Evidence map›Paper›PMID 21124917›Full record

ArticlePloS one2010

An essential role of the cytoplasmic tail of CXCR4 in G-protein signaling and organogenesis.

Darran G Cronshaw, Yuchun Nie, Janelle Waite, Yong-Rui Zou

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. 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
1.1field-weighted citation impact, top 24% 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, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. CXCR4/CXCL12 blockade therapy; a new horizon in TNBC therapy.Medical oncology (Northwood, London, England) · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. CXCR4 in breast cancer: oncogenic role and therapeutic targeting.Drug design, development and therapy · 2015
    Review
  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

4 authors at 1 institution in 1 country.

Darran G CronshawCenter for Autoimmune and Musculoskeletal Diseases, Feinstein Institute for Medical Research, Manhasset, New York, USA.
Yuchun Nie
Janelle Waite
Yong-Rui Zou
Feinstein Institute for Medical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CXCR4 regulates cell proliferation, enhances cell survival and induces chemotaxis, yet molecular mechanisms underlying its signaling remain elusive. Like all other G-protein coupled receptors (GPCRs), CXCR4 delivers signals through G-protein-dependent and -independent pathways, the latter involving its serine-rich cytoplasmic tail. To evaluate the signaling and biological contribution of this G-protein-independent pathway, we generated mutant mice that express cytoplasmic tail-truncated CXCR4 (ΔT) by a gene knock-in approach. We found that ΔT mice exhibited multiple developmental defects, with not only G-protein-independent but also G-protein-dependent signaling events completely abolished, despite ΔT's ability to still associate with G-proteins. These results reveal an essential positive regulatory role of the cytoplasmic tail in CXCR4 signaling and suggest the tail is crucial for mediating G-protein activation and initiating crosstalk between G-protein-dependent and G-protein-independent pathways for correct GPCR signaling.

Indexed as

OrganogenesisSignal TransductionAnimalsCell AdhesionChemokine CXCL12ChemotaxisFemaleFlow CytometryGastric MucosaGTP-Binding ProteinsHEK293 CellsHumansImmunoblottingImmunoprecipitationMaleMiceChemokine CXCL12Cxcl12 protein, mouseCXCR4 protein, mouseGTP-Binding ProteinsReceptors, CXCR4

Identifiers

PMID21124917
PMCPMC2988825
OpenAlexW1970837859

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.