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Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independent Mechanism
Author(s) -
José J. Fuster,
Herminia GonzálezNavarro,
Ángela Vinué,
Pedro Molina-Sánchez,
María J. AndrésManzano,
Keiichi I. Nakayama,
Keiko Nakayama,
Antonio Dı́ez-Juan,
António Bernad,
Cristina Rodrı́guez,
José MartínezGonzález,
Vicente Andrés
Publication year - 2011
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.111.235580
Subject(s) - foam cell , phosphorylation , mechanism (biology) , serine , macrophage , microbiology and biotechnology , cell growth , chemistry , biology , biochemistry , physics , quantum mechanics , in vitro
Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein.

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