Nf1+/- mice have increased neointima formation via hyperactivation of a Gleevec sensitive molecular pathway
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چکیده
منابع مشابه
Nf1+/- mice have increased neointima formation via hyperactivation of a Gleevec sensitive molecular pathway.
Neurofibromatosis type I (NF1) is a genetic disorder caused by mutations in the NF1 tumor suppressor gene. Neurofibromin is encoded by NF1 and functions as a negative regulator of Ras activity. Somatic mutations in the residual normal NF1 allele within cancers of NF1 patients is consistent with NF1 functioning as a tumor-suppressor. However, the prevalent non-malignant manifestations of NF1, in...
متن کاملHeterozygous inactivation of the Nf1 gene in myeloid cells enhances neointima formation via a rosuvastatin-sensitive cellular pathway.
Mutations in the NF1 tumor suppressor gene cause Neurofibromatosis type 1 (NF1). Neurofibromin, the protein product of NF1, functions as a negative regulator of Ras activity. Some NF1 patients develop cardiovascular disease, which represents an underrecognized disease complication and contributes to excess morbidity and mortality. Specifically, NF1 patients develop arterial occlusion resulting ...
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To begin to dissect atherogenesis as a complex genetic disorder affected by genetic makeup and environment, we have ( a ) generated a reproducible mouse model of neointimal growth; ( b ) evaluated the effect of disruption of a single gene, endothelial nitric oxide synthase, believed to be central to intimal growth, and ( c ) examined the modifying effects of gender and pregnancy upon the vascul...
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BACKGROUND AND PURPOSE The pathophysiology of vascular lesions after balloon angioplasty remains poorly understood. A major limitation of most experimental studies in this regard is that injury was assessed in healthy arteries. Our aim was to study the effects of hypercholesterolemia in a mouse vascular injury model that mimics human balloon angioplasty. METHODS Carotid balloon distension was...
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In response to arterial injury, medial vascular smooth muscle cells (VSMCs) proliferate and migrate into the intima, contributing to the development of occlusive vascular disease. The LIM protein cysteine-rich protein (CRP) 2 associates with the actin cytoskeleton and may maintain the cytoarchitecture. CRP2 also interacts with transcription factors in the nucleus to mediate SMC gene expression....
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ژورنال
عنوان ژورنال: Human Molecular Genetics
سال: 2008
ISSN: 0964-6906,1460-2083
DOI: 10.1093/hmg/ddn134