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Regulation of the Trafficking and Function of G Protein-Coupled Receptors by Rab1 GTPase in Cardiomyocytes

*Corresponding author for this work
  • Louisiana State University Health Sciences Center
Scholary Output:
Chapter in Book/Report/Conference proceeding
Chapter

Abstract

G protein-coupled receptors (GPCRs) play a crucial role in regulating cardiac growth and function under normal and diseased conditions. It has been well documented that the precise function of GPCRs is controlled by intracellular trafficking of the receptors. Compared with the extensive studies on the events of the endocytic pathway, molecular mechanism underlying the transport process of GPCRs from the endoplasmic reticulum (ER) through the Golgi to the cell surface and regulation of receptor signaling by these processes in cardiac myocytes remain poorly defined. This chapter describes the methods to characterize the function of Rab1 GTPase, which modulates protein transport from the ER to the Golgi apparatus, in the trafficking and signaling of angiotensin II type 1 receptor (AT1R), α1-adrenergic receptor (AR), and β-AR, and in hypertrophic growth in response to agonist stimulation in neonatal cardiac myocytes.

Publication Information

Output type

Scholary Output:
Chapter in Book/Report/Conference proceeding
Chapter

Original language

English (US)

Pages from-to (Number of pages)

Pages 227-238 (12 pages)

Publication milestones

  • Published - 2008

Publication status

Published - 2008

Publication series

  • Publication series name: Methods in Enzymology
    ISSN (Print): 0076-6879
    Volume: 438
9780123739681

Publication IDs

  • Scopus: 45549107702
  • PubMed: 18413252

Host publication title

Small GTPases in Disease, Part A

Host publication editors

  • William Balch
  • Alan Hall
  • Channing Der

Publication metrics

Metrics

Scopus
citations
Fractional count
1
Fractional count
1
Fractional count
1
Fractional count
1
SciVal
citations
4
SciVal
FWCI
0.04
SciVal
Author count
1
SciVal
Paper percentile
47

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Captures
10
Citation count
6

Funding Details

This work was supported by the National Institutes of Health grants R01‐GM076167 and P20‐R018766. The author thanks Stephen M. Lanier, John D. Hildebrandt (Medical University of South Carolina), Kenneth P. Minneman, and Kenneth E. Bernstein (Emory University) for sharing reagents.