Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence. - Test2 - elhamkhani - TriplyDB

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

http://www.wikidata.org/entity/Q34124543

about

Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts Cellular Senescence as the Causal Nexus of Aging Molecular insights into the premature aging disease progeria Cellular senescence in aging and age-related disease: from mechanisms to therapy New look at the role of progerin in skin aging When lamins go bad: nuclear structure and disease Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions Potential therapeutic approaches for modulating expression and accumulation of defective lamin A in laminopathies and age-related diseases TRF2 and lamin A/C interact to facilitate the functional organization of chromosome ends p53-dependent gene repression through p21 is mediated by recruitment of E2F4 repression complexes.Mitotic defects lead to pervasive aneuploidy and accompany loss of RB1 activity in mouse LmnaDhe dermal fibroblasts Inner nuclear membrane proteins: impact on human disease.Clinical strategies and animal models for developing senolytic agents.DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.Progerin, the protein responsible for the Hutchinson-Gilford progeria syndrome, increases the unrepaired DNA damages following exposure to ionizing radiation.Rapamycin activates autophagy in Hutchinson-Gilford progeria syndrome: implications for normal aging and age-dependent neurodegenerative disorders Lamin B1 loss is a senescence-associated biomarker.Progerin reduces LAP2α-telomere association in Hutchinson-Gilford progeria.Mutant lamin A links prophase to a p53 independent senescence program.Oxydative stress alters nuclear shape through lamins dysregulation: a route to senescence.Progerin-Induced Replication Stress Facilitates Premature Senescence in Hutchinson-Gilford Progeria Syndrome.Lamins in development, tissue maintenance and stress.Lamin B1 fluctuations have differential effects on cellular proliferation and senescence.Nuclear lamin functions and disease.Atrx deficiency induces telomere dysfunction, endocrine defects, and reduced life span.DNA damage accumulation and TRF2 degradation in atypical Werner syndrome fibroblasts with LMNA mutations.Prelamin A causes progeria through cell-extrinsic mechanisms and prevents cancer invasion.Management of multicellular senescence and oxidative stress.The contrasting roles of lamin B1 in cellular aging and human disease Adult Stem Cells and Diseases of Aging.Lamin A, farnesylation and aging Nuclear damages and oxidative stress: new perspectives for laminopathies.Implications of multipotent mesenchymal stromal cell aging.Hutchinson-Gilford progeria syndrome through the lens of transcription.Nuclear lamina remodelling and its implications for human disease.Progeria, rapamycin and normal aging: recent breakthrough.Hutchinson-Gilford progeria syndrome as a model for vascular aging.Translating the Science of Aging into Therapeutic Interventions.Tying up loose ends: telomeres, genomic instability and lamins.Mammalian telomeres and their partnership with lamins.

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Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

http://www.wikidata.org/entity/Q34124543

description

2010 nî lūn-bûn

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2010 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2010 թվականի հուլիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@ast

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

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Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

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type

label

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

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Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@en

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@nl

prefLabel

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@ast

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@en

Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@nl

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Journal of Cell Science

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Role of progerin-induced telomere dysfunction in HGPS premature cellular senescence.

@en

P2093

Erica K Benson

http://www.w3.org/2001/XMLSchema#string

Sam W Lee

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Stuart A Aaronson

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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

Nuclear lamins: building blocks of nuclear architecture

Telomerase modulates Wnt signalling by association with target gene chromatin

SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin

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

Control of human telomere length by TRF1 and TRF2

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

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Phenotype and course of Hutchinson-Gilford progeria syndrome

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

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2605-2612

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scholarly article

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10.1242/JCS.067306

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Pt 15

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123

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2010-07-06T00:00:00Z

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45096904

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20605919

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