TAX1BP1 manual deep research

Generated on 2026-04-24 as a manual fallback after provider-based deep research did not produce a usable report in this worktree.

Update on 2026-04-25: a provider-generated focused OpenAI report was subsequently created at
TAX1BP1-deep-research-openai.md. This manual memo is retained as a fallback synthesis and
local provenance record for the earlier provider failures.

Provenance

• Attempted just deep-research-falcon human TAX1BP1; the Edison/Falcon job remained active for several minutes without producing an output file.
• Attempted just deep-research-openai human TAX1BP1; the OpenAI deep-research job likewise remained long-running without producing an output file in a usable window.
• Attempted just deep-research-perplexity-lite human TAX1BP1; this failed immediately with 401 insufficient_quota.
• This fallback memo synthesizes the locally cached publications already used for the PN-focused review.

PN-focused conclusion

TAX1BP1 is best supported as a ubiquitin-binding selective-autophagy cargo adaptor/receptor rather than as a general signaling adaptor or a dedicated mitophagy/fusion factor.

• Xenophagy/selective-autophagy receptor function is directly supported by Salmonella and structural/autophagy-receptor studies PMID:26451915 PMID:29940186 PMID:30459273.
• Cargo-coupled macroautophagy initiation is supported by FIP200 recruitment around ubiquitin-positive cargo PMID:33226137 PMID:34471133.
• Innate immune pathway effects are real but are best interpreted as contextual consequences of selective autophagic cargo handling in the PN frame PMID:28898289 PMID:28898289.
• Older A20/NF-kappaB pathway papers support a broader adaptor role, but not one that should displace the autophagy-centered core call PMID:17703191 PMID:18239685.

Conservative boundaries

• Mitophagy should remain non-core here. The local evidence shows mitochondrial localization in a MAVS setting PMID:27736772, but this does not by itself justify a standalone core mitophagy annotation.
• Autophagosome-lysosome fusion should also remain below the threshold for direct promotion. PMID:26451915 supports a Myosin VI-linked maturation connection PMID:26451915, but the available TAX1BP1-specific evidence is still indirect for a direct fusion term.
• Broad signaling-adaptor annotations are acceptable as contextual/non-core descriptions, but the GO-facing core remains better captured by autophagy cargo adaptor activity plus the selective-autophagy process calls.

Impact on the local review

The current PN-focused YAML remains appropriately conservative. This manual fallback does not justify promoting additional core terms beyond:

• autophagy cargo adaptor activity
• macroautophagy
• xenophagy

It also does not justify promoting standalone core annotations for:

• mitophagy
• autophagosome-lysosome fusion
• broad inflammatory-signaling adaptor terms