TGF-?/NF1/Smad4-mediated suppression of ANT2 contributes to oxidative stress in cellular senescence

Result code in IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F14%3A00435869" target="_blank" >RIV/68378050:_____/14:00435869 - isvavai.cz</a>

Result on the web

<a href="http://dx.doi.org/10.1016/j.cellsig.2014.08.029" target="_blank" >http://dx.doi.org/10.1016/j.cellsig.2014.08.029</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.cellsig.2014.08.029" target="_blank" >10.1016/j.cellsig.2014.08.029</a>

Result language

angličtina

Original language name

TGF-?/NF1/Smad4-mediated suppression of ANT2 contributes to oxidative stress in cellular senescence

Original language description

Oxidative stress and persistent activation of DNA damage response (DDR) are causally involved in the development of cellular senescence, a phenomenon implicated in fundamental (patho)physiological processes such as aging, fetal development and tumorigenesis. Here, we report that adenine nucleotide translocase-2 (ANT2) is consistently down-regulated in all three major forms of cellular senescence: replicative, oncogene-induced and drug-induced, in both normal and cancerous human cells. We previously reported formation of novel NF1/Smad transcription repressor complexes in growth-arrested fibroblasts. Here we show that such complexes form in senescent cells. Mechanistically, binding of the NF1/Smad complexes to the NF1-dependent repressor elements in theANT2 gene promoter repressed ANT2 expression. Etoposide-induced formation of these complexes and repression of ANT2 were relatively late events co-incident with production and secretion of, and dependent on, TGF-?. siRNA-mediated knock-d

Czech name

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Czech description

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Type

J_x - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

CEP classification

EB - Genetics and molecular biology

OECD FORD branch

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Project

Result was created during the realization of more than one project. More information in the Projects tab.

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2014

Confidentiality

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Name of the periodical

Cellular Signalling

ISSN

0898-6568

e-ISSN

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Volume of the periodical

26

Issue of the periodical within the volume

12

Country of publishing house

GB - UNITED KINGDOM

Number of pages

9

Pages from-to

2903-2911

UT code for WoS article

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EID of the result in the Scopus database

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