase, Recepteur d'Origine Nantais (RON). A non-synonymous coding variant in MSP (689C) has been associated with genetic susceptibility to both Crohn's disease and ulcerative colitis, two major types of inflammatory bowel disease (IBD) characterized by chronic inflammation of the digestive tract. We investigated the consequences of this polymorphism for MSP-RON pathway activity and IBD pathogenesis.

methodsRON expression patterns were examined on mouse and human cells and tissues under normal and disease conditions to identify cell types regulated by MSP-RON. Recombinant MSP variants were tested for their ability to bind and stimulate RON and undergo proteolytic activation. MSP concentrations were quantified in the serum of individuals carrying the MSP 689R and 689C alleles.

resultsIn intestinal tissue, RON was primarily expressed by epithelial cells under normal and disease conditions. The 689C polymorphism had no impact on the ability of MSP to bind to or signal through RON. In a cohort of normal individuals and IBD patients, carriers of the 689C polymorphism had lower concentrations of MSP in their serum.

conclusionsBy reducing the quantities of circulating MSP, the 689C polymorphism, or a variant in linkage disequilibrium with this polymorphism, may impact RON ligand availability and thus receptor activity. Given the known functions of RON in regulating wound healing and our analysis of RON expression patterns in human intestinal tissue, these data suggest that decreased RON activity may impact the efficiency of epithelial repair and thus underlie the increased IBD susceptibility associated with the MSP 689C allele.

Indexed as

AllelesGenetic Predisposition to DiseasePolymorphism, Genetic3T3 CellsAnimalsEpithelial CellsGene Expression RegulationHepatocyte Growth FactorHumansInflammatory Bowel DiseasesIntestinesMiceModels, MolecularProtein ConformationProteolysisProto-Oncogene ProteinsHepatocyte Growth Factormacrophage stimulating proteinProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRON protein

Identifiers

PMID24409221
PMCPMC3884107
OpenAlexW2053150767

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.