Stress-induced expression of p53 target genes is insensitive to SNW1/SKIP downregulation

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F11%3A10104653" target="_blank" >RIV/00216208:11310/11:10104653 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.2478/s11658-011-0012-1" target="_blank" >http://dx.doi.org/10.2478/s11658-011-0012-1</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.2478/s11658-011-0012-1" target="_blank" >10.2478/s11658-011-0012-1</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Stress-induced expression of p53 target genes is insensitive to SNW1/SKIP downregulation

Popis výsledku v původním jazyce

Pharmacological inhibition of protein kinases that are responsible for the phosphorylation of the carboxy-terminal domain (CTD) of RNA Pol II during transcription by 5,6-dichloro-1-beta-D-ribofuranosyl-benzimidazole (DRB) leads to severe inhibition of mRNA synthesis and activates p53. Transcription of the p53 effectors that are induced under these conditions, such as p21 or PUMA, must bypass the requirement for CTD phosphorylation by the positive elongation factor P-TEFb. Here, we have downregulated SNW1/SKIP, a splicing factor and a transcriptional co-regulator, which was found to interact with P-TEFb and synergistically affect Tat-dependent transcription elongation of HIV 1. Using the colon cancer derived cell line HCT116, we have found that both doxorubicin- and DRB-induced expression of p21 or PUMA is insensitive to SNW1 downregulation by siRNA. This suggests that transcription of stress response genes, unlike, e.g., the SNW1-sensitive mitosis-specific genes, can proceed uncoupled

Název v anglickém jazyce

Stress-induced expression of p53 target genes is insensitive to SNW1/SKIP downregulation

Popis výsledku anglicky

Pharmacological inhibition of protein kinases that are responsible for the phosphorylation of the carboxy-terminal domain (CTD) of RNA Pol II during transcription by 5,6-dichloro-1-beta-D-ribofuranosyl-benzimidazole (DRB) leads to severe inhibition of mRNA synthesis and activates p53. Transcription of the p53 effectors that are induced under these conditions, such as p21 or PUMA, must bypass the requirement for CTD phosphorylation by the positive elongation factor P-TEFb. Here, we have downregulated SNW1/SKIP, a splicing factor and a transcriptional co-regulator, which was found to interact with P-TEFb and synergistically affect Tat-dependent transcription elongation of HIV 1. Using the colon cancer derived cell line HCT116, we have found that both doxorubicin- and DRB-induced expression of p21 or PUMA is insensitive to SNW1 downregulation by siRNA. This suggests that transcription of stress response genes, unlike, e.g., the SNW1-sensitive mitosis-specific genes, can proceed uncoupled

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/LC06061" target="_blank" >LC06061: Centrum buněčné invazivity v embryonálním vývoji a metastázách nádorů</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>Z - Vyzkumny zamer (s odkazem do CEZ)<br>S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2011

Kód důvěrnosti údajů

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

Název periodika

Cellular and Molecular Biology Letters

ISSN

1425-8153

e-ISSN

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Svazek periodika

16

Číslo periodika v rámci svazku

3

Stát vydavatele periodika

PL - Polská republika

Počet stran výsledku

12

Strana od-do

373-384

Kód UT WoS článku

000293019200002

EID výsledku v databázi Scopus

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