| 2018 |
STX7 (lysosomal) forms a SNARE complex with SNAP29 and autophagosomal YKT6 to mediate autophagosome-lysosome fusion independently of STX17; YKT6 depletion completely blocked fusion in STX17-knockout cells, establishing two independent SNARE complexes for autophagosomal fusion. |
STX17 knockout HeLa cells, siRNA depletion of YKT6, co-immunoprecipitation of SNARE complex, fluorescence microscopy of autophagosome-lysosome fusion |
The Journal of cell biology |
High |
29789439
|
| 2011 |
STX7 is required for lytic granule release from cytotoxic T lymphocytes (CTLs); it localizes to the immunological synapse and late endosomes (co-localizing with Rab7), and its loss prevents both TCR recycling through endosomes and lytic granule accumulation at the IS, without reducing total granule number. |
Dominant-negative STX7 expression, siRNA knockdown, evanescent wave microscopy of individual lytic granules, high-resolution STED nanoscopy, CTL killing assay |
Traffic (Copenhagen, Denmark) |
High |
21438968
|
| 2011 |
STX7 participates in SNARE complexes STX6/STX7/Vti1b and STX7/STX8/Vti1b on endosomal membranes; STX11 regulates late endosome-to-lysosome fusion by controlling availability of Vti1b to form these Q-SNARE complexes, establishing STX7 as a component of the endosomal fusion machinery in macrophages. |
Co-immunoprecipitation of SNARE complexes, siRNA depletion, rescue with siRNA-resistant construct, live imaging of endocytic compartments in macrophages |
Traffic (Copenhagen, Denmark) |
High |
21388490
|
| 2008 |
CSF-1 upregulates STX7 expression in primary macrophages and induces rapid serine phosphorylation of STX7, enhancing its binding to SNARE partners Vti1b, STX8, and VAMP8; mutagenesis of serine residues in the Habc domain and/or linker region identified these as the sites through which CSF-1 regulates SNARE complex assembly. |
Primary mouse macrophage culture, kinase inhibitor studies, mutagenesis of STX7 serine residues, co-immunoprecipitation of SNARE partners, western blotting |
Molecular and cellular biology |
High |
18710945
|
| 2014 |
UVRAG mediates viral endocytic transport through interaction with endosomal Q-SNAREs including STX7, STX8, and Vti1b, leading to assembly of a fusogenic trans-SNARE complex with VAMP8; inhibition of VAMP8 (but not VAMP7) significantly reduces viral entry, placing STX7 in the specific SNARE complex required for influenza A and VSV entry. |
Co-immunoprecipitation, siRNA depletion, viral infection assays, VAMP isoform-selective inhibition |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
24550300
|
| 2015 |
γ-SNAP mediates disassembly of endosomal STX7-containing SNARE complexes; immunoprecipitation combined with mass spectrometry showed γ-SNAP preferentially interacts with endosomal SNAREs, and its depletion altered endosome morphology and delayed EGFR and transferrin trafficking from early endosomes. |
Immunoprecipitation, mass spectrometry, siRNA depletion, overexpression, endosome morphology analysis |
Journal of cell science |
Medium |
26101353
|
| 2017 |
STX7 is required for homotypic fusion of phagophores to generate HCV-induced autophagosomes; in vitro membrane fusion assay demonstrated STX7-dependent phagophore-phagophore fusion, and STX7 knockdown blocked autophagosome formation without affecting HCV RNA replication on phagophore membranes. |
In vitro membrane fusion assay, electron microscopy, siRNA knockdown, live-cell imaging |
PLoS pathogens |
High |
28931085
|
| 2019 |
SGK3 phosphorylates STX7 at Ser126 at endosomes; phosphoproteomic screening and in vitro kinase assays confirmed STX7 Ser126 as an SGK3-specific substrate (poorly phosphorylated by Akt), and IGF1 stimulation in HEK293 cells promoted endogenous STX7 phosphorylation in an SGK3-dependent manner. |
Phosphoproteomic screen, in vitro kinase assay with purified SGK3 and Akt, Phos-tag gel analysis, SGK3 knockout cells, pan-SGK inhibitor treatment |
The Biochemical journal |
High |
31665227
|
| 2019 |
UNC13D binds STX7 on late endosomes and regulates endosomal maturation; a STX7-binding-deficient UNC13D mutant failed to rescue defective endosomal trafficking in unc13d-null cells, establishing that the UNC13D-STX7 interaction is required for endolysosomal flux. |
unc13d-null cells, rescue with STX7-binding-deficient UNC13D mutant, endocytic flux assays, biochemical and microscopy methods |
Autophagy |
Medium |
30892133
|
| 2020 |
STX7, STX8, VTI1B, and VAMP7/8 form a complete late endo-/lysosomal SNARE fusion machinery required for Salmonella-induced filament (SIF) formation; RNAi screen showed each component is individually required for SIF morphology in conjunction with RAB7 and HOPS tethering complex. |
Sub-genomic RNAi screen, high-resolution live-cell imaging, SIF morphology scoring |
PLoS pathogens |
Medium |
32658937
|
| 2021 |
STX7 (endosomal Q-SNARE) defines a rapidly replenishing synaptic vesicle pool in hippocampal neurons; disruption of STX7 function by overexpressing its N-terminal domain selectively abolished this pool, and recruitment of STX7-marked vesicles requires actin polymerization and Ca2+/calmodulin signaling. |
Optical imaging of presynaptic endosomal SNARE proteins, dominant-negative N-terminal domain overexpression, pharmacological inhibition of actin polymerization and Ca2+/calmodulin signaling in cultured hippocampal neurons |
Communications biology |
Medium |
34408265
|
| 2021 |
The trans-SNARE complex VAMP4/STX6/STX7/Vti1b mediates Golgi-to-late-endosome trafficking of MT1-MMP in macrophages; depletion of any SNARE in this complex reduced surface MT1-MMP and gelatin degradation, while overexpression of STX6/STX7/Vti1b increased surface MT1-MMP. |
Fixed and live imaging, siRNA depletion, overexpression, gelatin degradation assay in LPS-activated macrophages |
Traffic (Copenhagen, Denmark) |
Medium |
34476885
|
| 2022 |
STX7 promotes invadopodia formation and breast cancer cell invasion by forming distinct SNARE complexes with VAMP2, VAMP3, VAMP7, STX4, and SNAP23; STX7 depletion reduced invadopodia number and associated MT1-MMP at invadopodia, while increasing non-invadosomal MT1-MMP pools. |
siRNA screening of 13 SNAREs, TIRF microscopy, co-trafficking with MT1-MMP, immunoprecipitation, invasion assays in MDA-MB-231 cells |
Journal of cell science |
Medium |
35762511
|
| 2023 |
STX7 modulates seizure susceptibility by regulating presynaptic GABA release; overexpression of STX7 reduced seizure susceptibility in kainic acid and PTZ kindling models, affecting excitation/inhibition ratio and inhibitory vesicle density without changing intrinsic neuronal excitability or inhibitory synapse density. |
Kainic acid and PTZ kindling mouse models, STX7 overexpression and knockdown, whole-cell patch-clamp recordings, transmission electron microscopy |
Neurobiology of disease |
Medium |
37031804
|
| 2024 |
YKT6 forms a priming complex with STX17 and SNAP29 on autophagosomes via its SNARE domain; VAMP8 displaces YKT6 from this complex to form the fusogenic STX17-SNAP29-VAMP8 complex, with the YKT6-SNAP29-STX17 complex facilitating both lipid and content mixing to promote autophagy flux. STX7 (lysosomal) participates in the parallel STX7-SNAP29-YKT6 fusogenic complex. |
Co-immunoprecipitation, lipid mixing assay, content mixing assay, autophagy flux measurement |
Cell reports |
High |
38340317
|
| 2024 |
IFITM3 binds STX7 in cells and in vitro via a SNARE-like motif in its CD225 domain; mutations that abrogate STX7 binding cause loss of antiviral activity against influenza A virus, and mechanistically IFITM3 disrupts assembly of the STX7-containing SNARE complex controlling homotypic late endosome fusion, accelerating cargo trafficking to lysosomes. |
Co-immunoprecipitation in cells, in vitro binding assay, mutagenesis of SNARE-like motif, influenza A virus infection assay, endosomal cargo trafficking assay |
The EMBO journal |
High |
39653855
|
| 2024 |
Chlamydia effector IncE binds STX7- and STX12-containing vesicles via a proximal SNARE-mimetic short linear motif (SLiM) in its C-terminus, recruiting these vesicles to the Chlamydia inclusion to facilitate intracellular bacterial development. |
SLiM mutagenesis, vesicle recruitment assays, co-localization microscopy, functional bacterial development assays |
Cell reports |
Medium |
39154341
|
| 2025 |
Munc13-4 specifically interacts with STX7 to regulate endolysosomal flux and endosomal TLR signaling; small-molecule ENDOtollins inhibiting the Munc13-4-STX7 interaction blocked endolysosomal cargo degradation and reduced TLR3/7/9-driven inflammatory cytokine production in dendritic cells and neutrophils without affecting plasma membrane TLR responses. |
High-throughput small-molecule screening, orthogonal cell-based validation, endolysosomal flux assay, TLR ligand stimulation assays, in vivo CpG-induced inflammation model |
Nature chemical biology |
High |
41942734
|
| 2025 |
Salmonella Typhimurium hijacks STX7 to evade lysosomal fusion and maintain its intracellular vacuolar niche; STX7 knockdown reduced bacterial survival rescued by STX7 overexpression, STX7 is recruited to SCVs with altered distribution at late infection stages, and SPI-2 effectors SifA and SopD2 interact with STX7 by BioID proximity labeling. |
BioID proximity labeling, siRNA knockdown, overexpression rescue, live cell imaging, bacterial survival assay in HeLa and RAW264.7 cells |
Traffic (Copenhagen, Denmark) |
Medium |
40444290
|
| 2025 |
STX7 is identified as a direct binding target of capsazepine in astrocytes; drug affinity responsive target stability (DARTS) analysis, cellular thermal shift assay, and molecular docking demonstrated capsazepine binding to STX7, and STX7 siRNA knockdown phenocopied capsazepine's anti-inflammatory effects on astrocyte activation. |
DARTS analysis, cellular thermal shift assay (CETSA), molecular docking, siRNA knockdown, in vitro and in vivo astrocyte inflammation models |
FASEB journal |
Medium |
40386937
|
| 2025 |
STX7, VAMP8, VTI1B, and VAMP7 are recruited to the Plasmodium parasitophorous vacuole membrane (PVM) with distinct temporal profiles; combinatorial CRISPR knockouts showed VAMP7-VAMP8 and VAMP7-VTI1B double KOs significantly reduced parasite infection and growth, with STX7 appearing at PVM ~24 hpi during nutrient acquisition, indicating host SNARE machinery is co-opted for lysosome-PVM fusion. |
CRISPR/Cas9 knockout in HeLa cells, advanced fluorescence microscopy of P. berghei-infected cells, combinatorial knockout analysis |
Cells |
Medium |
41972675
|
| 2025 |
siRNA screening identified STX7, STX8, and VTI1B as components of the lysosomal SNARE machinery required for secretory granule-lysosome fusion (crinophagy); Munc13-4 associates with these SNAREs and regulates docking and fusion of secretory granules with lysosomes in a calcium-dependent manner. |
siRNA screening with live-cell SG-lysosome fusion assay, co-immunoprecipitation of Munc13-4 with SNARE partners, calcium manipulation experiments |
Research square (preprint)preprint |
Medium |
40951263
|