Provides electronic SNARE-family (SNAP receptor activity, SNARE binding, vesicle-mediated transport) annotations for VTI1A via InterPro VTI1/SNARE-domain mapping.

Transfers experimentally-supported endosome/TGN localization and endosome-to-TGN trafficking process annotations to VTI1A from characterised orthologous SNAREs (Vti1a/Vti1b/Vti1) by curator judgment of sequence similarity.

PAINT/IBA phylogenetic-inference annotations propagate SNAP receptor activity, SNARE binding, endosome-to-Golgi/TGN retrograde transport, and Golgi/endosome localization from experimentally annotated VTI1-family SNAREs to VTI1A.

Provides electronic Golgi apparatus, endosome, and TGN localizations for VTI1A from UniProt subcellular-location vocabulary, consistent with the experimental IDA evidence.

Provides electronic membrane-fusion process annotation for VTI1A via inter-ontology logical inference, consistent with VTI1A's role as a SNARE catalysing vesicle-membrane fusion.

ARBA machine-learning rule assigns broad vesicle/membrane-associated terms to VTI1A based on generalized sequence/annotation features; correct but non-specific relative to VTI1A's Golgi/endosome-SNARE role.

Accessible text supports a syntaxin5/Ykt6/GS28/GS15 complex, not VTI1A; VTI1A terms citing this PMID are accepted only on independent evidence and should be checked as possible source/reference errors.

STX10, STX16, Vti1a, and VAMP3 form a SNARE-complex route required for MPR transport from endosomes/late endosomes to the TGN/Golgi.

ARL1/ARFRP1 work supports Vti1a-containing SNARE involvement in Shiga-toxin retrograde transport downstream of ARL1.

This is a VAMP1 spastic ataxia paper and does not support VTI1A movement annotation.

Vti1a depletion phenocopies VAMP4-cognate SNARE disruption of Golgi ribbon structure, supporting early-endosome-to-TGN retrograde traffic.

Vti1a knockdown with STX13 blocks autophagic flux and supports autophagy/autophagosome context.

RAB6:GTP recruits the GARP tethering complex (VPS54/53/52/51) to the TGN, where GARP interacts with TGN SNAREs STX10 and STX16 and with a vesicle fraction containing the v-SNARE VAMP4; in the same pathway, the COG complex facilitates retrograde traffic in a STX6/STX16/VTI1A and VAMP4-dependent manner.

The Golgi-localized COG tethering complex interacts with Golgi SNAREs STX6, STX16, GOSR1, GOSR2, BET1L, SNAP29, VPS45 and VTI1A during intra-Golgi and endosome-to-TGN retrograde vesicle capture.

After capture at the TGN, late-endosome-derived vesicles undergo SNARE-mediated membrane fusion (involving VTI1A as part of the STX10/STX16/VTI1A t-SNARE complex) to deliver cargo and the resulting cis-SNARE to the TGN membrane.

RAB9-positive late-endosome-derived vesicles are tethered at the TGN by GARP, the golgin GCC2, and the STX10/STX16/VTI1A t-SNARE complex — the primary Reactome step in which VTI1A directly participates.

After late-endosome-to-TGN fusion, the 4-membered cis-SNARE complex containing VTI1A binds α/γ-SNAP and NSF hexamer, priming it for ATP-dependent disassembly.

NSF-driven ATP hydrolysis disassembles the post-fusion cis-SNARE complex containing VTI1A, releasing SNAREs (including VTI1A) for further rounds of endosome-to-TGN membrane fusion.

Early-endosome-derived retrograde vesicles fuse at the TGN via a SNARE complex that includes VTI1A (with STX6, STX16, VAMP4), delivering cargo such as TGOLN2 and internalised toxins back to the Golgi.

NSF-driven ATP hydrolysis disassembles the post-fusion cis-SNARE complex (containing VTI1A) after early-endosome-derived vesicle fusion at the TGN, recycling VTI1A and partner SNAREs.

After early-endosome-derived vesicle fusion, the 4-membered cis-SNARE complex (containing VTI1A) binds α/γ-SNAP and NSF hexamer at the TGN, priming it for ATP-dependent disassembly.

VAMP7/Vti1a defines a non-conventional KChIP1/Kv4 traffic pathway to the cell surface in HeLa and Neuro2A cells.

VTI1A is a VTI1-family SNARE involved in vesicle transport, lipid-bilayer fusion, late-endosome-to-TGN transport, and non-conventional cell-surface trafficking.

Local synthesis identifies SNARE-mediated endosome-to-Golgi/TGN traffic as core, autophagy as PN-relevant, and ESCRT-III complex membership as inappropriate.