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PI3K kinase and scaffold functions in heart
Author(s) -
Damilano Federico,
Perino Alessia,
Hirsch Emilio
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05081.x
Subject(s) - signal transduction , microbiology and biotechnology , scaffold protein , second messenger system , phosphoinositide 3 kinase , pi3k/akt/mtor pathway , gene isoform , receptor tyrosine kinase , kinase , tyrosine kinase , protein kinase a , phosphorylation , g protein coupled receptor , biology , chemistry , biochemistry , gene
Signal transduction events are key modulators of cellular function and, in the cardiovascular system, an emerging role is played by phosphoinositide 3‐kinases (PI3Ks), a family of enzymes containing a 3‐phosphorylated phosphoinositide that produce lipid second messengers. In the heart, multiple PI3K isoforms are expressed, but play potentially distinct roles. Among cardiac PI3Ks, PI3Kα is triggered by tyrosine kinase receptors and plays a role in adaptive hypertrophy, while PI3Kγ is triggered by G protein–coupled receptors and is involved in maladaptive heart remodeling. This view has been recently complicated by the finding that PI3Ks can also be involved in protein–protein interactions and affect signaling independently of their kinase activity. This review will thus focus on the effects of these multiple signaling events, with particular emphasis on their involvement in cardiac hypertrophy and failure.