| 2018 |
YKT6 forms a SNARE complex with SNAP29 and lysosomal STX7 on autophagosomes, providing a second pathway for autophagosome-lysosome fusion that is independent of STX17; depletion of YKT6 completely blocked autophagosome-lysosome fusion in STX17 KO cells. |
STX17 knockout HeLa cells, SNARE screen, co-immunoprecipitation, fluorescence microscopy |
The Journal of cell biology |
High |
29789439
|
| 2024 |
YKT6 forms a priming complex with STX17 and SNAP29 on autophagosomes via its SNARE domain; VAMP8 then displaces YKT6 to form the fusogenic STX17-SNAP29-VAMP8 complex, with STX7 participating in the YKT6-SNAP29-STX7 complex at lysosomes to mediate content and lipid mixing. |
Co-immunoprecipitation, lipid and content mixing assays, dominant-negative constructs, autophagy flux assays |
Cell reports |
High |
38340317
|
| 2011 |
STX7 is required for lytic granule release from cytotoxic T lymphocytes (CTLs); it localizes preferentially to the immunological synapse and mediates trafficking of recycling TCRs through late endosomes (colocalizing with Rab7), which is a prerequisite for lytic granule accumulation and CTL-mediated killing. |
Dominant-negative STX7 expression, siRNA knockdown, evanescent wave microscopy, high-resolution nanoscopy, functional CTL killing assay |
Traffic (Copenhagen, Denmark) |
High |
21438968
|
| 2008 |
CSF-1 induces serine phosphorylation of STX7 via PKC and Akt downstream of PI3K activation; this phosphorylation, mapped to the Habc domain and/or linker region by mutagenesis, enhances STX7 binding to its SNARE partners Vti1b, STX8, and VAMP8 and upregulates STX7 expression in macrophages. |
Primary mouse macrophage culture, kinase inhibitor pharmacology, site-directed mutagenesis, co-immunoprecipitation, Western blot |
Molecular and cellular biology |
High |
18710945
|
| 2014 |
UVRAG mediates viral endocytic transport and membrane penetration through interactions with endosomal Q-SNAREs STX7, STX8, and Vti1b, leading to assembly of a fusogenic trans-SNARE complex involving VAMP8 (but not VAMP7); inhibition of VAMP8 significantly reduces influenza A and VSV entry. |
Co-immunoprecipitation, viral entry assays, siRNA knockdown, VAMP8/VAMP7 inhibition |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
24550300
|
| 2011 |
STX11 binds Vti1b and regulates the availability of Vti1b to form Q-SNARE complexes including STX6/STX7/Vti1b and STX7/STX8/Vti1b that mediate late endosome to lysosome fusion in macrophages; mutant STX11 sequesters Vti1b from these complexes. |
Co-immunoprecipitation, siRNA depletion, confocal microscopy, functional endosomal trafficking assays in macrophages |
Traffic (Copenhagen, Denmark) |
Medium |
21388490
|
| 2019 |
SGK3 directly phosphorylates STX7 at Ser126 in a site that is inefficiently phosphorylated by Akt; IGF1-stimulated STX7 phosphorylation in HEK293 cells is blocked by SGK3 knockout or pan-SGK inhibitor, identifying STX7 as a specific endosomal substrate of SGK3. |
Phosphoproteomics screen, in vitro kinase assay, SGK3 knockout cells, Phos-tag gel electrophoresis, IGF1 stimulation |
The Biochemical journal |
High |
31665227
|
| 2015 |
γ-SNAP mediates disassembly of endosomal STX7-containing SNARE complexes (alongside α-SNAP) and regulates endocytic trafficking of EGFR and transferrin; depletion of γ-SNAP delayed exit of EGFR and transferrin from EEA1-positive early endosomes. |
Immunoprecipitation, mass spectrometry, siRNA knockdown, SNARE disassembly assay, fluorescence microscopy of EGFR/transferrin trafficking |
Journal of cell science |
Medium |
26101353
|
| 2017 |
STX7 is required for homotypic fusion of HCV-induced phagophores to generate autophagosomes; knockdown of STX7 inhibits autophagosome formation but does not affect HCV RNA replication, which occurs on phagophore precursors. |
siRNA knockdown, in vitro membrane fusion assay, electron microscopy, live-cell imaging, fluorescence microscopy |
PLoS pathogens |
Medium |
28931085
|
| 2021 |
STX7 defines a rapidly replenishing synaptic vesicle (SV) recycling pool in hippocampal neurons; this Stx7-marked pool is preferentially mobilized during high-frequency stimulation and its recruitment requires actin polymerization and Ca2+/calmodulin signaling; overexpression of the STX7 N-terminal domain as a dominant negative selectively abolished this pool. |
Optical imaging of presynaptic SNARE proteins in cultured hippocampal neurons, dominant-negative overexpression, pharmacological inhibition (actin, Ca2+/CaM pathway), electrophysiology |
Communications biology |
Medium |
34408265
|
| 2022 |
STX7 localizes near invadopodia and co-traffics with MT1-MMP; STX7 depletion reduces invadopodium number and associated degradative activity; STX7 forms SNARE complexes with VAMP2, VAMP3, VAMP7, STX4, and SNAP23; depletion of VAMP2, VAMP3, or STX4 phenocopies STX7 loss by abolishing invadopodia formation in MDA-MB-231 cells. |
siRNA knockdown, TIRF microscopy, immunoprecipitation, gelatin degradation assays |
Journal of cell science |
Medium |
35762511
|
| 2021 |
The trans-SNARE complex VAMP4/STX6/STX7/Vti1b regulates Golgi-to-late-endosome trafficking of MT1-MMP in LPS-activated macrophages; depletion of any complex member reduces surface MT1-MMP and gelatin degradation, while overexpression of STX6/STX7/Vti1b increases surface MT1-MMP. |
siRNA knockdown, overexpression, fixed and live imaging, surface protein assays, gelatin degradation assay |
Traffic (Copenhagen, Denmark) |
Medium |
34476885
|
| 2019 |
UNC13D regulates late endosomal trafficking via binding to STX7; a STX7-binding-deficient mutant of UNC13D fails to rescue the defective endosomal trafficking and endocytic flux phenotype of unc13d-null cells, demonstrating that STX7 interaction is functionally required for UNC13D's role in endosomal maturation. |
unc13d-null cell rescue experiments with wild-type vs. STX7-binding-deficient UNC13D mutant, biochemical and microscopy assays of endocytic flux |
Autophagy |
Medium |
30892133
|
| 2026 |
Small-molecule inhibitors (ENDOtollins) of the Munc13-4–STX7 interaction block endolysosomal flux and specifically inhibit endosomal TLR signaling (ERK in neutrophils; IRF in plasmacytoid DCs) without affecting plasma membrane TLR agonists; ENDO12 reduced CpG-induced systemic inflammation in vivo. |
High-throughput small-molecule screening, cell-based validation of Munc13-4-STX7 interaction inhibition, functional TLR signaling assays, in vivo CpG challenge model |
Nature chemical biology |
Medium |
41942734
|
| 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; mechanistically, IFITM3 disrupts assembly of the STX7-containing SNARE complex controlling homotypic late endosome fusion and accelerates trafficking of endosomal cargo to lysosomes. |
Co-immunoprecipitation, in vitro binding assay, mutagenesis, influenza A infection assay, endosomal cargo trafficking assay |
The EMBO journal |
High |
39653855
|
| 2024 |
Chlamydia effector IncE recruits STX7-containing vesicles to the inclusion via a proximal SNARE-mimicking short linear motif (SLiM) that binds STX7 and STX12. |
Cell biological characterization of IncE SLiM mutants, vesicle recruitment assays, co-localization microscopy |
Cell reports |
Medium |
39154341
|
| 2025 |
STX7 knockdown reduces Salmonella survival in HeLa and RAW264.7 macrophages, and this is rescued by STX7 overexpression; live imaging shows STX7 is recruited to Salmonella-containing vacuoles (SCVs) at different infection stages, and BioID revealed STX7 interactions with SPI-2 effectors SifA and SopD2, indicating Salmonella hijacks STX7 to evade lysosomal fusion. |
STX7 siRNA knockdown and overexpression rescue, live cell imaging, BioID proximity labeling |
Traffic (Copenhagen, Denmark) |
Medium |
40444290
|
| 2025 |
STX7 is identified as a binding target of the anti-inflammatory compound capsazepine; STX7 siRNA knockdown phenocopied capsazepine's anti-inflammatory effects on astrocytes; interaction confirmed by drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA), and molecular docking. |
siRNA knockdown, DARTS, CETSA, molecular docking, astrocyte activation assays |
FASEB journal |
Medium |
40386937
|
| 2023 |
STX7 overexpression reduces seizure susceptibility and alleviated epileptic activity in kainic acid and pentylenetetrazole models; STX7 does not affect neuronal intrinsic excitability but affects the excitation/inhibition ratio by influencing presynaptic GABA neurotransmitter release and inhibitory vesicle density (but not inhibitory synapse density). |
Overexpression/knockdown in rodent epilepsy models, whole-cell patch-clamp electrophysiology, transmission electron microscopy |
Neurobiology of disease |
Medium |
37031804
|
| 2025 |
STX7 knockout in hepatocellular carcinoma cells suppresses proliferation, migration, and EMT via inhibition of NF-κB signaling. |
CRISPR knockout, in vitro proliferation/migration assays, in vivo xenograft, Western blot for NF-κB pathway markers |
BMC cancer |
Low |
40999361
|
| 2024 |
GORASP2 depletion attenuates assembly of both STX17-SNAP29-VAMP8 and YKT6-SNAP29-STX7 SNARE complexes required for autophagosome-lysosome fusion, placing STX7 downstream of GORASP2-regulated RAB7A-HOPS machinery. |
Super-resolution microscopy, siRNA depletion, SNARE complex assembly assays |
Autophagy |
Low |
39056394
|
| 2020 |
A trafficome-wide RNAi screen identified the late endo-/lysosomal SNARE complex STX7/STX8/VTI1B/VAMP7 or VAMP8 as required for Salmonella-induced filament (SIF) formation and intracellular Salmonella replication. |
Sub-genomic RNAi screen, high-resolution live cell imaging for SIF morphology and dynamics |
PLoS pathogens |
Low |
32658937
|
| 2025 |
STX7, STX8, and VTI1B are recruited to the Plasmodium parasitophorous vacuole membrane (PVM) ~24 h post-infection; combined knockouts with VAMP7 reveal partial redundancy; STX7/VAMP8 appear at PVM later than VAMP7/Vti1B suggesting a role in nutrient acquisition phase. |
CRISPR/Cas9 knockout in HeLa cells, confocal microscopy, combinatorial knockout infection assays |
Cells |
Low |
41972675
|
| 2025 |
STX7, STX8, and VTI1B are required for crinophagy (secretory granule-lysosome fusion) in endocrine cells; siRNA screening identified these SNAREs as necessary for SG-lysosome docking/fusion alongside Munc13-4, Rab27A, VAMP2, PLEKHM1, and HOPS subunits. |
siRNA screen with live-cell SG-lysosome fusion assay |
Research square (preprint)preprint |
Low |
40951263
|