Evidence map›Paper›PMID 25335894›Full record

ArticleJournal of cell science2014

Delivery of CSF-1R to the lumen of macropinosomes promotes its destruction in macrophages.

Jieqiong Lou, Shalini T Low-Nam, Jason G Kerkvliet, Adam D Hoppe

Open access · greenAbstract read
In one paragraph

Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Revealing macropinocytosis using nanoparticles.Molecular aspects of medicine · 2022
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Macropinosomes as units of signal transduction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  15. Constitutive and stimulated macropinocytosis in macrophages: roles in immunity and in the pathogenesis of atherosclerosis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019
    Review
  16. 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 1 institution in 1 country.

Jieqiong LouDepartment of Chemistry and Biochemistry, South Dakota State University, Brookings, 57007 SD, USA.
Shalini T Low-NamDepartment of Chemistry and Biochemistry, South Dakota State University, Brookings, 57007 SD, USA.
Jason G KerkvlietDepartment of Chemistry and Biochemistry, South Dakota State University, Brookings, 57007 SD, USA.
Adam D HoppeDepartment of Chemistry and Biochemistry, South Dakota State University, Brookings, 57007 SD, USA adam.hoppe@sdstate.edu.
South Dakota State University · US

Funding

Signaling complex remodeling on the surfaces of live macrophagesF32GM105277 · NIGMS · SOUTH DAKOTA STATE UNIVERSITY · PI LOW-NAM, SHALINI THERESE · 2013 to 2014
$54k
NIGMS NIH HHS 1F32GM105277NIGMS NIH HHS F32 GM105277
6 · The paper itself

Abstract

Activation of the macrophage colony stimulating factor-1 receptor (CSF-1R) by CSF-1 stimulates pronounced macropinocytosis and drives proliferation of macrophages. Although the role of macropinocytosis in CSF-1R signaling remains unknown, we show here that, despite internalizing large quantities of plasma membrane, macropinosomes contribute little to the internalization of the CSF-1-CSF-1R complex. Rather, internalization of the CSF-1R in small endocytic vesicles that are sensitive to clathrin disruption, outcompetes macropinosomes for CSF-1R endocytosis. Following internalization, small vesicles carrying the CSF-1R underwent homotypic fusion and then trafficked to newly formed macropinosomes bearing Rab5. As these macropinosomes matured, acquiring Rab7, the CSF-1R was transported into their lumen and degraded. Inhibition of macropinocytosis delayed receptor degradation despite no disruption to CSF-1R endocytosis. These data indicate that CSF-1-stimulated macropinosomes are sites of multivesicular body formation and accelerate CSF-1R degradation. Furthermore, we demonstrate that macropinocytosis and cell growth have a matching dose dependence on CSF-1, suggesting that macropinosomes might be a central mechanism coupling CSF-1R signaling and macrophage growth.

Indexed as

PinocytosisAnimalsBone Marrow CellsClathrinEndocytosisEndosomesHumansMacrophage Colony-Stimulating FactorMacrophagesMice, Inbred C57BLMitogensModels, BiologicalProtein TransportProteolysisrab5 GTP-Binding Proteinsrab7 GTP-Binding ProteinsClathrinMacrophage Colony-Stimulating FactorMitogensrab5 GTP-Binding Proteinsrab7 GTP-Binding Proteinsrab7 GTP-binding proteins, humanrab7 GTP-binding proteins, mouserab GTP-Binding ProteinsReceptor, Macrophage Colony-Stimulating FactorCSF-1REndocytosisMacrophageMacropinosomeM-CSF

Identifiers

PMID25335894
PMCPMC4265739
OpenAlexW2097851646

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.