Evidence map›Paper›PMID 28455789›Full record

ArticleMolecular and cellular biochemistry2017

Functional and structural consequences of chemokine (C-X-C motif) receptor 4 activation with cognate and non-cognate agonists.

Jonathan M Eby, Hazem Abdelkarim, Lauren J Albee, Abhishek Tripathi, Xianlong Gao, Brian F Volkman, Vadim Gaponenko, Matthias Majetschak

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2017. 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
1.2field-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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Almost 50 Years of Monomeric Extracellular Ubiquitin (eUb).Pharmaceuticals (Basel, Switzerland) · 2024
    Review
  2. Article
  3. αPharmacological research · 2023
    Article
  4. Heteromerization between αFEBS letters · 2022
    Article
  5. Novel allosteric ligands of the angiotensin receptor AT1R as autoantibody blockers.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

8 authors at 3 institutions in 1 country.

Jonathan M EbyDepartment of Surgery, Burn and Shock Trauma Research Institute, Loyola University Chicago Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL, 60153, USA.
Hazem AbdelkarimDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, 900 S Ashland, Chicago, IL, 60607, USA.
Lauren J AlbeeDepartment of Surgery, Burn and Shock Trauma Research Institute, Loyola University Chicago Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL, 60153, USA.
Abhishek TripathiDepartment of Surgery, Burn and Shock Trauma Research Institute, Loyola University Chicago Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL, 60153, USA.
Xianlong GaoDepartment of Surgery, Burn and Shock Trauma Research Institute, Loyola University Chicago Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL, 60153, USA.
Brian F VolkmanDepartment of Biochemistry, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI, 53226, USA.
Vadim GaponenkoDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, 900 S Ashland, Chicago, IL, 60607, USA.
Matthias MajetschakDepartment of Surgery, Burn and Shock Trauma Research Institute, Loyola University Chicago Stritch School of Medicine, 2160 S. First Avenue, Maywood, IL, 60153, USA. mmajetschak@luc.edu.
Loyola University Chicago · USAshland (United States) · USMedical College of Wisconsin · US

Funding

Structural Basis for Chemokine FunctionR01AI058072 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI VOLKMAN, BRIAN F · 2004 to 2019
$4.1M
Structural Basis for Chemokine FunctionR37AI058072 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI Brian F Volkman · 2020 to 2026
$2.8M
Regulation of tyrosine kinase signaling through interaction with membrane lipidsR01CA188427 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GAPONENKO, VADIM V, TYNER, ANGELA L · 2015 to 2019
$2.1M
Chemokine control of cardiovascular function during hemorrhagic shockR01GM107495 · NIGMS · UNIVERSITY OF SOUTH FLORIDA · PI MAJETSCHAK, MATTHIAS · 2014 to 2017
$1.1M
Peptide-based nanoparticle inhibition of CCR3-mediated inflammatory cell recruitmR21HL118588 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GAPONENKO, VADIM V · 2013 to 2014
$423k
NCI NIH HHS R01 CA188427NCI NIH HHS R01CA188427NHLBI NIH HHS R21 HL118588NIAID NIH HHS R01 AI058072NIAID NIH HHS R37 AI058072NIGMS NIH HHS R01 GM107495NIGMS NIH HHS R01GM107495Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program W81XWH-15-1-0262the National Heart, Lung, and Blood Institute R21HL118588
6 · The paper itself

Abstract

Chemokine (C-X-C motif) receptor 4 (CXCR4) regulates cell trafficking and plays important roles in the immune system. Ubiquitin has recently been identified as an endogenous non-cognate agonist of CXCR4, which activates CXCR4 via interaction sites that are distinct from those of the cognate agonist C-X-C motif chemokine ligand 12 (CXCL12). As compared with CXCL12, chemotactic activities of ubiquitin in primary human cells are poorly characterized. Furthermore, evidence for functional selectivity of CXCR4 agonists is lacking, and structural consequences of ubiquitin binding to CXCR4 are unknown. Here, we show that ubiquitin and CXCL12 have comparable chemotactic activities in normal human peripheral blood mononuclear cells, monocytes, vascular smooth muscle, and endothelial cells. Chemotactic activities of the CXCR4 ligands could be inhibited with the selective CXCR4 antagonist AMD3100 and with a peptide analogue of the second transmembrane domain of CXCR4. In human monocytes, ubiquitin- and CXCL12-induced chemotaxis could be inhibited with pertussis toxin and with inhibitors of phospholipase C, phosphatidylinositol 3 kinase, and extracellular signal-regulated kinase 1/2. Both agonists induced inositol trisphosphate production in vascular smooth muscle cells, which could be inhibited with AMD3100. In β-arrestin recruitment assays, ubiquitin did not sufficiently recruit β-arrestin2 to CXCR4 (EC

Indexed as

Chemokine CXCL12ChemotaxisEnzyme-Linked Immunosorbent AssayHumansNuclear Magnetic Resonance, BiomolecularProtein ConformationReceptors, CXCR4Signal TransductionUbiquitinChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanReceptors, CXCR4UbiquitinBiased agonistChemotaxisCXCL12Nuclear magnetic resonance spectroscopyStromal cell-derived factor-1αUbiquitin

Identifiers

PMID28455789
PMCPMC5660673
OpenAlexW2609757728

What OpenQuestion holds

Textmetadata
LicenceTDM
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.