Evidence map›Paper›PMID 17938235›Full record

ArticleThe Journal of experimental medicine2007

Identification of an alternative G{alpha}q-dependent chemokine receptor signal transduction pathway in dendritic cells and granulocytes.

Guixiu Shi, Santiago Partida-Sánchez, Ravi S Misra, Michael Tighe, Michael T Borchers, James J Lee, Melvin I Simon, Frances E Lund

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  4. Review
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  6. Review
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  8. Article
  9. Article
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  11. Review
  12. Loss of Gαq impairs regulatory B-cell function.Arthritis research & therapy · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Cinacalcet Rectifies Hypercalcemia in a Patient With Familial Hypocalciuric Hypercalcemia Type 2 (FHH2) Caused by a Germline Loss-of-Function GαJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018
    Article
  17. Expression of GJournal of immunology research · 2018
    Article
  18. GMediators of inflammation · 2017
    Article
  19. Article
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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

8 authors at 4 institutions in 1 country.

Guixiu ShiTrudeau Institute, Saranac Lake, NY 12983, USA.
Santiago Partida-Sánchez
Ravi S Misra
Michael Tighe
Michael T Borchers
James J Lee
Melvin I Simon
Frances E Lund
Trudeau Institute · USCalifornia Institute of Technology · USMayo Clinic in Arizona · USUniversity of Cincinnati Medical Center · US

Funding

Ecto-enzyme CD38: Regulator of dendritic cell migrationR01AI057996 · NIAID · TRUDEAU INSTITUTE, INC. · PI LUND, FRANCES E. · 2004 to 2006
$1.0M
NIAID NIH HHS AI-057996NIAID NIH HHS R01 AI057996
6 · The paper itself

Abstract

CD38 controls the chemotaxis of leukocytes to some, but not all, chemokines, suggesting that chemokine receptor signaling in leukocytes is more diverse than previously appreciated. To determine the basis for this signaling heterogeneity, we examined the chemokine receptors that signal in a CD38-dependent manner and identified a novel "alternative" chemokine receptor signaling pathway. Similar to the "classical" signaling pathway, the alternative chemokine receptor pathway is activated by Galpha(i2)-containing Gi proteins. However, unlike the classical pathway, the alternative pathway is also dependent on the Gq class of G proteins. We show that Galpha(q)-deficient neutrophils and dendritic cells (DCs) make defective calcium and chemotactic responses upon stimulation with N-formyl methionyl leucyl phenylalanine and CC chemokine ligand (CCL) 3 (neutrophils), or upon stimulation with CCL2, CCL19, CCL21, and CXC chemokine ligand (CXCL) 12 (DCs). In contrast, Galpha(q)-deficient T cell responses to CXCL12 and CCL19 remain intact. Thus, the alternative chemokine receptor pathway controls the migration of only a subset of cells. Regardless, the novel alternative chemokine receptor signaling pathway appears to be critically important for the initiation of inflammatory responses, as Galpha(q) is required for the migration of DCs from the skin to draining lymph nodes after fluorescein isothiocyanate sensitization and the emigration of monocytes from the bone marrow into inflamed skin after contact sensitization.

Indexed as

Signal TransductionADP-ribosyl Cyclase 1AnimalsAntigens, CDCD4-Positive T-LymphocytesChemotaxis, LeukocyteDendritic CellsGranulocytesGTP-Binding Protein alpha Subunits, Gq-G11MiceMice, KnockoutReceptors, ChemokineADP-ribosyl Cyclase 1Antigens, CDGTP-Binding Protein alpha Subunits, Gq-G11Receptors, Chemokine

Identifiers

PMID17938235
PMCPMC2118484
OpenAlexW2153091412

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.