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Permanently Farnesylated Prelamin A, Progeria, and Atherosclerosis.

作者信息

Worman Howard J, Michaelis Susan

机构信息

Department of Medicine and Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, New York (H.J.W.).

Department of Cell Biology, The Johns Hopkins University School of Medicine, Baltimore, MD (S.M.).

出版信息

Circulation. 2018 Jul 17;138(3):283-286. doi: 10.1161/CIRCULATIONAHA.118.034480.

Abstract
摘要

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本文引用的文献

1
Vascular Smooth Muscle-Specific Progerin Expression Accelerates Atherosclerosis and Death in a Mouse Model of Hutchinson-Gilford Progeria Syndrome.
Circulation. 2018 Jul 17;138(3):266-282. doi: 10.1161/CIRCULATIONAHA.117.030856. Epub 2018 Feb 28.
2
A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder.
J Cell Sci. 2016 May 15;129(10):1975-80. doi: 10.1242/jcs.187302. Epub 2016 Mar 31.
3
Modulation of LMNA splicing as a strategy to treat prelamin A diseases.
J Clin Invest. 2016 Apr 1;126(4):1592-602. doi: 10.1172/JCI85908. Epub 2016 Mar 21.
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Biochemistry. A protease for the ages.
Science. 2013 Mar 29;339(6127):1529-30. doi: 10.1126/science.1236764.
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Hum Mol Genet. 2012 Sep 15;21(18):4084-93. doi: 10.1093/hmg/dds233. Epub 2012 Jun 19.
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Splicing-directed therapy in a new mouse model of human accelerated aging.
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Prelamin A acts to accelerate smooth muscle cell senescence and is a novel biomarker of human vascular aging.
Circulation. 2010 May 25;121(20):2200-10. doi: 10.1161/CIRCULATIONAHA.109.902056. Epub 2010 May 10.
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Laminopathies and the long strange trip from basic cell biology to therapy.
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