Crosstalk of JNK1-STAT3 is critical for RAW264.7 cell survival

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18450%2F14%3A50002644" target="_blank" >RIV/62690094:18450/14:50002644 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.cellsig.2014.09.013" target="_blank" >http://dx.doi.org/10.1016/j.cellsig.2014.09.013</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.cellsig.2014.09.013" target="_blank" >10.1016/j.cellsig.2014.09.013</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Crosstalk of JNK1-STAT3 is critical for RAW264.7 cell survival

Popis výsledku v původním jazyce

T-2 toxin, a major compound of trichothecenes, inhibits protein synthesis and induces inflammation and cell apoptosis through the activation ofMAPK pathway. The JAK/STAT pathway has recently been shown to be downstream targets of trichothecenes. However,whether there is any crosstalk between JNK and JAK/STAT pathways in trichothecene toxicity has not been studied. In the present study, we explored this potential in RAW264.7 cells treatedwith T-2 toxin. Our results revealed a crosstalk between JNK1 andSTAT3 after T-2 toxin treatment,which was mediated by K-Ras. T-2 toxin treatment resulted in rapid phosphorylation, and more importantly, JNK1- STAT3 signaling pathway was shown to maintain the normal function of the mitochondria and to inhibit T-2 toxin-induced apoptosis. Therefore, this pathway was considered to be a potential cell survival pathway. Breakdown and degranulation of ribosomes in the rough endoplasmic reticulum and swelling of mitochondria were clearly visible after the ce

Název v anglickém jazyce

Crosstalk of JNK1-STAT3 is critical for RAW264.7 cell survival

Popis výsledku anglicky

T-2 toxin, a major compound of trichothecenes, inhibits protein synthesis and induces inflammation and cell apoptosis through the activation ofMAPK pathway. The JAK/STAT pathway has recently been shown to be downstream targets of trichothecenes. However,whether there is any crosstalk between JNK and JAK/STAT pathways in trichothecene toxicity has not been studied. In the present study, we explored this potential in RAW264.7 cells treatedwith T-2 toxin. Our results revealed a crosstalk between JNK1 andSTAT3 after T-2 toxin treatment,which was mediated by K-Ras. T-2 toxin treatment resulted in rapid phosphorylation, and more importantly, JNK1- STAT3 signaling pathway was shown to maintain the normal function of the mitochondria and to inhibit T-2 toxin-induced apoptosis. Therefore, this pathway was considered to be a potential cell survival pathway. Breakdown and degranulation of ribosomes in the rough endoplasmic reticulum and swelling of mitochondria were clearly visible after the ce

Druh

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

CEP obor

FP - Ostatní lékařské obory

OECD FORD obor

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Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2014

Kód důvěrnosti údajů

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

Název periodika

Cellular signalling

ISSN

0898-6568

e-ISSN

—

Svazek periodika

26

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

2951-2960

Kód UT WoS článku

000345107700040

EID výsledku v databázi Scopus

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