Open AccessA novel truncated form of eNOS associates with altered vascular function
Author(s) -
Elena Galluccio,
Laura Cassina,
Isabella Russo,
Fabrizio Gelmini,
Emanuela Setola,
Luca Rampoldi,
Lorena Citterio,
Alessandra Rossodivita,
Mikel Kamami,
Antonio Colombo,
Ottavio Alfieri,
M. Carini,
Emanuele Bosi,
Mariella Trovati,
PierMarco Piatti,
Lucilla D. Monti,
Giorgio Casari
Publication year - 2013
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvt267
Subject(s) - enos , medicine , biology , homeostasis , intron , coronary artery disease , endothelial nitric oxide synthase , gene , endocrinology , nitric oxide synthase , genetics , nitric oxide
Nitric oxide (NO) plays a key role in vascular homeostasis and is produced by endothelial NO synthase (eNOS), encoded by NOS3 gene. We previously reported the genetic association between NOS3 rs753482-A>C polymorphism on intron 19 and coronary artery disease (CAD). In the attempt of conferring functional implication to the rs753482-A>C polymorphism, we investigated its influence on transcript maturation.
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