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Krüppel-Like Factor-11, a Transcription Factor Involved in Diabetes Mellitus, Suppresses Endothelial Cell Activation via the Nuclear Factor-κB Signaling Pathway
Author(s) -
Yanbo Fan,
Yanhong Guo,
Jifeng Zhang,
Malayannan Subramaniam,
Chao-Zhong Song,
Raúl Urrutia,
Y. Eugene Chen
Publication year - 2012
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.112.300349
Subject(s) - proinflammatory cytokine , transcription factor , cell adhesion molecule , gene knockdown , tumor necrosis factor alpha , microbiology and biotechnology , signal transduction , cell adhesion , endothelial stem cell , biology , inflammation , cancer research , chemistry , medicine , immunology , cell , biochemistry , apoptosis , gene , in vitro
Endothelial cell (EC) inflammatory status is critical to many vascular diseases. Emerging data demonstrate that mutations of Krüppel-like factor-11 (KLF11), a gene coding maturity-onset diabetes mellitus of the young type 7 (MODY7), contribute to the development of neonatal diabetes mellitus. However, the function of KLF11 in the cardiovascular system still remains to be uncovered. In this study, we aimed to investigate the role of KLF11 in vascular endothelial inflammation.

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