PMID- 24576550
OWN - NLM
STAT- MEDLINE
DCOM- 20141125
LR  - 20140401
IS  - 1873-3913 (Electronic)
IS  - 0898-6568 (Linking)
VI  - 26
IP  - 6
DP  - 2014 Jun
TI  - The eIF2B-interacting domain of RGS2 protects against GPCR agonist-induced 
      hypertrophy in neonatal rat cardiomyocytes.
PG  - 1226-34
LID - S0898-6568(14)00066-7 [pii]
LID - 10.1016/j.cellsig.2014.02.006 [doi]
AB  - The protective effect of Regulator of G protein Signaling 2 (RGS2) in cardiac 
      hypertrophy is thought to occur through its ability to inhibit the chronic GPCR 
      signaling that promotes pathogenic growth both in vivo and in cultured 
      cardiomyocytes. However, RGS2 is known to have additional functions beyond its 
      activity as a GTPase accelerating protein, such as the ability to bind to 
      eukaryotic initiation factor, eIF2B, and inhibit protein synthesis. The RGS2 
      eIF2B-interacting domain (RGS2(eb)) was examined for its ability to regulate 
      hypertrophy in neonatal ventricular myocytes. Both full-length RGS2 and RGS2(eb) 
      were able to inhibit agonist-induced cardiomyocyte hypertrophy, but RGS2(eb) had 
      no effect on receptor-mediated inositol phosphate production, cAMP production, or 
      ERK 1/2 activation. These results suggest that the protective effects of RGS2 in 
      cardiac hypertrophy may derive at least in part from its ability to govern 
      protein synthesis.
CI  - Copyright (c) 2014 Elsevier Inc. All rights reserved.
FAU - Chidiac, Peter
AU  - Chidiac P
AD  - Department of Physiology and Pharmacology, Schulich School of Medicine and 
      Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
FAU - Sobiesiak, Alina J
AU  - Sobiesiak AJ
AD  - Department of Physiology and Pharmacology, Schulich School of Medicine and 
      Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
FAU - Lee, Katherine N
AU  - Lee KN
AD  - Department of Physiology and Pharmacology, Schulich School of Medicine and 
      Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
FAU - Gros, Robert
AU  - Gros R
AD  - Department of Physiology and Pharmacology, Schulich School of Medicine and 
      Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
FAU - Nguyen, Chau H
AU  - Nguyen CH
AD  - Department of Physiology and Pharmacology, Schulich School of Medicine and 
      Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada; School of 
      Pharmacy, D'Youville College, Buffalo, NY 14201, USA. Electronic address: 
      nguyenc@dyc.edu.
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140224
PL  - England
TA  - Cell Signal
JT  - Cellular signalling
JID - 8904683
RN  - 0 (Eukaryotic Initiation Factor-2B)
RN  - 0 (Inositol Phosphates)
RN  - 0 (RGS Proteins)
RN  - 0 (RGS2 protein, rat)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 1WS297W6MV (Phenylephrine)
RN  - E0399OZS9N (Cyclic AMP)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Cardiomegaly/*metabolism
MH  - Cell Size/drug effects
MH  - Cells, Cultured
MH  - Cyclic AMP/metabolism
MH  - Eukaryotic Initiation Factor-2B
MH  - Gene Expression
MH  - Inositol Phosphates/metabolism
MH  - Isoproterenol/pharmacology
MH  - Myocytes, Cardiac/drug effects/*metabolism/pathology
MH  - Phenylephrine/pharmacology
MH  - Protein Biosynthesis
MH  - Protein Interaction Domains and Motifs
MH  - RGS Proteins/chemistry/*physiology
MH  - Rats
MH  - Receptors, G-Protein-Coupled/*agonists/physiology
MH  - Second Messenger Systems
OTO - NOTNLM
OT  - Cardiac hypertrophy
OT  - G protein
OT  - GPCR
OT  - Protein synthesis
OT  - RGS protein
EDAT- 2014/03/01 06:00
MHDA- 2014/12/15 06:00
CRDT- 2014/03/01 06:00
PHST- 2013/08/27 00:00 [received]
PHST- 2014/02/05 00:00 [revised]
PHST- 2014/02/11 00:00 [accepted]
PHST- 2014/03/01 06:00 [entrez]
PHST- 2014/03/01 06:00 [pubmed]
PHST- 2014/12/15 06:00 [medline]
AID - S0898-6568(14)00066-7 [pii]
AID - 10.1016/j.cellsig.2014.02.006 [doi]
PST - ppublish
SO  - Cell Signal. 2014 Jun;26(6):1226-34. doi: 10.1016/j.cellsig.2014.02.006. Epub 
      2014 Feb 24.