Mitochondrial Dysfunction in Gliomas

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F13%3A00423057" target="_blank" >RIV/68378050:_____/13:00423057 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1016/j.spen.2013.09.003" target="_blank" >http://dx.doi.org/10.1016/j.spen.2013.09.003</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.spen.2013.09.003" target="_blank" >10.1016/j.spen.2013.09.003</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Mitochondrial Dysfunction in Gliomas

Popis výsledku v původním jazyce

Mitochondrial (mt) dysfunction in gliomas has been linked to abnormalities of mt energy metabolism, marked by a metabolic shift from oxidative phosphorylation to glycolysis ("Warburg effect"), disturbances in mt membrane potential regulation and apoptotic signaling, as well as to somatic mutations involving the Krebs cycle enzyme isocitrate dehydrogenase. Evolving biological concepts with potential therapeutic implications include interaction between microtubule proteins and mitochondria (mt) in the control of closure of voltage-dependent anion channels and in the regulation of mt dynamics and the mt-endoplasmic reticulum network. The cytoskeletal protein beta III-tubulin, which is overexpressed in malignant gliomas, has emerged as a prosurvival factorassociated in part with nit and also as a marker of chemoresistance. Mt-targeted therapeutic strategies that are discussed include the following: (1) metabolic modulation with emphasis on dichloroacetate, a pyruvate dehydrogenase kinase

Název v anglickém jazyce

Mitochondrial Dysfunction in Gliomas

Popis výsledku anglicky

Mitochondrial (mt) dysfunction in gliomas has been linked to abnormalities of mt energy metabolism, marked by a metabolic shift from oxidative phosphorylation to glycolysis ("Warburg effect"), disturbances in mt membrane potential regulation and apoptotic signaling, as well as to somatic mutations involving the Krebs cycle enzyme isocitrate dehydrogenase. Evolving biological concepts with potential therapeutic implications include interaction between microtubule proteins and mitochondria (mt) in the control of closure of voltage-dependent anion channels and in the regulation of mt dynamics and the mt-endoplasmic reticulum network. The cytoskeletal protein beta III-tubulin, which is overexpressed in malignant gliomas, has emerged as a prosurvival factorassociated in part with nit and also as a marker of chemoresistance. Mt-targeted therapeutic strategies that are discussed include the following: (1) metabolic modulation with emphasis on dichloroacetate, a pyruvate dehydrogenase kinase

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/LH12050" target="_blank" >LH12050: Regulace tvorby mikrotubulů u nádorových buněk mozku</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

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

Název periodika

Seminars in Pediatric Neurology

ISSN

1071-9091

e-ISSN

—

Svazek periodika

20

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

12

Strana od-do

216-227

Kód UT WoS článku

000328262000007

EID výsledku v databázi Scopus

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