Related references
Note: Only part of the references are listed.Severe hepatocellular disease in mice lacking one or both CaaX prenyltransferases
Shao H. Yang et al.
JOURNAL OF LIPID RESEARCH (2012)
Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome
Leslie B. Gordon et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2012)
Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA
Hea-Jin Jung et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2012)
MEDICINE Drug Trial Offers Uncertain Start in Race to Save Children With Progeria
Jennifer Couzin-Frankel
SCIENCE (2012)
Unique Preservation of Neural Cells in Hutchinson-Gilford Progeria Syndrome Is Due to the Expression of the Neural-Specific miR-9 MicroRNA
Xavier Nissan et al.
CELL REPORTS (2012)
Absence of progeria-like disease phenotypes in knock-in mice expressing a non-farnesylated version of progerin
Shao H. Yang et al.
HUMAN MOLECULAR GENETICS (2011)
Splicing-Directed Therapy in a New Mouse Model of Human Accelerated Aging
Fernando G. Osorio et al.
SCIENCE TRANSLATIONAL MEDICINE (2011)
Rapamycin Reverses Cellular Phenotypes and Enhances Mutant Protein Clearance in Hutchinson-Gilford Progeria Syndrome Cells
Kan Cao et al.
SCIENCE TRANSLATIONAL MEDICINE (2011)
Genetic studies on the functional relevance of the protein prenyltransferases in skin keratinocytes
Roger Lee et al.
HUMAN MOLECULAR GENETICS (2010)
An accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria
Brandon S. J. Davies et al.
HUMAN MOLECULAR GENETICS (2010)
Direct Synthesis of Lamin A, Bypassing Prelamin A Processing, Causes Misshapen Nuclei in Fibroblasts but No Detectable Pathology in Mice
Catherine Coffinier et al.
JOURNAL OF BIOLOGICAL CHEMISTRY (2010)
Assessing the efficacy of protein farnesyltransferase inhibitors in mouse models of progeria
Shao H. Yang et al.
JOURNAL OF LIPID RESEARCH (2010)
Activating the synthesis of progerin, the mutant prelamin A in Hutchinson-Gilford progeria syndrome, with antisense oligonucleotides
Loren G. Fong et al.
HUMAN MOLECULAR GENETICS (2009)
Laminopathies and the long strange trip from basic cell biology to therapy
Howard J. Worman et al.
JOURNAL OF CLINICAL INVESTIGATION (2009)
Treatment with a farnesyltransferase inhibitor improves survival in mice with a Hutchinson-Gilford progeria syndrome mutation
Shao H. Yang et al.
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS (2008)
Progerin elicits disease phenotypes of progeria in mice whether or not it is farnesylated
Shao H. Yang et al.
JOURNAL OF CLINICAL INVESTIGATION (2008)
Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging
Ignacio Varela et al.
NATURE MEDICINE (2008)
A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model
Brian C. Capell et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2008)
Increased progerin expression associated with unusual LMNA mutations causes severe progeroid syndromes
Casey L. Moulson et al.
HUMAN MUTATION (2007)
A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation
Shao H. Yang et al.
JOURNAL OF CLINICAL INVESTIGATION (2006)
A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria
LG Fong et al.
SCIENCE (2006)
Prelamin A and lamin A appear to be dispensable in the nuclear lamina
LG Fong et al.
JOURNAL OF CLINICAL INVESTIGATION (2006)
Prelamin A, Zmpste24, misshapen cell nuclei, and progeria - new evidence suggesting that protein farnesylation could be important for disease pathogenesis
SG Young et al.
JOURNAL OF LIPID RESEARCH (2005)
Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy
CL Moulson et al.
JOURNAL OF INVESTIGATIVE DERMATOLOGY (2005)
Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome
BC Capell et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2005)
Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes
JI Toth et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2005)
Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation
SH Yang et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2005)
Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome
P Scaffidi et al.
NATURE MEDICINE (2005)
Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice
LG Fong et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2004)
Nuclear envelope alterations in fibroblasts from patients with muscular dystrophy, cardiomyopathy, and partial lipodystrophy carrying lamin A/C gene mutations
A Muchir et al.
MUSCLE & NERVE (2004)
Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
M Eriksson et al.
NATURE (2003)
Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect
MO Bergo et al.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2002)