SH3GLB1 PN Consistency Notes
- Generated: 2026-06-18
- Project: PROTEOSTASIS
- Scope: PN consistency rereview against local AIGR review and available deep-research artifacts
- UniProt: Q9Y371
- AIGR review status: COMPLETE
- Review batch: proteostasis-pr-1217 (PR 1217)
- Batch change status: added
Source Files Checked
Deep Research Files
- No
*-deep-research*.md file found in this gene directory.
AIGR Review Snapshot
- Description: SH3GLB1 encodes endophilin B1/Bif-1, an N-BAR/SH3 membrane-curvature adaptor that links UVRAG/BECN1/PI3KC3-C2 autophagy signaling to ATG9-positive Golgi membrane fission and autophagosome assembly. Its core functions include PI3KC3 activation, adaptor-mediated association with UVRAG/Beclin 1, and membrane fission/tubulation at Golgi/autophagosome membranes. SH3GLB1 also has supported non-core roles in mitochondrial outer membrane dynamics, Bax/Bak-dependent apoptosis, receptor degradation, cytokinesis, and older lipid-binding/acyltransferase biochemistry.
- Existing/core annotation action counts: ACCEPT: 14; KEEP_AS_NON_CORE: 14; MARK_AS_OVER_ANNOTATED: 21; MODIFY: 12
PN Consistency Summary
- Consistency: Consistent. Notes, review, and PN agree SH3GLB1/Bif-1/endophilin B1 is a POSITIVE N-BAR/SH3 adaptor that activates PI3KC3 via UVRAG (PMID:17891140) and drives ATG9/Golgi membrane fission (PMID:21068542). PN Notes ("binds to UVRAG and promotes activity") correctly state the positive direction — contrast with the RUBCNL row, which was mislabeled. No contradictions.
- PN story / NEW pressure: PN asserts GO:0034272 membership. GOA has only generic GO:0032991 (protein-containing complex, IDA+IEA), so GO:0034272 is
more_specific_than_existing_goa. Review handles this via MODIFY of GO:0032991 → proposed_replacement GO:0034272 (rather than a standalone NEW row). GO:0034272 verified real. Review also adds membrane-fission (GO:0090148) and positive regulation of membrane tubulation (GO:1903527) as core — both verified real, non-obsolete, and beyond the PN story. Verdict: ADD/refine to GO:0034272 (review does via MODIFY) — aligned with PN.
- Evidence alignment: PN cites Annual Review, a cardiovascular review, and PMID:19270696. Review uses primary PMID:17891140 (Bif-1/UVRAG autophagy), 21068542 (ATG9/Golgi fission), 11604418 (endophilin membrane tubulation), 15452144/16227588 (mitochondria/Bax, non-core), 12456676 (LPAAT, non-core). PMID:19270696 is not cited in this review; the PN reference list is shared-branch boilerplate, only loosely SH3GLB1-specific.
- Verdict: Consistent; PN GO:0034272 refines the gene's generic GO:0032991 (more_specific) and the review captures it via MODIFY plus richer membrane-fission/tubulation MF/BP terms (all verified). No edits required.
Full Consistency Review
- UniProt: Q9Y371 · batch: proteostasis-pr-1217 · review status: COMPLETE
- PN placement:
ALP|Autophagosome closure maturation and lysosome fusion|Class 3 PI3K complex 2, direct|Class 3 PI3K complex 2 component ; PN-node mapping: type leaf mapped, ok_for_propagation_to_go → GO:0034272, goa_status more_specific_than_existing_goa; ancestors GO:0035032 / GO:0016236 context_only.
- Consistency: Consistent. Notes, review, and PN agree SH3GLB1/Bif-1/endophilin B1 is a POSITIVE N-BAR/SH3 adaptor that activates PI3KC3 via UVRAG (PMID:17891140) and drives ATG9/Golgi membrane fission (PMID:21068542). PN Notes ("binds to UVRAG and promotes activity") correctly state the positive direction — contrast with the RUBCNL row, which was mislabeled. No contradictions.
- PN story / NEW pressure: PN asserts GO:0034272 membership. GOA has only generic GO:0032991 (protein-containing complex, IDA+IEA), so GO:0034272 is
more_specific_than_existing_goa. Review handles this via MODIFY of GO:0032991 → proposed_replacement GO:0034272 (rather than a standalone NEW row). GO:0034272 verified real. Review also adds membrane-fission (GO:0090148) and positive regulation of membrane tubulation (GO:1903527) as core — both verified real, non-obsolete, and beyond the PN story. Verdict: ADD/refine to GO:0034272 (review does via MODIFY) — aligned with PN.
- Mapping strategy: Supports the C2-component mapping; the PN-projected GO:0034272 is NARROWER than the gene's existing generic GO:0032991, which is exactly the intended refinement (not an over-broad projection). As with the other C2 binders,
part_of for an associating membrane-fission adaptor is defensible but borderline vs. an associated/recruitment relation — review flags this in suggested_questions. Ancestors correctly held too_broad.
- Evidence alignment: PN cites Annual Review, a cardiovascular review, and PMID:19270696. Review uses primary PMID:17891140 (Bif-1/UVRAG autophagy), 21068542 (ATG9/Golgi fission), 11604418 (endophilin membrane tubulation), 15452144/16227588 (mitochondria/Bax, non-core), 12456676 (LPAAT, non-core). PMID:19270696 is not cited in this review; the PN reference list is shared-branch boilerplate, only loosely SH3GLB1-specific.
- Verdict: Consistent; PN GO:0034272 refines the gene's generic GO:0032991 (more_specific) and the review captures it via MODIFY plus richer membrane-fission/tubulation MF/BP terms (all verified). No edits required.
PN Dossier Context
- review_batch: proteostasis-pr-1217
- review_yaml: genes/human/SH3GLB1/SH3GLB1-ai-review.yaml
- PN workbook rows: 1
PN row 1: Autophagy-Lysosome Pathway | Autophagosome closure maturation and lysosome fusion | Class 3 PI3K complex 2, direct | Class 3 PI3K complex 2 component
- UniProt: Q9Y371
- In branches: ALP
- Notes: Member of class III PI3K complex 2 that binds to UVRAG and promotes activity
- PN references (titles):
- Mammalian Autophagy: How Does It Work? | Annual Review of Biochemistry (annualreviews.org)
- role of autophagy in cardiovascular pathology | Cardiovascular Research | Oxford Academic (oup.com)
- Two Beclin 1-binding proteins, Atg14L and Rubicon, reciprocally regulate autophagy at different stages | Nature Cell Biology
- PN-node mapping records (path + ancestors):
- [type] Autophagy-Lysosome Pathway|Autophagosome closure maturation and lysosome fusion|Class 3 PI3K complex 2, direct|Class 3 PI3K complex 2 component
status=mapped scope=ok_for_propagation_to_go GO=[GO:0034272 phosphatidylinositol 3-kinase complex, class III, type II]
rationale: This PN type denotes component membership in the direct class III PI3K complex 2 module used during autophagosome maturation and lysosome fusion. The corresponding GO complex term is the right propagation target.
- [group] Autophagy-Lysosome Pathway|Autophagosome closure maturation and lysosome fusion|Class 3 PI3K complex 2, direct
status=context_only scope=too_broad_to_propagate GO=[GO:0035032 phosphatidylinositol 3-kinase complex, class III]
rationale: Reviewed as a class-III PI3K complex context or regulator bucket. This node is useful for curator interpretation, but it should not project cellular-component membership; only explicit complex-component leaves propagate to GO complex terms.
- [class] Autophagy-Lysosome Pathway|Autophagosome closure maturation and lysosome fusion
status=context_only scope=too_broad_to_propagate GO=[GO:0016236 macroautophagy]
rationale: This class is a late macroautophagy context, but the subtree mixes docking, fusion, localization, membrane-composition, and unknown late-stage roles. The class-level relation is useful for display while propagation is restricted to narrower mechanism nodes.
- [branch] Autophagy-Lysosome Pathway
status=no_mapping scope= GO=[]
rationale: Reviewed as the top-level PN branch. It is a project taxonomy umbrella rather than a direct GO assertion; all propagation must come from manually curated child nodes.
Projected GO annotations (1)
- GO:0034272 phosphatidylinositol 3-kinase complex, class III, type II | scope=ok_for_propagation_to_go | goa_status=more_specific_than_existing_goa | from=Autophagy-Lysosome Pathway|Autophagosome closure maturation and lysosome fusion|Class 3 PI3K complex 2, direct|Class 3 PI3K complex 2 component
Note
This file is generated from the current PROTEOSTASIS phase-1 dossier and local gene-review artifacts. Edit the source review, PN mapping, or dossier rather than this generated note when correcting the underlying curation.