ArticleThe Journal of cell biology2003
HIV Gag mimics the Tsg101-recruiting activity of the human Hrs protein.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
135 citing papers in PubMed, 1 synthesis or guideline pooled it, 254 citations in OpenAlex.
- Multiple Inhibitory Factors Act in the Late Phase of HIV-1 Replication: a Systematic Review of the Literature.Microbiology and molecular biology reviews : MMBR · 2018Pooled it
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- Identification of membrane curvature sensing motifs essential for VPS37A phagophore recruitment and autophagosome closure.Communications biology · 2024Article
- ALIX and TSG101 are essential for cellular entry and replication of two porcine alphacoronaviruses.PLoS pathogens · 2024Article
- Non-bone-derived exosomes: a new perspective on regulators of bone homeostasis.Cell communication and signaling : CCS · 2024Review
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- The multifaceted interactions between pathogens and host ESCRT machinery.PLoS pathogens · 2023Review
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- Exosomal transmission of viruses, a two-edged biological sword.Cell communication and signaling : CCS · 2023Review
- Plant autophagosomes mature into amphisomes prior to their delivery to the central vacuole.The Journal of cell biology · 2022Article
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- Tsg101/ESCRT-I recruitment regulated by the dual binding modes of K63-linked diubiquitin.Structure (London, England : 1993) · 2022Article
- Updating on Roles of HIV Intrinsic Factors: A Review of Their Antiviral Mechanisms and Emerging Functions.Intervirology · 2022Review
75 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The HIV-1 Gag protein recruits the cellular factor Tsg101 to facilitate the final stages of virus budding. A conserved P(S/T)AP tetrapeptide motif within Gag (the "late domain") binds directly to the NH2-terminal ubiquitin E2 variant (UEV) domain of Tsg101. In the cell, Tsg101 is required for biogenesis of vesicles that bud into the lumen of late endosomal compartments called multivesicular bodies (MVBs). However, the mechanism by which Tsg101 is recruited from the cytoplasm onto the endosomal membrane has not been known. Now, we report that Tsg101 binds the COOH-terminal region of the endosomal protein hepatocyte growth factor-regulated tyrosine kinase substrate (Hrs; residues 222-777). This interaction is mediated, in part, by binding of the Tsg101 UEV domain to the Hrs 348PSAP351 motif. Importantly, Hrs222-777 can recruit Tsg101 and rescue the budding of virus-like Gag particles that are missing native late domains. These observations indicate that Hrs normally functions to recruit Tsg101 to the endosomal membrane. HIV-1 Gag apparently mimics this Hrs activity, and thereby usurps Tsg101 and other components of the MVB vesicle fission machinery to facilitate viral budding.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.