Evidence map›Paper›PMID 20519440›Full record

ArticleMolecular biology of the cell2010

S100A4 regulates macrophage chemotaxis.

Zhong-Hua Li, Natalya G Dulyaninova, Reniqua P House, Steven C Almo, Anne R Bresnick

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
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  8. Article
  9. bioRxiv : the preprint server for biology · 2025
    Article
  10. Nonmuscle myosin 2 turnover in cells is synergistically controlled by the tail and the motor domain.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  18. Article
  19. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
  20. Article

28 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Zhong-Hua LiDepartment of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Natalya G Dulyaninova
Reniqua P House
Steven C Almo
Anne R Bresnick
Albert Einstein College of Medicine · US

Funding

Molecular and Structural Basis for T Cell CostimulationR01AI007289 · NIAID · YESHIVA UNIVERSITY · PI NATHENSON, STANLEY G · 1985 to 2012
$7.7M
Old Drugs and New Strategies for Tumor MetastasisR01CA129598 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI BRESNICK, ANNE R · 2008 to 2011
$989k
Molecular and Structural Basis for T Cell CostimulationR56AI007289 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI NATHENSON, STANLEY G · 2007 to 2007
$553k
BIOCHEMICAL STUDIES ON HISTOCOMPATIBILITY ANTIGENSR37AI007289 · NIAID · YESHIVA UNIVERSITY · PI NATHENSON, STANLEY G · 1987 to 1996
–
NCI NIH HHS CA-129598NCI NIH HHS R01 CA129598NIAID NIH HHS AI-07289NIAID NIH HHS R01 AI007289NIAID NIH HHS R56 AI007289
6 · The paper itself

Abstract

S100A4, a member of the S100 family of Ca(2+)-binding proteins, is directly involved in tumor metastasis. In addition to its expression in tumor cells, S100A4 is expressed in normal cells and tissues, including fibroblasts and cells of the immune system. To examine the contribution of S100A4 to normal physiology, we established S100A4-deficient mice by gene targeting. Homozygous S100A4(-/-) mice are fertile, grow normally and exhibit no overt abnormalities; however, the loss of S100A4 results in impaired recruitment of macrophages to sites of inflammation in vivo. Consistent with these observations, primary bone marrow macrophages (BMMs) derived from S100A4(-/-) mice display defects in chemotactic motility in vitro. S100A4(-/-) BMMs form unstable protrusions, overassemble myosin-IIA, and exhibit altered colony-stimulating factor-1 receptor signaling. These studies establish S100A4 as a regulator of physiological macrophage motility and demonstrate that S100A4 mediates macrophage recruitment and chemotaxis in vivo.

Indexed as

ChemotaxisActomyosinAnimalsBone Marrow CellsCell CountCell Surface ExtensionsCytoskeletonHeterocyclic Compounds, 4 or More RingsHumansInflammationMacrophage Colony-Stimulating FactorMacrophagesMiceMice, KnockoutModels, BiologicalReceptor, Macrophage Colony-Stimulating FactorActomyosinblebbistatinHeterocyclic Compounds, 4 or More RingsMacrophage Colony-Stimulating FactorReceptor, Macrophage Colony-Stimulating FactorS100a4 protein, mouseS100 Calcium-Binding Protein A4S100 Proteins

Identifiers

PMID20519440
PMCPMC2912347
OpenAlexW2131313137

What OpenQuestion holds

Textmetadata
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.