Evidence map›Paper›PMID 15650218›Full record

ArticleJournal of virology2005

Anti-CXCR4 monoclonal antibodies recognizing overlapping epitopes differ significantly in their ability to inhibit entry of human immunodeficiency virus type 1.

Xavier Carnec, Lan Quan, William C Olson, Uriel Hazan, Tatjana Dragic

Abstract read
In one paragraph

Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

  1. Article
  2. CXCR4 coordinates adhesion, migration, and development of human NK cells.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
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  12. Article
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  15. Design and evaluation of a CXCR4 targeting peptide 4DV3 as an HIV entry inhibitor and a ligand for targeted drug delivery.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2019
    Article
  16. Article
  17. Detecting Cell Surface Expression of the G Protein-Coupled Receptor CXCR4.Methods in molecular biology (Clifton, N.J.) · 2018
    Article
  18. Review
  19. Article
  20. 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

5 authors.

Xavier CarnecAlbert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461, USA.
Lan Quan
William C Olson
Uriel Hazan
Tatjana Dragic

Funding

STRUCTURE/FUNCTION STUDY OF HIV AND SIV CORECEPTORSR01AI043847 · NIAID · YESHIVA UNIVERSITY · PI DRAGIC, TATJANA · 1998 to 2005
$2.2M
INHIBITION OF HIV1 ENTRY BY CHEMOKINESR43AI040810 · NIAID · PROGENICS PHARMACEUTICALS, INC. · PI ALLAWAY, GRAHAM P · 1997 to 1997
–
NIAID NIH HHS R01 AI043847NIAID NIH HHS R01 AI43847NIAID NIH HHS R43 AI40810
6 · The paper itself

Abstract

CXCR4 is one of two physiologically relevant human immunodeficiency type 1 (HIV-1) entry coreceptors. Studies of CXCR4 mutants have not clearly identified the determinants of coreceptor function and specificity. We therefore used a panel of monoclonal antibodies to further elucidate CXCR4 expression, structure, and function. Our findings show the existence of conformational subpopulations of CXCR4 that are in equilibrium on the cell surface but are not cell type specific as previously reported. HIV-1 X4 isolates can interact with multiple CXCR4 conformations in order to gain entry into target cells.

Indexed as

Epitope MappingAntibodies, MonoclonalCell LineHeLa CellsHIV-1HumansPoint MutationProtein ConformationReceptors, CXCR4T-LymphocytesAntibodies, MonoclonalReceptors, CXCR4

Identifiers

PMID15650218
PMCPMC544137

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.