A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model - Test2 - elhamkhani - TriplyDB

A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model

A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model

http://www.wikidata.org/entity/Q24657266

about

Molecular ageing in progeroid syndromes: Hutchinson-Gilford progeria syndrome as a model Progeria: a rare genetic premature ageing disorder Targeting protein prenylation in progeria Human ZMPSTE24 disease mutations: residual proteolytic activity correlates with disease severity Exome sequencing and functional analysis identifies BANF1 mutation as the cause of a hereditary progeroid syndrome Blocking protein farnesylation improves nuclear shape abnormalities in keratinocytes of mice expressing the prelamin A variant in Hutchinson-Gilford progeria syndrome Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts When lamins go bad: nuclear structure and disease Mouse models of laminopathies The nuclear envelope: an intriguing focal point for neurogenetic disease Recent advances in understanding the role of lamins in health and disease Potential therapeutic approaches for modulating expression and accumulation of defective lamin A in laminopathies and age-related diseases Cardiovascular genomics, personalized medicine, and the National Heart, Lung, and Blood Institute: part I: the beginning of an era Protein farnesylation inhibitors cause donut-shaped cell nuclei attributable to a centrosome separation defect Calcific aortic valve stenosis: methods, models, and mechanisms Dynamics of lamin-A processing following precursor accumulation.Defective lamin A-Rb signaling in Hutchinson-Gilford Progeria Syndrome and reversal by farnesyltransferase inhibition.Tipifarnib prevents development of hypoxia-induced pulmonary hypertension.Nuclear localization signal deletion mutants of lamin A and progerin reveal insights into lamin A processing and emerin targeting Activation of Rho GTPases in Smith-Lemli-Opitz syndrome: pathophysiological and clinical implications.Mechanisms controlling the smooth muscle cell death in progeria via down-regulation of poly(ADP-ribose) polymerase 1.The posttranslational processing of prelamin A and disease.2014 Association of American Physicians George M. Kober Medal. Introduction of Elizabeth G. Nabel Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.Isoprenoids, small GTPases and Alzheimer's disease.Differential temporal and spatial progerin expression during closure of the ductus arteriosus in neonates Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson-Gilford progeria syndrome.Costello and cardio-facio-cutaneous syndromes: Moving toward clinical trials in RASopathies.Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells.Inner nuclear membrane proteins: impact on human disease.Progeria: translational insights from cell biology.DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.A mutation abolishing the ZMPSTE24 cleavage site in prelamin A causes a progeroid disorder Sulforaphane enhances progerin clearance in Hutchinson-Gilford progeria fibroblasts.Isoprenoids and related pharmacological interventions: potential application in Alzheimer's disease.Automated image analysis of nuclear shape: what can we learn from a prematurely aged cell?Rapamycin activates autophagy in Hutchinson-Gilford progeria syndrome: implications for normal aging and age-dependent neurodegenerative disorders Nuclear mechanics in disease Biogenesis of the Saccharomyces cerevisiae pheromone a-factor, from yeast mating to human disease.Arterial ageing.

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P2860

A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model

http://www.wikidata.org/entity/Q24657266

description

2008 nî lūn-bûn

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2008 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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Proceedings of the National Academy of Sciences of the United States of America

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A farnesyltransferase inhibito ...... ease in a progeria mouse model

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Dina A Faddah

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Elizabeth G Nabel

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Frank D Kolodgie

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Hedwig Avallone

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Hong San

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Kan Cao

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Karen N Conneely

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Michael R Erdos

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Michelle Olive

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Renu Virmani

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P2860

The mutant form of lamin A that causes Hutchinson-Gilford progeria is a biomarker of cellular aging in human skin

Structural organization of the human gene encoding nuclear lamin A and nuclear lamin C

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome

Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome

Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

Phenotype and course of Hutchinson-Gilford progeria syndrome

Lamin A-dependent misregulation of adult stem cells associated with accelerated ageing

Lamin A-dependent nuclear defects in human aging

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

Human laminopathies: nuclei gone genetically awry

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Francis Collins

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18838683

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cardiovascular disease

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