PMID- 10066418
OWN - NLM
STAT- MEDLINE
DCOM- 19990413
LR  - 20190612
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 256
IP  - 1
DP  - 1999 Mar 5
TI  - G protein-mediated mitogen-activated protein kinase activation by two dopamine D2 
      receptors.
PG  - 33-40
AB  - Two isoforms of dopamine D2 receptor, D2L (long) and D2S (short), differ by the 
      insertion of 29 amino acids specific to D2L within the putative third 
      intracellular loop of the receptor, which appears to be important in selectivity 
      for G-protein coupling. We have generated D2L- and D2S-expressing Chinese hamster 
      ovary (CHO) cells, and regulation of the mitogen-activated protein kinase (MAPK) 
      pathway was examined in these cells. Both D2L and D2S mediated a rapid and 
      transient activation of MAPK with dominant activation of p42-kDa MAPK. Pertussis 
      toxin treatment completely abrogated stimulation of MAPK mediated by D2L and D2S, 
      demonstrating that both receptors couple to pertussis toxin-sensitive G proteins 
      in this signaling. Stimulation of MAPK mediated by both D2L and D2S receptor was 
      markedly attenuated by coexpression of the C-terminus of beta-adrenergic receptor 
      kinase (betaARKct), which selectively inhibits Gbetagamma-mediated signal 
      transduction. Further analysis of D2L- and D2S-mediated MAPK activation 
      demonstrated that D2L-mediated MAPK activation was not significantly affected by 
      PKC depletion or partially affected by genistein. In contrast, D2S-mediated MAPK 
      activation was potentially inhibited by PKC depletion and genistein was capable 
      of completely inhibiting D2S-mediated MAPK activation. Together, these results 
      suggest that D2L- and D2S-mediated MAPK activation is predominantly Gbetagamma 
      subunit-mediated signaling and that protein kinase C and tyrosine 
      phosphorylations are involved in these signaling pathways.
CI  - Copyright 1999 Academic Press.
FAU - Choi, E Y
AU  - Choi EY
AD  - Medical Research Center, College of Medicine, Yonsei University, Seoul, 120-752, 
      South Korea.
FAU - Jeong, D
AU  - Jeong D
FAU - Park, K W
AU  - Park KW
FAU - Baik, J H
AU  - Baik JH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Dopamine D2 Receptor Antagonists)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Lysophospholipids)
RN  - 0 (Peptide Fragments)
RN  - 0 (Protein Isoforms)
RN  - 0 (Receptors, Dopamine D2)
RN  - 0 (Virulence Factors, Bordetella)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 2.7.11.15 (beta-Adrenergic Receptor Kinases)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - CHO Cells
MH  - Calcium-Calmodulin-Dependent Protein Kinases/*metabolism
MH  - Cricetinae
MH  - Cyclic AMP-Dependent Protein Kinases/metabolism
MH  - Dopamine/pharmacology
MH  - Dopamine Antagonists/pharmacology
MH  - Dopamine D2 Receptor Antagonists
MH  - Enzyme Activation/drug effects
MH  - Enzyme Inhibitors/pharmacology
MH  - GTP-Binding Proteins/antagonists & inhibitors/*metabolism
MH  - Lysophospholipids/antagonists & inhibitors/pharmacology
MH  - Mice
MH  - Peptide Fragments/metabolism
MH  - Pertussis Toxin
MH  - Phosphorylation/drug effects
MH  - Protein Isoforms/metabolism
MH  - Protein Kinase C/metabolism
MH  - Protein-Tyrosine Kinases/antagonists & inhibitors/metabolism
MH  - Receptors, Dopamine D2/*metabolism
MH  - *Signal Transduction/drug effects
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Transfection
MH  - Virulence Factors, Bordetella/pharmacology
MH  - beta-Adrenergic Receptor Kinases
EDAT- 1999/03/06 00:00
MHDA- 1999/03/06 00:01
CRDT- 1999/03/06 00:00
PHST- 1999/03/06 00:00 [pubmed]
PHST- 1999/03/06 00:01 [medline]
PHST- 1999/03/06 00:00 [entrez]
AID - S0006291X99902863 [pii]
AID - 10.1006/bbrc.1999.0286 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 1999 Mar 5;256(1):33-40. doi: 10.1006/bbrc.1999.0286.