p53-mediated control of gene expression via mRNA translation during Endoplasmic Reticulum stress

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F15%3A%230000661" target="_blank" >RIV/00209805:_____/15:#0000661 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1080/15384101.2015.1090066" target="_blank" >http://dx.doi.org/10.1080/15384101.2015.1090066</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1080/15384101.2015.1090066" target="_blank" >10.1080/15384101.2015.1090066</a>

Jazyk výsledku

angličtina

Název v původním jazyce

p53-mediated control of gene expression via mRNA translation during Endoplasmic Reticulum stress

Popis výsledku v původním jazyce

p53 is activated by different stress and damage pathways and regulates cell biological responses including cell cycle arrest, repair pathways, apoptosis and senescence. Following DNA damage, the levels of p53 increase and via binding to target gene promoters, p53 induces expression of multiple genes including p21(CDKN1A) and mdm2. The effects of p53 on gene expression during the DNA damage response are well mimicked by overexpressing p53 under normal conditions. However, stress to the Endoplasmic Reticulum (ER) and the consequent Unfolded Protein Response (UPR) leads to the induction of the p53/47 isoform that lacks the first 40 aa of p53 and to an active suppression of p21(CDKN1A) transcription and mRNA translation. We now show that during ER stress p53 also suppresses MDM2 protein levels via a similar mechanism. These observations not only raise questions about the physiological role of MDM2 during ER stress but it also reveals a new facet of p53 as a repressor toward 2 of its major

Název v anglickém jazyce

p53-mediated control of gene expression via mRNA translation during Endoplasmic Reticulum stress

Popis výsledku anglicky

p53 is activated by different stress and damage pathways and regulates cell biological responses including cell cycle arrest, repair pathways, apoptosis and senescence. Following DNA damage, the levels of p53 increase and via binding to target gene promoters, p53 induces expression of multiple genes including p21(CDKN1A) and mdm2. The effects of p53 on gene expression during the DNA damage response are well mimicked by overexpressing p53 under normal conditions. However, stress to the Endoplasmic Reticulum (ER) and the consequent Unfolded Protein Response (UPR) leads to the induction of the p53/47 isoform that lacks the first 40 aa of p53 and to an active suppression of p21(CDKN1A) transcription and mRNA translation. We now show that during ER stress p53 also suppresses MDM2 protein levels via a similar mechanism. These observations not only raise questions about the physiological role of MDM2 during ER stress but it also reveals a new facet of p53 as a repressor toward 2 of its major

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

<a href="/cs/project/LO1413" target="_blank" >LO1413: RECAMO2020</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Cell cycle

ISSN

1538-4101

e-ISSN

—

Svazek periodika

14

Číslo periodika v rámci svazku

21

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

6

Strana od-do

3373-3378

Kód UT WoS článku

000364559400011

EID výsledku v databázi Scopus

2-s2.0-84959491839