Evidence map›Paper›PMID 25263281›Full record

ArticleEuropean journal of immunology2015

Class I myosin Myo1e regulates TLR4-triggered macrophage spreading, chemokine release, and antigen presentation via MHC class II.

Jens Wenzel, Jessica L Ouderkirk, Mira Krendel, Roland Lang

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. MYO1F Regulates IgE and MRGPRX2-Dependent Mast Cell Exocytosis.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  10. Review
  11. Article
  12. Long-Tailed Unconventional Class I Myosins in Health and Disease.International journal of molecular sciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Osteoclast stimulation factor 1 (Ostf1) KNOCKOUT increases trabecular bone mass in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2017
    Article
  18. Myosin-I molecular motors at a glance.Journal of cell science · 2016
    Review
  19. 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

4 authors at 3 institutions in 2 countries.

Jens WenzelInstitute of Clinical Microbiology, Immunology and Hygiene, University Hospital Erlangen, Friedrich Alexander Universität Erlangen-Nürnberg, Erlangen, Germany.
Jessica L Ouderkirk
Mira Krendel
Roland Lang
SUNY Upstate Medical University · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversitätsklinikum Erlangen · DE

Funding

Role of myosin 1e in podocyte biology and renal filtrationR01DK083345 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI Mira Krendel · 2011 to 2026
$6.8M
NIDDK NIH HHS 1R01DK083345NIDDK NIH HHS R01 DK083345
6 · The paper itself

Abstract

TLR-mediated recognition of microbial danger induces substantial changes in macrophage migration, adherence, and phagocytosis. Recently, we described the LPS-regulated phosphorylation of many cytoskeleton-associated proteins by phosphoproteomics. The functional role of these cytoskeletal and motor proteins in innate immune cell responses is largely unexplored. Here, we first identified both long-tailed class I myosins Myo1e and Myo1f as important contributors to LPS-triggered macrophage spreading. Mouse bone marrow-derived macrophages and DCs deficient in Myo1e selectively secreted increased amounts of the chemokine CCL2. In addition, the cell surface expression of MHC class II (MHC-II) on both cell types was reduced in the absence of Myo1e. However, transcriptional changes in CCL2 and MHC-II were not observed in the absence of Myo1e, indicating that Myo1e regulates specific intracellular transport processes. The capacity of macrophages and DCs lacking Myo1e to stimulate antigen-specific CD4(+) T-cell proliferation was impaired, consistent with the reduced MHC-II surface protein levels. Surprisingly, in Myo1e-deficient DCs, the proteolytic cleavage of endocytosed antigen was also increased. Together, our results provide evidence for a non-redundant function of the motor protein Myo1e in the regulation of TLR4-controlled, cytoskeleton-associated functional properties of macrophages and DCs, and in induction of a full MHC-II-restricted adaptive immune response.

Indexed as

AnimalsAntigen PresentationBone Marrow CellsCD4-Positive T-LymphocytesCell ProliferationChemokine CCL2CytoskeletonDendritic CellsGene Expression RegulationHistocompatibility Antigens Class IILipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMyosinsCcl2 protein, mouseChemokine CCL2Histocompatibility Antigens Class IILipopolysaccharidesMyo1e protein, mouseMyo1f protein, mouseMyosinsMyosin Type ITlr4 protein, mouseToll-Like Receptor 4CytoskeletonMacrophagesMHC class IIMyosinToll-like receptors

Identifiers

PMID25263281
PMCPMC4293287
OpenAlexW1576433667

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.