Evidence map›Paper›PMID 14555957›Full record

ArticleNature biotechnology2003

A genetic approach to inactivating chemokine receptors using a modified viral protein.

V McNeil Coffield, Qi Jiang, Lishan Su

Open access · greenAbstract read
In one paragraph

Article in Nature biotechnology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. CXCR4 blockade induces atherosclerosis by affecting neutrophil function.Journal of molecular and cellular cardiology · 2014
    Article
  3. Article
  4. Article
  5. SDF-1α and CXCR4 as therapeutic targets in cardiovascular disease.American journal of cardiovascular disease · 2012
    Article
  6. Article
  7. Article
  8. Article
  9. Maraviroc in the treatment of HIV infection.Drug design, development and therapy · 2009
    Article
  10. Article
  11. Article
  12. Cryopyrin/NALP3 binds ATP/dATP, is an ATPase, and requires ATP binding to mediate inflammatory signaling.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. 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

3 authors at 1 institution in 1 country.

V McNeil CoffieldCurriculum in Genetics and Molecular Biology, and 22-048 Lineberger Cancer Center, School of Medicine, The University of North Carolina, Chapel Hill, NC 27599-7295, USA.
Qi Jiang
Lishan Su
University of North Carolina at Chapel Hill · US

Funding

HIV-1 Replication and Pathogenesis in the Human ThymusR01AI041356 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 1998 to 2007
$2.2M
Novel genetic approach to dissecting homing /engraftmentR21HL072240 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2002 to 2004
$651k
Genetic Analy. of Chemokine Receptors in T Cell Develop.R21AI053804 · NIAID · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SU, LISHAN · 2002 to 2003
$361k
NHLBI NIH HHS HL72240NHLBI NIH HHS R21 HL072240NIAID NIH HHS AI53804NIAID NIH HHS R01 AI041356NIAID NIH HHS R21 AI053804
6 · The paper itself

Abstract

We have developed a genetic system, called degrakine, that specifically and stably inactivates chemokine receptors (CKR) by redirecting the ability of the HIV-1 protein, Vpu, to degrade CD4 in the endoplasmic reticulum (ER) via the host proteasome machinery. To harness Vpu's proteolytic targeting capability to degrade new receptors, we fused a chemokine with the C terminal region of Vpu. The fusion protein, or degrakine, accumulates in the ER, trapping and functionally inactivating its target CKR. We have demonstrated that degrakines based on SDF-1 (CXCL12), MDC (CCL22) and RANTES (CCL5) specifically inactivate their respective receptor functions. Using a retroviral vector expressing the SDF-1 degrakine, we have established that CXCR4 is required for the homing of hematopoietic stem/progenitor cells (HSPC) to the bone marrow immediately after transplantation. Thus the degrakine provides an effective genetic tool to dissect receptor functions in a number of biological systems in vitro and in vivo.

Indexed as

AnimalsCells, CulturedChemokinesDrug Delivery SystemsEndoplasmic ReticulumGene TargetingHuman Immunodeficiency Virus ProteinsHumansMiceOsteitisProtein EngineeringReceptors, ChemokineRecombinant Fusion ProteinsViral Regulatory and Accessory ProteinsViroporin ProteinsChemokinesHuman Immunodeficiency Virus ProteinsReceptors, ChemokineRecombinant Fusion ProteinsViral Regulatory and Accessory ProteinsViroporin Proteinsvpu protein, Human immunodeficiency virus 1

Identifiers

PMID14555957
PMCPMC4414054
OpenAlexW1968513047

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.