ArticleScientific reports2019
SQSTM-1/p62 potentiates HTLV-1 Tax-mediated NF-κB activation through its ubiquitin binding function.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- A multi-omics approach reveals specific oncogenic and inflammatory potential of viral oncoproteins Tax from neglected HTLV-1b and -1c genotypes.PLoS pathogens · 2026Article
- Calcium oxalate crystals exacerbate the damage and inflammation of renal tubular epithelial cells by blocking autophagic flux.Urolithiasis · 2026Article
- The Pathology of Viral Infections.Advances in experimental medicine and biology · 2026Review
- PIKfyve controls dendritic cell function and tumor immunity.bioRxiv : the preprint server for biology · 2024Article
- PIKfyve, expressed by CD11c-positive cells, controls tumor immunity.Nature communications · 2024Article
- Treatment of Rheumatoid Arthritis Based on the Inherent Bioactivity of Black Phosphorus Nanosheets.Aging and disease · 2024Article
- PCBP1 interacts with the HTLV-1 Tax oncoprotein to potentiate NF-κB activation.Frontiers in immunology · 2024Article
- The helicase-like transcription factor redirects the autophagic flux and restricts human T cell leukemia virus type 1 infection.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Interplay between ADP-ribosyltransferases and essential cell signaling pathways controls cellular responses.Cell discovery · 2021Review
- Article
- HTLV-1 Infection and Pathogenesis: New Insights from Cellular and Animal Models.International journal of molecular sciences · 2021Review
- Autophagy in Human T-Cell Leukemia Virus Type 1 (HTLV-1) Induced Leukemia.Frontiers in oncology · 2021Review
- How Oncogenic Viruses Exploit p62-Mediated Selective Autophagy for Cancer Development.Annals of immunology & immunotherapy · 2021Article
- The E3/E4 ubiquitin conjugation factor UBE4B interacts with and ubiquitinates the HTLV-1 Tax oncoprotein to promote NF-κB activation.PLoS pathogens · 2020Article
- A novel positive feedback-loop between the HTLV-1 oncoprotein Tax and NF-κB activity in T-cells.Retrovirology · 2020Article
- p62: Friend or Foe? Evidences forInternational journal of molecular sciences · 2020Review
- Mechanisms of Oncogenesis by HTLV-1 Tax.Pathogens (Basel, Switzerland) · 2020Review
- NF-κB and MicroRNA Deregulation Mediated by HTLV-1 Tax and HBZ.Pathogens (Basel, Switzerland) · 2019Review
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Authors and funding
14 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NF-κB pathway is constitutively activated in adult T cell leukemia, an aggressive malignancy caused by Human T Leukemia Virus type 1 (HTLV-1). The viral oncoprotein Tax triggers this constitutive activation by interacting with the ubiquitin-rich IKK complex. We previously demonstrated that Optineurin and TAX1BP1, two members of the ubiquitin-binding, Sequestosome-1 (SQSTM-1/p62)-like selective autophagy receptor family, are involved in Tax-mediated NF-κB signaling. Here, using a proximity-dependent biotinylation approach (BioID), we identify p62 as a new candidate partner of Tax and confirm the interaction in infected T cells. We then demonstrate that p62 knock-out in MEF cells as well as p62 knock-down in HEK293T cells significantly reduces Tax-mediated NF-κB activity. We further show that although p62 knock-down does not alter NF-κB activation in Jurkat T cells nor in infected T cells, p62 does potentiate Tax-mediated NF-κB activity upon over-expression in Jurkat T cells. We next show that p62 associates with the Tax/IKK signalosome in cells, and identify the 170-206 domain of p62 as sufficient for the direct, ubiquitin-independent interaction with Tax. However, we observe that this domain is dispensable for modulating Tax activity in cells, and functional analysis of p62 mutants indicates that p62 could potentiate Tax activity in cells by facilitating the association of ubiquitin chains with the Tax/IKK signalosome. Altogether, our results identify p62 as a new ubiquitin-dependent modulator of Tax activity on NF-κB, further highlighting the importance of ubiquitin in the signaling activity of the viral Tax oncoprotein.
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