Daxx inhibuje apoptózu indukovanou stresem v kardiomyocytech

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F08%3A00325125" target="_blank" >RIV/86652036:_____/08:00325125 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Daxx inhibits stress-induced apoptosis in cardiac myocytes

Popis výsledku v původním jazyce

The role of the death-associated protein Daxx in modulation of apoptosis induced in cardiac myocytes by oxidative stress was studied. Exposure of cardiomyocyte-like cells to oxidative stress or simulated hypoxia increased the level of accumulated ROS andapoptosis. Under conditions of sub-apoptotic stimulation of cardiac myocytes, there was no increase in the level of the Daxx protein, but it translocated from the nucleus to the cytoplasm. Daxx overexpression protected the cells from apoptosis, while they were sensitised to cell death following its down-regulation by siRNA. Lowering the level of the Daxx protein sensitised cardiac myocytes to spontaneous apoptosis, suggesting that the protein may also have a prosurvival role under physiological conditions. Finally, it was shown that DJ-1, a protein suggested previously to sequester Daxx in the nucleus under conditions of oxidative stress preventing thus its cytosolic translocation, was localised in the cytoplasm of cardiac myocytes

Název v anglickém jazyce

Daxx inhibits stress-induced apoptosis in cardiac myocytes

Popis výsledku anglicky

The role of the death-associated protein Daxx in modulation of apoptosis induced in cardiac myocytes by oxidative stress was studied. Exposure of cardiomyocyte-like cells to oxidative stress or simulated hypoxia increased the level of accumulated ROS andapoptosis. Under conditions of sub-apoptotic stimulation of cardiac myocytes, there was no increase in the level of the Daxx protein, but it translocated from the nucleus to the cytoplasm. Daxx overexpression protected the cells from apoptosis, while they were sensitised to cell death following its down-regulation by siRNA. Lowering the level of the Daxx protein sensitised cardiac myocytes to spontaneous apoptosis, suggesting that the protein may also have a prosurvival role under physiological conditions. Finally, it was shown that DJ-1, a protein suggested previously to sequester Daxx in the nucleus under conditions of oxidative stress preventing thus its cytosolic translocation, was localised in the cytoplasm of cardiac myocytes

Druh

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

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/GA305%2F07%2F1008" target="_blank" >GA305/07/1008: Úloha mitochondrií v apoptóze kardiomyocytů při infarktu myokardu: od buněk k celému zvířeti</a><br>

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2008

Kód důvěrnosti údajů

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

Název periodika

Redox Report

ISSN

1351-0002

e-ISSN

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Svazek periodika

13

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

8

Strana od-do

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Kód UT WoS článku

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EID výsledku v databázi Scopus

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