Fibroblast clones from patients with Hutchinson–Gilford progeria can senesce despite the presence of telomerase-Reference-Cited by-同舟云学术

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Fibroblast clones from patients with Hutchinson–Gilford progeria can senesce despite the presence of telomerase

Published:2004-04 Issue:4 Volume:39 Page:461-467
ISSN:0531-5565
Container-title:Experimental Gerontology
language:en
Short-container-title:Experimental Gerontology

Author:

Wallis Corrin V.,Sheerin Angela N.,Green Michael H.L.,Jones Christopher J.,Kipling David,Faragher Richard G.A.

Publisher

Elsevier BV

Subject

Cell Biology,Endocrinology,Genetics,Molecular Biology,Ageing,Biochemistry

Reference14 articles.

1. Extension of life-span by introduction of telomerase into normal human cells;Bodnar;Science,1998

2. A standard strain of human ocular keratocytes;Dropcova;Ophthalmic Res.,1999

3. Rate of DNA repair in progeric and normal human fibroblasts;Epstein;Biochem Biophys Res Commun.,1974

4. Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome;Eriksson;Nature,2003

5. How might replicative senescence contribute to human ageing?;Faragher;Bioessays,1998

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1. Progerin Can Induce DNA Damage in the Absence of Global Changes in Replication or Cell Proliferation;2024-07-02

2. Hutchinson-Gilford Progeria Syndrome;Neurocutaneous Disorders;2022

3. Progerin impairs 3D genome organization and induces fragile telomeres by limiting the dNTP pools;Scientific Reports;2021-06-23

4. Hutchinson-Gilford Progeria Syndrome;Encyclopedia of Gerontology and Population Aging;2021

5. Telomere elongation through hTERT immortalization leads to chromosome repositioning in control cells and genomic instability in Hutchinson‐Gilford progeria syndrome fibroblasts, expressing a novel SUN1 isoform;Genes, Chromosomes and Cancer;2019-01-07

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