2007 Fiscal Year Final Research Report Summary
Identification of activator of G-protein signaling involved in cardiovascular disease
| Project/Area Number |
18599006
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Yokohama City University |
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Principal Investigator |
SATO Motohiko Yokohama City University, Cardiovascular Research Institute, School of Medicine, Associate professor (40292122)
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| Co-Investigator(Kenkyū-buntansha) |
OKUMURA Satoshi Yokohama city University, Cardiovascular Research Institute, School of Medicine, Associate professor (60233475)
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| Project Period (FY) |
2006 – 2007
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| Keywords | G-protein / Signal trasnduction / Cardiovascular disease |
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| Research Abstract |
Recent data indicate the existence of signal regulators that directly influence the activation state of G-proteins independent of a GPCR. As part of a strategy to identify such entities involved in the development of cardiovascular disease, we utilized a functional screen in the yeast for the receptor-independent activators of heterotrimeric G-protein signaling and identified activators of G-protein signaling (AGS) 8 from rat heart following treatment of repetitive ischemia. We report here the extension of this approach to identify AGS involved in the development of cardiac hypertrophy. cDNA libraries were generated from hypertrophic heart of the mouse following treatment of isoproterenol (60 ug/g/day) or transverse aorta constriction for 7-9 days. The libraries were applied to the yeast system expressing Gsα or Giα3 as well as Gα16. Using the Giα3 yeast strain, we isolated cDNAs encoding AGS2 and 3 as well as RGS12. Using the Gα16 yeast strain, we isolated 3 candidates for novel AGS (novel-AGSs) representing 3 unique coding sequences belonged to the same functional group. The bioactivity of novel-AGSs was also observed in yeast strains expressing Gas, but not Gαi3. By interfacing to Gαl 6 or Gas signaling pathways, novel-AGSs may contribute to the development of cardiac hypertrophy.
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Research Products
(24 results)
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[Journal Article] AGS32007
Author(s)
Blumer J, et. al.
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Journal Title
UCSD-Nature Molecule Pages
Pages: doi:10.1038/mp.a000228.01
Description
「研究成果報告書概要(和文)」より
Peer Reviewed
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[Journal Article] Developmental changes in gene expression of Epac and its upregulation in myocardial hypertrophy2007
Author(s)
Ulcan, C, Wang, X, Baljinnyam, E, Bai, YZ, Okumura, S, Sato, M, Minamisawa, S, Hirotani, S, Ishikawa, Y
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Journal Title
Am J Physiol Cell Physiol 293
Pages: 1662-72
Description
「研究成果報告書概要(欧文)」より
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