| Category | Key points | Best supporting citations (pqac ids) | Source URL + pub year |
|---|---|---|---|
| Identity/domains | Verified target is human **TAX1BP1 / T6BP / Tax1-binding protein 1** (UniProt Q86VP1). Current evidence supports classification as a **selective autophagy receptor** with a **SKICH** domain, **LC3-interacting regions (LIRs)**, and **two C-terminal UBZ (ubiquitin-binding zinc finger) domains**; the second UBZ is essential for ubiquitin binding and shows preference for **K63-linked** chains, with reported binding also to linear tetra-Ub and K48-linked chains. | (pqac-00000010, pqac-00000002, pqac-00000006) | https://doi.org/10.1002/bies.202300076 (2023); https://doi.org/10.1080/15548627.2024.2394306 (2025) |
| Molecular function | TAX1BP1 functions primarily as a **ubiquitin-binding adaptor/cargo receptor** that links ubiquitinated cargo to autophagy machinery and suppresses excessive inflammatory signaling. Evidence supports roles in **aggrephagy**, **lysophagy**, pathogen-directed selective autophagy, and negative regulation of **NF-κB** and **RLR/MAVS** signaling. | (pqac-00000005, pqac-00000006, pqac-00000013) | https://doi.org/10.1080/15548627.2024.2394306 (2025); https://doi.org/10.1038/s41580-022-00542-2 (2023) |
| Key pathways | Best-supported pathways include: **NF-κB termination** via A20/TNFAIP3-associated inhibitory complexes; **RLR/MAVS** pathway suppression through autophagic clearance of MAVS aggregates; **lysophagy** where TAX1BP1 is sufficient to promote damaged-lysosome clearance; and broader roles in **mitophagy/selective autophagy receptor networks**. Recent work also places TAX1BP1 among receptors that can restore mitophagy when multiple SARs are removed. | (pqac-00000005, pqac-00000006, pqac-00000013, pqac-00000010) | https://doi.org/10.1080/15548627.2024.2394306 (2025); https://doi.org/10.1038/s41580-022-00542-2 (2023); https://doi.org/10.1002/bies.202300076 (2023) |
| Key binding partners | Supported partners include **A20/TNFAIP3** (anti-inflammatory adaptor function), **TRAF6** (historical alternate name TRAF6-binding protein), **TBK1** and **IKBKE/IKKi** (phosphorylate TAX1BP1), **RB1CC1/FIP200**, **ATG8-family proteins**, **NDP52/CALCOCO2**, **OPTN**, **p62/SQSTM1**, **MAVS**, and **myosin VI**. Myosin VI is a recent structural/biophysical partner supported by 2024 cryo-EM work on the motor and by prior receptor-binding evidence. | (pqac-00000005, pqac-00000004, pqac-00000015, pqac-00000012) | https://doi.org/10.1080/15548627.2024.2394306 (2025); https://doi.org/10.1038/s41467-024-45424-7 (2024); https://doi.org/10.1186/s12890-024-03351-9 (2024) |
| Localization | TAX1BP1 acts mainly in the **cytosol** and at sites of selective autophagy cargo capture, with evidence for localization to **autophagosomes/autophagic vacuoles**, **lysosomes** (including increased LAMP1 colocalization when phosphorylated), and likely the **outer autophagosome membrane** through ubiquitin/myosin VI coupling. Later work also implicates TAX1BP1 in **Golgi-associated autophagic regulation**, but strongest directly gathered support here is for cytosol-autophagosome-lysosome trafficking. | (pqac-00000005, pqac-00000007, pqac-00000010, pqac-00000015) | https://doi.org/10.1080/15548627.2024.2394306 (2025); https://doi.org/10.1038/s41467-024-45424-7 (2024) |
| Recent 2023-2024 developments | 2023 reviews place TAX1BP1 firmly within the **mammalian selective autophagy receptor** toolkit and note a role in **mitophagy restoration** relative to other SARs. A 2024 review of autophagosome-lysosome fusion lists TAX1BP1 among cargo receptors relevant to autophagy completion. A 2024 cryo-EM study of **myosin VI** highlights TAX1BP1 as a cargo adaptor for the motor. A 2024 asthma study links **UBE2N-TAX1BP1 signaling** to ferroptosis/inflammation phenotypes, though this is more disease-model evidence than core mechanistic annotation. A 2024 HTLV-1 paper provides contextual relevance to Tax/NF-κB biology but not direct TAX1BP1 mechanism. | (pqac-00000010, pqac-00000014, pqac-00000015, pqac-00000012, pqac-00000011) | https://doi.org/10.1002/bies.202300076 (2023); https://doi.org/10.1038/s41580-022-00542-2 (2023); https://doi.org/10.3390/cells13060500 (2024); https://doi.org/10.1038/s41467-024-45424-7 (2024); https://doi.org/10.1186/s12890-024-03351-9 (2024); https://doi.org/10.3389/fimmu.2024.1375168 (2024) |
| Quantitative/statistical notes | Direct quantitative TAX1BP1 mechanistic evidence in gathered sources is limited for 2023-2024. The strongest numbers come from a later mechanistic study showing **13 putative IKBKE/IKKi-induced phosphosites**, with **S254, S593, S666** highlighted; phosphomimetic mutants showed stronger lysosomal colocalization and MAVS-clearance phenotypes, with reported statistics including **p < 0.01**, **p < 0.001**, and **p < 0.0001** across experiments. A 2024 lysophagy review cites **~20%** reduced repair in FBXO27-KO cells in a related damaged-lysosome model and notes TAX1BP1 is sufficient to promote lysophagy. | (pqac-00000007, pqac-00000005, pqac-00000013) | https://doi.org/10.1080/15548627.2024.2394306 (2025); https://doi.org/10.1038/s41580-022-00542-2 (2023) |
| Applications/disease links | TAX1BP1 is not yet an established drug target, but disease-oriented evidence connects it to **inflammatory regulation**, **viral signaling**, **bacterial infection biology**, **ferroptosis/asthma models**, and possible **oncology** associations. Open Targets lists associations including **prostate carcinoma/prostate cancer**, **hypospadias**, **hallux valgus**, and **type 2 diabetes mellitus**; these are association-level signals rather than definitive functional causality. The asthma study explicitly proposes the **TRIM11–UBE2N–TAX1BP1 axis** as a potential therapeutic avenue. | (pqac-00000000, pqac-00000012) | Open Targets platform context (current); https://doi.org/10.1186/s12890-024-03351-9 (2024) |


*Table: This table summarizes the best-supported functional annotation of human TAX1BP1 (UniProt Q86VP1), emphasizing domain architecture, molecular role, pathways, localization, and recent 2023-2024 developments. It is useful as a compact evidence map for building a full narrative report with source-linked claims.*