Cardiovascular pathology in Hutchinson-Gilford progeria: correlation with the vascular pathology of aging. - sprookjes - yvandenbroek - TriplyDB

Cardiovascular pathology in Hutchinson-Gilford progeria: correlation with the vascular pathology of aging.

Cardiovascular pathology in Hutchinson-Gilford progeria: correlation with the vascular pathology of aging.

http://www.wikidata.org/entity/Q34248086

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Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cells DNA Damage: A Main Determinant of Vascular Aging Molecular insights into the premature aging disease progeria Search and insights into novel genetic alterations leading to classical and atypical Werner syndrome Mouse models of laminopathies Cellular and molecular biology of aging endothelial cells How Research on Human Progeroid and Antigeroid Syndromes Can Contribute to the Longevity Dividend Initiative A pathway linking oxidative stress and the Ran GTPase system in progeria.Otologic and audiologic manifestations of Hutchinson-Gilford progeria syndrome Calcific aortic valve stenosis: methods, models, and mechanisms Expression of progerin in aging mouse brains reveals structural nuclear abnormalities without detectible significant alterations in gene expression, hippocampal stem cells or behavior.Mechanisms controlling the smooth muscle cell death in progeria via down-regulation of poly(ADP-ribose) polymerase 1.Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome.Discordant gene expression signatures and related phenotypic differences in lamin A- and A/C-related Hutchinson-Gilford progeria syndrome (HGPS).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.Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in Hutchinson-Gilford progeria syndrome cells.Progeria: translational insights from cell biology.A prospective study of radiographic manifestations in Hutchinson-Gilford progeria syndrome DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome Sulforaphane enhances progerin clearance in Hutchinson-Gilford progeria fibroblasts.Signaling pathway activation drift during aging: Hutchinson-Gilford Progeria Syndrome fibroblasts are comparable to normal middle-age and old-age cells Age-dependent loss of MMP-3 in Hutchinson-Gilford progeria syndrome Dementia and Alzheimer's disease: a new direction.The 2010 Jay L. Foster Memorial Lecture.Mechanisms of premature vascular aging in children with Hutchinson-Gilford progeria syndrome.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 Comparative endocrinology of aging and longevity regulation The adventitia: a dynamic interface containing resident progenitor cells.Nuclear mechanics in disease Progerin sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in laminopathy-related progeroid syndromes.Reprogramming progeria fibroblasts re-establishes a normal epigenetic landscape.Risk of dementia and death in the long-term follow-up of the Pittsburgh Cardiovascular Health Study-Cognition Study.Correlated alterations in genome organization, histone methylation, and DNA-lamin A/C interactions in Hutchinson-Gilford progeria syndrome.Truncated prelamin A expression in HGPS-like patients: a transcriptional study.Nuclear lamin functions and disease.Skeletal muscle contractile function and neuromuscular performance in Zmpste24 -/- mice, a murine model of human progeria.The Mechanobiology of Aging

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Cardiovascular pathology in Hutchinson-Gilford progeria: correlation with the vascular pathology of aging.

http://www.wikidata.org/entity/Q34248086

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2010 nî lūn-bûn

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2010 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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Arteriosclerosis, Thrombosis, and Vascular Biology

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Birgit Funke

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Elizabeth G Nabel

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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

Prelamin A acts to accelerate smooth muscle cell senescence and is a novel biomarker of human vascular aging

Hutchinson-Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody.

Phenotype and course of Hutchinson-Gilford progeria syndrome

Lamin A-dependent nuclear defects in human aging

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

Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors

Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice

Molecular regulation of vascular smooth muscle cell differentiation in development and disease

Effect of progerin on the accumulation of oxidized proteins in fibroblasts from Hutchinson Gilford progeria patients.

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Francis Collins

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2010-08-26T00:00:00Z

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Aparato circulatorio

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