PUBLICATION

Allosteric modulation of the CXCR4:CXCL12 axis by targeting receptor nanoclustering via the TMV-TMVI domain

Authors
García-Cuesta, E.M., Martínez, P., Selvaraju, K., Ulltjärn, G., Gómez Pozo, A.M., D'Agostino, G., Gardeta, S., Quijada-Freire, A., Blanco Gabella, P., Roca, C., Hoyo, D.D., Jiménez-Saiz, R., García-Rubia, A., Soler Palacios, B., Lucas, P., Ayala-Bueno, R., Santander Acerete, N., Carrasco, Y., Oscar Sorzano, C., Martinez, A., Campillo, N.E., Jensen, L.D., Rodriguez Frade, J.M., Santiago, C., Mellado, M.
ID
ZDB-PUB-240910-3
Date
2024
Source
eLIFE   13: (Journal)
Registered Authors
Keywords
allosteric inhibitors, cell migration, chemokine receptors, human, immunology, inflammation, zebrafish
MeSH Terms
  • Chemokine CXCL12*/metabolism
  • Models, Molecular
  • Protein Domains
  • Protein Binding
  • Humans
  • Receptors, CXCR4*/chemistry
  • Receptors, CXCR4*/metabolism
  • Animals
  • Allosteric Regulation
PubMed
39248648 Full text @ Elife
Abstract
CXCR4 is a ubiquitously expressed chemokine receptor that regulates leukocyte trafficking and arrest in both homeostatic and pathological states. It also participates in organogenesis, HIV-1 infection, and tumor development. Despite the potential therapeutic benefit of CXCR4 antagonists, only one, plerixafor (AMD3100), which blocks the ligand-binding site, has reached the clinic. Recent advances in imaging and biophysical techniques have provided a richer understanding of the membrane organization and dynamics of this receptor. Activation of CXCR4 by CXCL12 reduces the number of CXCR4 monomers/dimers at the cell membrane and increases the formation of large nanoclusters, which are largely immobile and are required for correct cell orientation to chemoattractant gradients. Mechanistically, CXCR4 activation involves a structural motif defined by residues in TMV and TMVI. Using this structural motif as a template, we performed in silico molecular modeling followed by in vitro screening of a small compound library to identify negative allosteric modulators of CXCR4 that do not affect CXCL12 binding. We identified AGR1.137, a small molecule that abolishes CXCL12-mediated receptor nanoclustering and dynamics and blocks the ability of cells to sense CXCL12 gradients both in vitro and in vivo while preserving ligand binding and receptor internalization.
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping