Evidence map›Paper›PMID 24846720›Full record

ReviewInflammatory bowel diseases2014

Tyro3, Axl, and Mertk receptor signaling in inflammatory bowel disease and colitis-associated cancer.

Carla V Rothlin, Jonathan A Leighton, Sourav Ghosh

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammatory bowel diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. AXL-dependent autophagy impairment differentiates monocyte-derived macrophages from Crohn's disease and intestinal tuberculosis.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026
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  15. Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022
    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 2 institutions in 1 country.

Carla V Rothlin*Department of Immunobiology, School of Medicine, Yale University, New Haven, Connecticut; †Division of Gastroenterology, Mayo Clinic, Scottsdale, Arizona; and ‡Department of Cellular and Molecular Medicine and Arizona Cancer Center, University of Arizona, Tucson, Arizona.
Jonathan A Leighton
Sourav Ghosh
Mayo Clinic in Arizona · USYale University · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
SPORE in Gastrointestinal CancerP50CA095060 · NCI · UNIVERSITY OF ARIZONA · PI GERNER, EUGENE W · 2002 to 2012
$25.3M
TAM receptor tyrosine kinases in inflammatory boweldiseaseR01AI089824 · NIAID · YALE UNIVERSITY · PI ROTHLIN, CARLA · 2010 to 2018
$3.9M
NCI NIH HHS CA95060NCI NIH HHS P30 CA016359NCI NIH HHS P50 CA095060NIAID NIH HHS R01 AI089824
6 · The paper itself

Abstract

Three receptor tyrosine kinases, Tyro3, Axl, and Mertk (TAM) and their ligands Gas6 and Protein S, have emerged as potent negative regulators of innate immune responses. A number of studies using genetic ablation of TAM loci in mice have elucidated the mechanism of TAM engagement and function during the immune response and removal of apoptotic cells. Following phagocytosis of apoptotic cells or the induction of T-cell dependent adaptive immune responses, ligand-induced TAM signaling dampens proinflammatory cytokine production and thus prevents exaggerated or prolonged inflammation. It is believed that the TAM pathway may play an important role in the pathogenesis of inflammatory bowel disease. Suppression of inflammation and removal of apoptotic cells followed by tissue repair are essential processes for disease remission and the successful management of inflammatory bowel disease. In light of the key role of TAMs in controlling inflammatory responses, here, we review the recent advances on TAM research vis-à-vis the resolution of intestinal inflammation. Targeted activation of TAM receptor tyrosine kinases may represent a potent therapeutic opportunity in inflammatory bowel disease.

Indexed as

AnimalsAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseColitisGene Expression Regulation, NeoplasticHumansInflammatory Bowel DiseasesMiceNeoplasmsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesSignal TransductionAxl Receptor Tyrosine Kinasec-Mer Tyrosine KinaseMERTK protein, humanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTYRO3 protein, human

Identifiers

PMID24846720
PMCPMC4343000
OpenAlexW1974242686

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.