Viral Hijacking of BET Proteins.
BET inhibitors
BET proteins
BRD4
Coronavirus
Flavivirus
Hepatitis B virus
Herpesvirus
JQ1
Papillomavirus
Polyomavirus
RVX-208
Retrovirus
host-pathogen interactions
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
17 10 2022
17 10 2022
Historique:
received:
21
09
2022
revised:
09
10
2022
accepted:
11
10
2022
entrez:
27
10
2022
pubmed:
28
10
2022
medline:
29
10
2022
Statut:
epublish
Résumé
Proteins of the bromodomain and exterminal domain (BET) family mediate critical host functions such as cell proliferation, transcriptional regulation, and the innate immune response, which makes them preferred targets for viruses. These multidomain proteins are best known as transcriptional effectors able to read acetylated histone and non-histone proteins through their tandem bromodomains. They also contain other short motif-binding domains such as the extraterminal domain, which recognizes transcriptional regulatory proteins. Here, we describe how different viruses have evolved to hijack or disrupt host BET protein function through direct interactions with BET family members to support their own propagation. The network of virus-BET interactions emerges as highly intricate, which may complicate the use of small-molecule BET inhibitors-currently in clinical development for the treatment of cancer and cardiovascular diseases-to treat viral infections.
Identifiants
pubmed: 36298829
pii: v14102274
doi: 10.3390/v14102274
pmc: PMC9609653
pii:
doi:
Substances chimiques
Transcription Factors
0
Histones
0
Cell Cycle Proteins
0
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIAID NIH HHS
ID : R37 AI083139
Pays : United States
Organisme : NIAID NIH HHS
ID : F31 AI164671-01
Pays : United States
Organisme : NIAID NIH HHS
ID : 5R01AI083139-07
Pays : United States
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