Dissociation of ligand-induced internalization of CXCR-4 from its co-receptor activity for HIV-1 Env-mediated membrane fusion

Arch Virol. 1998;143(5):851-61. doi: 10.1007/s007050050337.

Abstract

The C-terminal cytoplasmic tail of chemokine receptors is important for their internalization upon ligand binding. We generated several deletion mutants of the C-terminal cytoplasmic tail of CXCR-4, a co-receptor for T cell line tropic strains of human immunodeficiency virus type 1 (HIV-1), to know whether or not co-receptor internalization is associated with HIV-1 entry. Our data showed that the removal of C-terminal 15 amino acid residues of the cytoplasmic tail from CXCR-4 completely abolished its internalization, but did not affect the co-receptor activity at all. Co-receptor activity was fully retained even when all 45 amino acid residues in the C-terminal cytoplasmic tail had been deleted. These data indicated that no cytoplasmic tail nor internalization of CXCR-4 is required for its co-receptor activity for HIV-1 entry.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • Cell Line
  • Chemokine CXCL12
  • Chemokines, CXC / pharmacology
  • DNA Primers / genetics
  • Down-Regulation / drug effects
  • Gene Products, env / physiology*
  • HIV-1 / pathogenicity*
  • HIV-1 / physiology
  • Humans
  • Ligands
  • Membrane Fusion / physiology*
  • Mice
  • Polymerase Chain Reaction
  • Receptors, CXCR4 / genetics
  • Receptors, CXCR4 / metabolism*
  • Recombinant Proteins / pharmacology
  • Sequence Deletion

Substances

  • CXCL12 protein, human
  • Chemokine CXCL12
  • Chemokines, CXC
  • Cxcl12 protein, mouse
  • DNA Primers
  • Gene Products, env
  • Ligands
  • Receptors, CXCR4
  • Recombinant Proteins