Heavy metals induce phosphorylation of the Bcl-2 protein by Jun N-terminal kinase

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F09%3A00028421" target="_blank" >RIV/00216224:14310/09:00028421 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11130/09:5137 RIV/68081707:_____/09:00345303

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Heavy metals induce phosphorylation of the Bcl-2 protein by Jun N-terminal kinase

Popis výsledku v původním jazyce

The Bcl-2 protein is one of the key components of biochemical pathways controling programmed cell death. Function of this protein can be regulated by posttranslational modifications. Phosphorylation of Bcl-2 has been considered to be significantly associated with cell cycle arrest in the G2/M phase of the cell cycle, and with cell death caused by defects of microtubule dynamics. This study shows that phosphorylation of Bcl-2 can be induced by heavy metals due to activation of the Jun N-terminal kinase pathway that is not linked to the G2/M cell cycle arrest. Furthermore, we show that hyperphosphorylated Bcl-2 protein is a more potent inhibitor of zinc-induced cell death than its hypophosphorylated mutant form. These data suggest that regulation of theBcl-2 protein function by phosphorylation is an important part of cell response to stress.

Název v anglickém jazyce

Heavy metals induce phosphorylation of the Bcl-2 protein by Jun N-terminal kinase

Popis výsledku anglicky

The Bcl-2 protein is one of the key components of biochemical pathways controling programmed cell death. Function of this protein can be regulated by posttranslational modifications. Phosphorylation of Bcl-2 has been considered to be significantly associated with cell cycle arrest in the G2/M phase of the cell cycle, and with cell death caused by defects of microtubule dynamics. This study shows that phosphorylation of Bcl-2 can be induced by heavy metals due to activation of the Jun N-terminal kinase pathway that is not linked to the G2/M cell cycle arrest. Furthermore, we show that hyperphosphorylated Bcl-2 protein is a more potent inhibitor of zinc-induced cell death than its hypophosphorylated mutant form. These data suggest that regulation of theBcl-2 protein function by phosphorylation is an important part of cell response to stress.

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

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2009

Kód důvěrnosti údajů

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

Název periodika

Biological Chemistry

ISSN

1431-6730

e-ISSN

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Svazek periodika

390/2009

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

9

Strana od-do

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Kód UT WoS článku

000263247800008

EID výsledku v databázi Scopus

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