Evidence map›Paper›PMID 15870290›Full record

ArticleMolecular and cellular biology2005

Vav activation and function as a rac guanine nucleotide exchange factor in macrophage colony-stimulating factor-induced macrophage chemotaxis.

Vidya Vedham, Hyewon Phee, K Mark Coggeshall

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Hematopoietic Stem Cells: Nature and Niche Nurture.Bioengineering (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Towards a New Understanding of Decision-Making by Hematopoietic Stem Cells.International journal of molecular sciences · 2020
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Macrophage motility is driven by frontal-towing with a force magnitude dependent on substrate stiffness.Integrative biology : quantitative biosciences from nano to macro · 2015
    Article
  13. Review
  14. Article
  15. CSF-1 receptor signaling in myeloid cells.Cold Spring Harbor perspectives in biology · 2014
    Review
  16. Article
  17. Article
  18. Review
  19. Interstitial leukocyte migration in vivo.Current opinion in cell biology · 2013
    Review
  20. Review
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

3 authors at 2 institutions in 2 countries.

Vidya VedhamThe Oklahoma Medical Research Foundation, Immunobiology and Cancer Program, 825 N.E. 13th St., Oklahoma City, OK 73104, USA.
Hyewon Phee
K Mark Coggeshall
Bipar · FRUniversity of California, San Francisco · US

Funding

Signaling by IgG receptors leading to phagocytosisR01AI049264 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI COGGESHALL, KENNETH MARK · 2002 to 2006
$1.6M
PHOSPHATIDYLINOSITOL 3 KINASE IN B CELL ACTIVATIONR01CA064268 · NCI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI COGGESHALL, KENNETH MARK · 1999 to 2003
$1.0M
REGULATION OF RAS ACTIVITY IN B LYMPHOCYTESR29CA064268 · NCI · OHIO STATE UNIVERSITY · PI COGGESHALL, KENNETH MARK · 1994 to 1998
–
NCI NIH HHS CA64268NCI NIH HHS R01 CA064268NIAID NIH HHS AI49264NIAID NIH HHS R01 AI049264
6 · The paper itself

Abstract

Signal transduction mediated by phosphatidylinositol 3-kinase (PI 3-kinase) is regulated by hydrolysis of its products, a function performed by the 145-kDa SH2 domain-containing inositol phosphatase (SHIP). Here, we show that bone marrow macrophages of SHIP(-/-) animals have elevated levels of phosphatidylinositol 3,4,5-trisphosphate [PI (3,4,5)P(3)] and displayed higher and more prolonged chemotactic responses to macrophage colony-stimulating factor (M-CSF) and elevated levels of F-actin relative to wild-type macrophages. We also found that the small GTPase Rac was constitutively active and its upstream activator Vav was constitutively phosphorylated in SHIP(-/-) macrophages. Furthermore, we show that Vav in wild-type macrophages is recruited to the membrane in a PI 3-kinase-dependent manner through the Vav pleckstrin homology domain upon M-CSF stimulation. Dominant inhibitory mutants of both Rac and Vav blocked chemotaxis. We conclude that Vav acts as a PI 3-kinase-dependent activator for Rac activation in macrophages stimulated with M-CSF and that SHIP regulates macrophage M-CSF-triggered chemotaxis by hydrolysis of PI (3,4,5)P(3).

Indexed as

AnimalsCell Cycle ProteinsCell MembraneCells, CulturedChemotaxisEnzyme ActivationMacrophage Colony-Stimulating FactorMacrophagesMiceMice, Inbred C57BLPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphoric Monoester HydrolasesProtein Structure, TertiaryProtein TransportCell Cycle ProteinsINPPL1 protein, humanMacrophage Colony-Stimulating Factorphosphatidylinositol 3,4,5-triphosphatePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPhosphoric Monoester HydrolasesProto-Oncogene ProteinsProto-Oncogene Proteins c-vavrac GTP-Binding ProteinsVav1 protein, mouse

Identifiers

PMID15870290
PMCPMC1087731
OpenAlexW2134591087

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.