Rapamycin Reverses Cellular Phenotypes and Enhances Mutant Protein Clearance in Hutchinson-Gilford Progeria Syndrome Cells-Reference-Cited by-同舟云学术

Rapamycin Reverses Cellular Phenotypes and Enhances Mutant Protein Clearance in Hutchinson-Gilford Progeria Syndrome Cells

Published:2011-06-29 Issue:89 Volume:3 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Cao Kan¹²,Graziotto John J.³,Blair Cecilia D.¹,Mazzulli Joseph R.³,Erdos Michael R.¹,Krainc Dimitri³,Collins Francis S.¹

Affiliation:

1. Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892–8004, USA.

2. Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.

3. Department of Neurology, Massachusetts General Hospital, MassGeneral Institute for Neurodegenerative Disease, Harvard Medical School, Charlestown, MA 02129, USA.

Abstract

Shown previously to extend longevity in animals, the drug rapamycin might serve as a treatment for a human premature aging syndrome.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference38 articles.

1. Human laminopathies: nuclei gone genetically awry

2. Hutchinson–Gilford Progeria Syndrome, Aging, and the Nuclear Lamina

3. Phenotype and Course of Hutchinson–Gilford Progeria Syndrome

4. A lamin A protein isoform overexpressed in Hutchinson-Gilford progeria syndrome interferes with mitosis in progeria and normal cells

5. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson–Gilford progeria syndrome

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