The role of the TP73 gene and its transcripts in neuro-oncology

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F14%3A00077492" target="_blank" >RIV/00216224:14110/14:00077492 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00159816:_____/14:00061124

Výsledek na webu

<a href="http://dx.doi.org/10.3109/02688697.2014.908162" target="_blank" >http://dx.doi.org/10.3109/02688697.2014.908162</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3109/02688697.2014.908162" target="_blank" >10.3109/02688697.2014.908162</a>

Jazyk výsledku

angličtina

Název v původním jazyce

The role of the TP73 gene and its transcripts in neuro-oncology

Popis výsledku v původním jazyce

Protein p73 is a member of the p53 protein family that can induce cell cycle arrest or apoptosis by the activation of p53-responsive genes as well as p53-independent pathways. Alternative promoter usage, together with differential splicing of the C-terminal exons, forms several distinct mRNAs that are translated into corresponding protein isoforms containing different domains. While TAp73 isoforms respond to genotoxic stress in a manner similar to tumor suppressor p53, Delta TAp73 isoforms inhibit apoptosis during normal development and in cancer cell lines. Thus, the impact of p73 on tumorigenesis depends on a subtle balance between tumor-promoting and-suppressing isoforms. Due to the structural homology between p53 and p73, a subtle balance among p53family members and their isoforms could influence glioma cell evolution toward malignancy. Thus, the p73 status has to be considered when studying the regulatory role of p53 protein in gliomagenesis.

Název v anglickém jazyce

The role of the TP73 gene and its transcripts in neuro-oncology

Popis výsledku anglicky

Protein p73 is a member of the p53 protein family that can induce cell cycle arrest or apoptosis by the activation of p53-responsive genes as well as p53-independent pathways. Alternative promoter usage, together with differential splicing of the C-terminal exons, forms several distinct mRNAs that are translated into corresponding protein isoforms containing different domains. While TAp73 isoforms respond to genotoxic stress in a manner similar to tumor suppressor p53, Delta TAp73 isoforms inhibit apoptosis during normal development and in cancer cell lines. Thus, the impact of p73 on tumorigenesis depends on a subtle balance between tumor-promoting and-suppressing isoforms. Due to the structural homology between p53 and p73, a subtle balance among p53family members and their isoforms could influence glioma cell evolution toward malignancy. Thus, the p73 status has to be considered when studying the regulatory role of p53 protein in gliomagenesis.

Druh

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

CEP obor

FH - Neurologie, neurochirurgie, neurovědy

OECD FORD obor

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Projekt

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

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

British journal of neurosurgery

ISSN

0268-8697

e-ISSN

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Svazek periodika

28

Číslo periodika v rámci svazku

5

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

8

Strana od-do

598-605

Kód UT WoS článku

000341753500004

EID výsledku v databázi Scopus

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