DCAF1 inhibits the NF-κB pathway by targeting p65
Author:
Funder
Nora Eccles Treadwell Foundation
National Natural Science Foundation of China
Publisher
Elsevier BV
Subject
Immunology,Immunology and Allergy
Reference42 articles.
1. Cytoplasmic retention of HIV-1 regulatory protein Vpr by protein-protein interaction with a novel human cytoplasmic protein VprBP;Zhang;Gene,2001
2. VprBP (DCAF1): a promiscuous substrate recognition subunit that incorporates into both RING-family CRL4 and HECT-family EDD/UBR5 E3 ubiquitin ligases;Nakagawa;BMC Mol. Biol.,2013
3. HIV1 Vpr arrests the cell cycle by recruiting DCAF1/VprBP, a receptor of the Cul4-DDB1 ubiquitin ligase;Transy;Cell Cycle,2009
4. DCAF1 (VprBP): emerging physiological roles for a unique dual-service E3 ubiquitin ligase substrate receptor;Schabla;J. Mol. Cell Biol.,2019
5. Incorporation of Vpr into human immunodeficiency virus type 1 virions: requirement for the p6 region of gag and mutational analysis;Paxton;J. Virol.,1993
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1. DOT1L/H3K79me2 represses HIV-1 reactivation via recruiting DCAF1;Cell Reports;2024-07
2. Enhanced NF-κB activation via HIV-1 Tat-TRAF6 cross-talk;Science Advances;2024-01-19
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4. Monacolin K Induces Apoptosis of Human Glioma U251 Cells by Triggering ROS-Mediated Oxidative Damage and Regulating MAPKs and NF-κB Pathways;ACS Chemical Neuroscience;2023-03-14
5. Corrigendum to ‘DCAF1 inhibits the NF-κB pathway by targeting p65’[Immunology Letters 249 (2022) 33–42];Immunology Letters;2022-12
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