Evidence map›Paper›PMID 26082487›Full record

ArticleThe Journal of biological chemistry2015

Down-regulation of Stathmin Is Required for the Phenotypic Changes and Classical Activation of Macrophages.

Kewei Xu, Rene E Harrison

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. [Research progress in the role of STMN1 in tumor].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

2 authors at 1 institution in 1 country.

Kewei XuFrom the Departments of Cell and Systems Biology and Biological Sciences, University of Toronto Scarborough, Toronto, Ontario M1C 1A4, Canada.
Rene E HarrisonFrom the Departments of Cell and Systems Biology and Biological Sciences, University of Toronto Scarborough, Toronto, Ontario M1C 1A4, Canada harrison@utsc.utoronto.ca.
University of Toronto · CA

Funding

Canadian Institutes of Health Research MOP-68992
6 · The paper itself

Abstract

Macrophages are important cells of innate immunity with specialized capacity for recognition and elimination of pathogens and presentation of antigens to lymphocytes for adaptive immunity. Macrophages become activated upon exposure to pro-inflammatory cytokines and pathogenic stimuli. Classical activation of macrophages with interferon-γ (IFNγ) and lipopolysaccharide (LPS) triggers a wide range of signaling events and morphological changes to induce the immune response. Our previous microtubule (MT) proteomic work revealed that the stathmin association with MTs is considerably reduced in activated macrophages, which contain significantly more stabilized MTs. Here, we show that there is a global decrease in stathmin levels, an MT catastrophe protein, in activated macrophages using both immunoblotting and immunofluorescent microscopy. This is an LPS-specific response that induces proteasome-mediated degradation of stathmin. We explored the functions of stathmin down-regulation in activated macrophages by generating a stable cell line overexpressing stathmin-GFP. We show that stathmin-GFP overexpression impacts MT stability, impairs cell spreading, and reduces activation-associated phenotypes. Furthermore, overexpressing stathmin reduces complement receptor 3-mediated phagocytosis and cellular activation, implicating a pivotal inhibitory role for stathmin in classically activated macrophages.

Indexed as

Macrophage ActivationAnimalsCDC2 Protein KinaseCell LineCell ShapeDown-RegulationInterferon-gammaLipopolysaccharidesMacrophagesMiceMicrotubulesPhagocytosisPhenotypeProteasome Endopeptidase ComplexProtein StabilityReceptors, ComplementCDC2 Protein KinaseInterferon-gammaLipopolysaccharidesProteasome Endopeptidase ComplexReceptors, ComplementStathminStmn1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4activationinnate immunitymacrophagemicrotubulemicrotubule-associated proteinphagocytosisstathmin

Identifiers

PMID26082487
PMCPMC4521045
OpenAlexW1577221282

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.