Regulator of G-protein signaling (RGS) proteins in cancer biology

The regulator of G-protein signaling (RGS) family is a diverse group of multifunctional proteins that regulate cellular signaling events downstream of G-protein coupled receptors (GPCRs). In recent years, GPCRs have been linked to the initiation and progression of multiple cancers; thus, regulators...

Full description

Saved in:
Bibliographic Details
Published in:Biochemical pharmacology 2009-11, Vol.78 (10), p.1289-1297
Main Authors: Hurst, Jillian H., Hooks, Shelley B.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cancer
G-protein coupled receptors
Guanine Nucleotide Exchange Factors - biosynthesis
Guanine Nucleotide Exchange Factors - genetics
Guanine Nucleotide Exchange Factors - physiology
Humans
Medical sciences
Neoplasms - genetics
Neoplasms - metabolism
Pharmacology. Drug treatments
Polymorphism, Single Nucleotide
Receptors, G-Protein-Coupled - biosynthesis
Receptors, G-Protein-Coupled - genetics
Receptors, G-Protein-Coupled - physiology
Regulator of G-protein signaling proteins
RGS Proteins - biosynthesis
RGS Proteins - genetics
RGS Proteins - physiology
Rho Guanine Nucleotide Exchange Factors
Signal Transduction
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The regulator of G-protein signaling (RGS) family is a diverse group of multifunctional proteins that regulate cellular signaling events downstream of G-protein coupled receptors (GPCRs). In recent years, GPCRs have been linked to the initiation and progression of multiple cancers; thus, regulators of GPCR signaling are also likely to be important to the pathophysiology of cancer. This review highlights recent studies detailing changes in RGS transcript expression during oncogenesis, single nucleotide polymorphisms in RGS proteins linked to lung and bladder cancers, and specific roles for RGS proteins in multiple cancer types.
ISSN:0006-2952
1873-2968
DOI:10.1016/j.bcp.2009.06.028