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2019/03/18
Zebrafish yolk sac microinjection of thalidomide for assessment of developmental toxicology

2019/02/18
Toxicological Evaluation of SiO2 Nanoparticles by Zebrafish Embryo Toxicity Test

2018/12/27
Increased susceptibility to oxidative stress-induced toxicological evaluation by genetically modified nrf2a-deficient zebrafish.

2018/01/18
EGF receptor kinase suppresses ciliogenesis through activation of USP8 deubiquitinase

2017/11/23
Chemokines protect vascular smooth muscle cells from cell death induced by cyclic mechanical stretch.

tNovel reciprocal regulation of cAMP signaling and apoptosis by orphan G-protein-coupled receptor GPRC5A gene expression.

                     
2006/12/08

Hirano M, Zang L, Oka T, Ito Y, Shimada Y, Nishimura Y, Tanaka T.
Biochem Biophys Res Commun. 2006 Dec 8;351(1):185-91. Epub 2006 Oct 11.


Abstract

GPRC5A is a member of G-protein-coupled receptors, which was originally identified as an all-trans-retinoic acid-induced gene. Although recent studies reported that this gene was highly expressed in the cancer cell lines and that GPRC5A might positively regulate cell proliferation, its mechanism remains unknown. We investigated the upstream and downstream signaling of GPRC5A and its biological function, and found that cAMP signaling is the novel GPRC5A induction pathway. When GPRC5A gene was overexpressed, intracellular cAMP concentration was decreased, and Gsalpha gene expression was downregulated. On the other hand, RNA interference of GPRC5A increased mRNA levels of Gsalpha and intracellular cAMP, reduced cell number, and induced apoptosis. Conversely, cell number was increased by GPRC5A overexpression. We first report the novel negative feedback model of cAMP signaling through GPRC5A gene expression. This evidence explains one of the mechanisms of the GPRC5A-regulated cell growth in some cancer cell lines.


PMID: 17055459 [PubMed - indexed for MEDLINE]

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