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Regulator of G-Protein Signaling Subtype 4 Mediates Antihypertrophic Effect of Locally Secreted Natriuretic Peptides in the Heart
Author(s) -
Takeshi Tokudome,
Ichiro Kishimoto,
Takeshi Horio,
Yuji Arai,
Daryl O. Schwenke,
Jun Hino,
Ichiro Okano,
Yuhei Kawano,
Masakazu Kohno,
Mikiya Miyazato,
Kazuwa Nakao,
Kenji Kangawa
Publication year - 2008
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.107.732990
Subject(s) - atrial natriuretic peptide , medicine , endocrinology , natriuretic peptide , regulator of g protein signaling , phosphorylation , cyclic guanosine monophosphate , protein kinase a , biology , g protein , receptor , heart failure , microbiology and biotechnology , nitric oxide , gtpase activating protein
Mice lacking guanylyl cyclase-A (GC-A), a natriuretic peptide receptor, have pressure-independent cardiac hypertrophy. However, the mechanism underlying GC-A-mediated inhibition of cardiac hypertrophy remains to be elucidated. In the present report, we examined the role of regulator of G-protein signaling subtype 4 (RGS4), a GTPase activating protein for G(q) and G(i), in the antihypertrophic effects of GC-A.

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