Evidence map›Paper›PMID 25194421›Full record

ArticleNature immunology2014

Diversification of TAM receptor tyrosine kinase function.

Anna Zagórska, Paqui G Través, Erin D Lew, Ian Dransfield, Greg Lemke

Open access · greenAbstract read
In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 306 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
306citing papers in PubMed, 1 pooled it
14.0field-weighted citation impact, top 1% 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

306 citing papers in PubMed, 1 synthesis or guideline pooled it, 426 citations in OpenAlex.

  1. Pooled it
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  8. NLRC5-Deficient Macrophages Promote a Tumor-Permissive Phenotype via AXL- and MERTK-Mediated Efferocytosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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246 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Anna ZagórskaMolecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA.
Paqui G TravésMolecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA.
Erin D LewMolecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA.
Ian DransfieldMRC Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK.
Greg Lemke1] Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA. [2] Immunobiology and Microbial Pathogenesis Laboratory, Salk Institute for Biological Studies, La Jolla, California, USA.
Salk Institute for Biological Studies · USCentre for Inflammation Research · GB

Funding

TAM Receptors and Virus InfectionR01AI101400 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI DIAMOND, MICHAEL S, KLEIN, ROBYN S. · 2012 to 2021
$5.8M
TAM receptor control of microglial function and nervous system homeostasisR01NS085296 · NINDS · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI LEMKE, GREG E · 2013 to 2017
$2.1M
TAM Receptor Regulation of Innate ImmunityR01AI077058 · NIAID · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI LEMKE, GREG E · 2008 to 2011
$1.9M
NIAID NIH HHS R01 AI077058NIAID NIH HHS R01 AI101400NINDS NIH HHS R01 NS085296
6 · The paper itself

Abstract

The clearance of apoptotic cells is critical for both tissue homeostasis and the resolution of inflammation. We found that the TAM receptor tyrosine kinases Axl and Mer had distinct roles as phagocytic receptors in these two settings, in which they exhibited divergent expression, regulation and activity. Mer acted as a tolerogenic receptor in resting macrophages and during immunosuppression. In contrast, Axl was an inflammatory response receptor whose expression was induced by proinflammatory stimuli. Axl and Mer differed in their ligand specificities, ligand-receptor complex formation in tissues, and receptor shedding upon activation. These differences notwithstanding, phagocytosis by either protein was strictly dependent on receptor activation triggered by bridging of TAM receptor-ligand complexes to the 'eat-me' signal phosphatidylserine on the surface of apoptotic cells.

Indexed as

AnimalsApoptosisAxl Receptor Tyrosine KinaseBone Marrow CellsCells, Culturedc-Mer Tyrosine KinaseDendritic CellsGene ExpressionGrowth Arrest-Specific Protein 6ImmunoblottingIntercellular Signaling Peptides and ProteinsLipopolysaccharidesMacrophagesMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalAxl Receptor Tyrosine KinaseAXL receptor tyrosine kinase, mousec-Mer Tyrosine KinaseGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsLipopolysaccharidesMertk protein, mouseProto-Oncogene ProteinsReceptor Protein-Tyrosine Kinases

Identifiers

PMID25194421
PMCPMC4169336
OpenAlexW2118374586

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.