CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.
Humans
Ubiquitin-Protein Ligases
/ metabolism
vpr Gene Products, Human Immunodeficiency Virus
/ metabolism
Ubiquitination
Virus Replication
Viral Regulatory and Accessory Proteins
/ metabolism
HIV Infections
/ virology
Host-Pathogen Interactions
HIV-1
/ physiology
Protein Serine-Threonine Kinases
Receptors, Interleukin-17
CRL4
DCAF1
G2 arrest
HIV
HuSH
SAMHD1
UNG2
Vpr
Vpx
ubiquitin
Journal
Viruses
ISSN: 1999-4915
Titre abrégé: Viruses
Pays: Switzerland
ID NLM: 101509722
Informations de publication
Date de publication:
17 Aug 2024
17 Aug 2024
Historique:
received:
15
07
2024
revised:
04
08
2024
accepted:
15
08
2024
medline:
1
9
2024
pubmed:
31
8
2024
entrez:
29
8
2024
Statut:
epublish
Résumé
The Human Immunodeficiency Virus (HIV) encodes several proteins that contort the host cell environment to promote viral replication and spread. This is often accomplished through the hijacking of cellular ubiquitin ligases. These reprogrammed complexes initiate or enhance the ubiquitination of cellular proteins that may otherwise act to restrain viral replication. Ubiquitination of target proteins may alter protein function or initiate proteasome-dependent destruction. HIV Viral Protein R (Vpr) and the related HIV-2 Viral Protein X (Vpx), engage the CRL4-DCAF1 ubiquitin ligase complex to target numerous cellular proteins. In this review we describe the CRL4-DCAF1 ubiquitin ligase complex and its interactions with HIV Vpr and Vpx. We additionally summarize the cellular proteins targeted by this association as well as the observed or hypothesized impact on HIV.
Identifiants
pubmed: 39205287
pii: v16081313
doi: 10.3390/v16081313
pii:
doi:
Substances chimiques
Ubiquitin-Protein Ligases
EC 2.3.2.27
vpr Gene Products, Human Immunodeficiency Virus
0
Viral Regulatory and Accessory Proteins
0
VPX protein, Human immunodeficiency virus 2
0
DCAF1 protein, human
EC 2.7.11.1
IL17RB protein, human
0
Protein Serine-Threonine Kinases
EC 2.7.11.1
Receptors, Interleukin-17
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM