PMID- 8639784
OWN - NLM
STAT- MEDLINE
DCOM- 19960716
LR  - 20210216
IS  - 0006-4971 (Print)
IS  - 0006-4971 (Linking)
VI  - 87
IP  - 10
DP  - 1996 May 15
TI  - Differential coupling of CC chemokine receptors to multiple heterotrimeric G 
      proteins in human interleukin-2-activated natural killer cells.
PG  - 4255-60
AB  - Using two different approaches, we have investigated the types of G proteins 
      coupled to CC chemokine receptors. First, permeabilization of 
      interleukin-2-activated natural killer (IANK) cells with streptolysin-O and 
      introduction of anti-G protein antibodies inside these cells resulted in the 
      following. (1) Anti-G(s), anti-G(o), and anti-G(z) inhibited the migration of 
      IANK cells in response to macrophage-inflammatory protein-1 alpha (MIP-1 alpha), 
      monocyte chemoattractant protein-1 (MCP-1), or regulated on activation normal T 
      cell expressed and secreted (RANTES). (2) Anti-Gi inhibited their migration in 
      response to MCP-1 or RANTES but not in response to MIP-1 alpha. Second, 
      incubation of IANK cell membranes with anti-G protein antibodies before 
      incubating with (gamma-35S) GTP or (gamma-32P) GTP, resulted in the following. 
      (1) Anti-G(s), anti-G(o), or anti-G(z) inhibited GTP binding and GTPase activity 
      in the presence of MIP-1 alpha, or RANTES. (2) Anti-G(i) inhibited GTP binding 
      and GTPase activity in the presence of MCP-1 or RANTES but not in the presence of 
      MIP-1 alpha. The inhibitory effect of anti-G protein antibodies was reversed upon 
      incubating these antibodies with their respective synthetic peptides before 
      addition to IANK cell membranes. These results suggest that MCP-1 and RANTES 
      receptors are promiscuously coupled to multiple G proteins in IANK cell membranes 
      and that this coupling is different from MIP-1 alpha receptors, which seem to be 
      coupled to G(s), G(o), and G(z) but not to G(i).
FAU - al-Aoukaty, A
AU  - al-Aoukaty A
AD  - Department of Anatomy, University of Oslo, Norway.
FAU - Schall, T J
AU  - Schall TJ
FAU - Maghazachi, A A
AU  - Maghazachi AA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Blood
JT  - Blood
JID - 7603509
RN  - 0 (CCR2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Interleukin-2)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monokines)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, CCR5)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Receptors, Cytokine)
RN  - 0 (macrophage inflammatory protein 1alpha receptor)
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - EC 3.6.1.- (GTP Phosphohydrolases)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Cell Membrane/drug effects/metabolism
MH  - Chemokine CCL2/*pharmacology
MH  - Chemokine CCL4
MH  - Chemokine CCL5/*pharmacology
MH  - Chemotaxis, Leukocyte/drug effects
MH  - GTP Phosphohydrolases/metabolism
MH  - GTP-Binding Proteins/*metabolism
MH  - Guanosine Triphosphate/pharmacology
MH  - Humans
MH  - Interleukin-2/pharmacology
MH  - Killer Cells, Natural/drug effects/*metabolism
MH  - Lymphocyte Activation/*drug effects
MH  - Macrophage Inflammatory Proteins
MH  - Molecular Sequence Data
MH  - Monokines/*pharmacology
MH  - Receptors, CCR2
MH  - Receptors, CCR5
MH  - *Receptors, Chemokine
MH  - Receptors, Cytokine/drug effects/*physiology
MH  - Signal Transduction/drug effects/*physiology
EDAT- 1996/05/15 00:00
MHDA- 1996/05/15 00:01
CRDT- 1996/05/15 00:00
PHST- 1996/05/15 00:00 [pubmed]
PHST- 1996/05/15 00:01 [medline]
PHST- 1996/05/15 00:00 [entrez]
AID - S0006-4971(20)63693-X [pii]
PST - ppublish
SO  - Blood. 1996 May 15;87(10):4255-60.