Overexpression of the ?Np73 isoform is associated with centrosome amplification in brain tumor cell lines

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F15%3A%230000654" target="_blank" >RIV/00209805:_____/15:#0000654 - isvavai.cz</a>

Výsledek na webu

<a href="http://link.springer.com/article/10.1007%2Fs13277-015-3474-3" target="_blank" >http://link.springer.com/article/10.1007%2Fs13277-015-3474-3</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1007/s13277-015-3474-3" target="_blank" >10.1007/s13277-015-3474-3</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Overexpression of the ?Np73 isoform is associated with centrosome amplification in brain tumor cell lines

Popis výsledku v původním jazyce

The p73 protein is a member of the p53 family, and this protein is known to be essential for the maintenance of genomic stability, DNA repair, and apoptosis regulation. Transcription from two promoters leads to two main N-terminal isoforms: the TAp73 isoform is reported to have tumor suppressor function, whereas the ?Np73 isoform likely has oncogenic potential. The present study is focused on the investigation of a possible role of both these p73 N-terminal isoforms in the process of centrosome amplification. HGG-02 and GM7 glioblastoma cell lines and the Daoy medulloblastoma cell line were used in this study. The cells were analyzed using indirect immunofluorescence to determine TAp73 and ?Np73 expression patterns and possible co-localization with theBubR1 protein, as well as the number of centrosomes. A transiently transfected GM7 cell line was used to verify the results concerning the N-terminal isoforms in relation to centrozome amplification. We found that increased immunoreactiv

Název v anglickém jazyce

Overexpression of the ?Np73 isoform is associated with centrosome amplification in brain tumor cell lines

Popis výsledku anglicky

The p73 protein is a member of the p53 family, and this protein is known to be essential for the maintenance of genomic stability, DNA repair, and apoptosis regulation. Transcription from two promoters leads to two main N-terminal isoforms: the TAp73 isoform is reported to have tumor suppressor function, whereas the ?Np73 isoform likely has oncogenic potential. The present study is focused on the investigation of a possible role of both these p73 N-terminal isoforms in the process of centrosome amplification. HGG-02 and GM7 glioblastoma cell lines and the Daoy medulloblastoma cell line were used in this study. The cells were analyzed using indirect immunofluorescence to determine TAp73 and ?Np73 expression patterns and possible co-localization with theBubR1 protein, as well as the number of centrosomes. A transiently transfected GM7 cell line was used to verify the results concerning the N-terminal isoforms in relation to centrozome amplification. We found that increased immunoreactiv

Druh

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

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

—

Projekt

<a href="/cs/project/ED2.1.00%2F03.0101" target="_blank" >ED2.1.00/03.0101: Regionální centrum aplikované molekulární onkologie (RECAMO)</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2015

Kód důvěrnosti údajů

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

Název periodika

Tumor biology

ISSN

1010-4283

e-ISSN

—

Svazek periodika

36

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

14

Strana od-do

7483-7491

Kód UT WoS článku

000362969900018

EID výsledku v databázi Scopus

2-s2.0-84944277548