Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. (Q39378063)

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26 January 2020

title

Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence (English)

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1

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Diana Jurk

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Morgan Taschuk

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Joao F Passos

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author name string

Francisco D M Marques

3

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Clara Correia-Melo

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Timothy Hardy

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Agata Gackowska

6

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Rhys Anderson

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Jelena Mann

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language of work or name

English

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publication date

28 February 2012

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26 January 2020

published in

Nature Communications

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volume

3

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page(s)

708

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Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported

26 January 2020

copyright license

start time

1 January 2012

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April 2022 Public Data File from Crossref

copyright status

copyrighted

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describes a project that uses

ImageJ

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11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC3292717/fullTextXML

inferred from PubMed Central ID database lookup

cites work

Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation

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A RAP1/TRF2 complex inhibits nonhomologous end-joining at human telomeric DNA ends

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Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence

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Pot1 deficiency initiates DNA damage checkpoint activation and aberrant homologous recombination at telomeres

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A telomeric repeat sequence adjacent to a DNA double-stranded break produces an anticheckpoint

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Shelterin: the protein complex that shapes and safeguards human telomeres

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DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion

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Oxidative damage in telomeric DNA disrupts recognition by TRF1 and TRF2

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Telomere shortening triggers senescence of human cells through a pathway involving ATM, p53, and p21(CIP1), but not p16(INK4a)

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Visualizing telomere dynamics in living mammalian cells using PNA probes

11 September 2017

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A DNA damage checkpoint response in telomere-initiated senescence

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The role of chondrocyte senescence in osteoarthritis

21 August 2018

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22426229

12 December 2020

inferred from PubMed ID database lookup

Telomerase does not counteract telomere shortening but protects mitochondrial function under oxidative stress

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22426229

12 December 2020

inferred from PubMed ID database lookup

DNA damage response and cellular senescence in tissues of aging mice

1 reference

PubMed

https://pubmed.ncbi.nlm.nih.gov/22426229

12 December 2020

inferred from PubMed ID database lookup

Identifiers

DOI

10.1038/NCOMMS1708

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:22426229 AND SRC:MED&resulttype=core&format=json

26 January 2020

0 references

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:22426229 AND SRC:MED&resulttype=core&format=json

26 January 2020

PubMed publication ID

22426229

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:22426229 AND SRC:MED&resulttype=core&format=json