ArticleScientific reports2016
Class B β-arrestin2-dependent CCR5 signalosome retention with natural antibodies to CCR5.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Targeted Immuno-Antiretroviral to Promote Dual Protection against HIV: A Proof-of-Concept Study.Nanomaterials (Basel, Switzerland) · 2022Article
- Effect of an Antagonistic Peptide of CCR5 on the Expression of Autophagy-related Genes and β-Arrestin 2 in Lung Tissues of Asthmatic Mice.Allergy, asthma & immunology research · 2021Article
- Beyond HIV infection: Neglected and varied impacts of CCR5 and CCR5Δ32 on viral diseases.Virus research · 2020Review
- Human papillomavirus type 38 alters wild-type p53 activity to promote cell proliferation via the downregulation of integrin alpha 1 expression.PLoS pathogens · 2020Article
- Dual CCR5/CCR2 targeting: opportunities for the cure of complex disorders.Cellular and molecular life sciences : CMLS · 2019Review
- Encoding the β-Arrestin Trafficking Fate of Ghrelin Receptor GHSR1a: C-Tail-Independent Molecular Determinants in GPCRs.ACS pharmacology & translational science · 2019Article
- The Abrogation of Phosphorylation Plays a Relevant Role in the CCR5 Signalosome Formation with Natural Antibodies to CCR5.Viruses · 2017Article
- The Role of Natural Antibodies to CC Chemokine Receptor 5 in HIV Infection.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCR5 stimulation with natural ligands, such as RANTES, classically induces short-term internalization with transient activation of β-arrestins and rapidly recycling on the cell surface. Here we discovered that, in T cells, natural CCR5 antibodies induce a CCR5-negative phenotype with the involvement of β-arrestin2, which leads to the formation of a stable CCR5 signalosome with both β-arrestin2 and ERK1. The activation of β-arrestin2 is necessary to CCR5 signaling for the signalosome formation and stabilization. When all stimuli were washed out, β-arrestin1 silencing favors the activity of β-arrestin2 for the CCR5 signalosome retention. Interestingly, CCR5 turn from Class A trafficking pattern, normally used for its internalization with natural modulating molecules (i.e. RANTES), into a long lasting Class B type specifically induced by stimulation with natural anti-CCR5 antibodies. This new CCR5 pathway is relevant not only to study in depth the molecular basis of all pathologies where CCR5 is involved but also to generate new antidody-based therapeutics.
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Registered trials
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