Transcriptional regulators of human oncoviruses: structural and functional implications for anticancer therapy
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68081707%3A_____%2F22%3A00569833" target="_blank" >RIV/68081707:_____/22:00569833 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216224:14310/22:00125582
Výsledek na webu
<a href="https://academic.oup.com/narcancer/article/4/1/zcac005/6541525?login=true" target="_blank" >https://academic.oup.com/narcancer/article/4/1/zcac005/6541525?login=true</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1093/narcan/zcac005" target="_blank" >10.1093/narcan/zcac005</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Transcriptional regulators of human oncoviruses: structural and functional implications for anticancer therapy
Popis výsledku v původním jazyce
Transcription is often the first biosynthetic event of viral infection. Viruses produce preferentially viral transcriptional regulators (vTRs) essential for expressing viral genes and regulating essential host cell proteins to enable viral genome replication. As vTRs are unique viral proteins that promote the transcription of viral nucleic acid, vTRs interact with host proteins to suppress detection and immune reactions to viral infection. Thus, vTRs are promising therapeutic targets that are sequentially and structurally distinct from host cell proteins. Here, we review vTRs of three human oncoviruses: HBx of hepatitis B virus, HBZ of human T-lymphotropic virus type 1, and Rta of Epstein-Barr virus. We present three cunningly exciting and dangerous transcription strategies that make viral infections so efficient. We use available structural and functional knowledge to critically examine the potential of vTRs as new antiviral-anticancer therapy targets. For each oncovirus, we describe (i) the strategy of viral genome transcription, (ii) vTRs' structure and binding partners essential for transcription regulation, and (iii) advantages and challenges of vTR targeting in antiviral therapies. We discuss the implications of vTR regulation for oncogenesis and perspectives on developing novel antiviral and anticancer strategies.
Název v anglickém jazyce
Transcriptional regulators of human oncoviruses: structural and functional implications for anticancer therapy
Popis výsledku anglicky
Transcription is often the first biosynthetic event of viral infection. Viruses produce preferentially viral transcriptional regulators (vTRs) essential for expressing viral genes and regulating essential host cell proteins to enable viral genome replication. As vTRs are unique viral proteins that promote the transcription of viral nucleic acid, vTRs interact with host proteins to suppress detection and immune reactions to viral infection. Thus, vTRs are promising therapeutic targets that are sequentially and structurally distinct from host cell proteins. Here, we review vTRs of three human oncoviruses: HBx of hepatitis B virus, HBZ of human T-lymphotropic virus type 1, and Rta of Epstein-Barr virus. We present three cunningly exciting and dangerous transcription strategies that make viral infections so efficient. We use available structural and functional knowledge to critically examine the potential of vTRs as new antiviral-anticancer therapy targets. For each oncovirus, we describe (i) the strategy of viral genome transcription, (ii) vTRs' structure and binding partners essential for transcription regulation, and (iii) advantages and challenges of vTR targeting in antiviral therapies. We discuss the implications of vTR regulation for oncogenesis and perspectives on developing novel antiviral and anticancer strategies.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
10608 - Biochemistry and molecular biology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2022
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
NAR CANCER
ISSN
2632-8674
e-ISSN
—
Svazek periodika
4
Číslo periodika v rámci svazku
1
Stát vydavatele periodika
GB - Spojené království Velké Británie a Severního Irska
Počet stran výsledku
16
Strana od-do
—
Kód UT WoS článku
000925421400008
EID výsledku v databázi Scopus
2-s2.0-85141079091