Affinage

STX17

Syntaxin-17 · UniProt P56962

Length
302 aa
Mass
33.4 kDa
Annotated
2026-06-10
38 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/7 claims corpus-supported (86%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

STX17 (syntaxin 17) is an autophagosomal Qa-SNARE that drives the fusion of autophagosomes with endosomes and lysosomes by assembling a trans-SNARE complex with SNAP29 and the lysosomal R-SNARE VAMP8, a function conserved from Drosophila to human cells (PMID:24113031). Its delivery to autophagosomal membranes is gated by multiple inputs: PtdIns4P binding through C-terminal Lys/Arg residues anchors it to the membrane (PMID:38411137), ULK-mediated phosphorylation at S289 directs autophagosomal localization and licenses interaction with the actin-binding linker FLNA that bridges STX17 to ATG8 proteins (PMID:37389864), and starvation-induced GCN5 acetylation at K254 (reversed by SIRT1) promotes myosin VI-dependent translocation (PMID:42062288). Productive SNARE assembly is staged through a YKT6-STX17-SNAP29 priming complex that is converted to the fusogenic STX17-SNAP29-VAMP8 complex when VAMP8 displaces YKT6 (PMID:38340317), and is reinforced by deacetylation of the SNARE domain (CREBBP/CBP versus HDAC2), which enhances SNAP29 and HOPS engagement upon nutrient stress (PMID:32264736). Tethering and lipid-kinase activity at the fusion site are coordinated by Pacer, which uses STX17 as an anchor to recruit the HOPS and PI3KC3 complexes (PMID:28306502). This fusion step is negatively regulated by RUNDC1, which traps the ATG14-STX17-SNAP29 complex to exclude VAMP8 (PMID:37684417), and by STING, which sequesters STX17 to suppress basal and starvation-induced autophagy (PMID:35510944). Beyond autophagosome maturation, STX17 shuttles between the ER and mitochondria under Fis1 control; loss of Fis1 drives its mitochondrial accumulation, N-terminal exposure, self-oligomerization, and ATG14-dependent, PINK1/Parkin-independent mitophagy (PMID:31053718). STX17 is exploited by pathogens, with PRRSV nsp5 binding to block SNARE assembly and incomplete autophagy (PMID:36815765), and is transcriptionally controlled by BMAL1 to promote autophagic clearance of amyloid-beta (PMID:39687016).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 2013 High

    Established the core identity of STX17 as the autophagosomal SNARE that executes autophagosome-lysosome/endosome fusion, defining its central role in autophagic flux.

    Evidence Drosophila Syx17 loss-of-function, human cell knockdown, and autophagy flux assays identifying the STX17-SNAP29-VAMP8/VAMP7 complex

    PMID:24113031

    Open questions at the time
    • Did not resolve how STX17 is recruited to autophagosomes
    • Regulatory inputs controlling complex assembly unaddressed
  2. 2017 Medium

    Defined functional sub-modules of STX17 — the N-terminal domain as essential for fusion and Pacer as an STX17-anchored recruiter of tethering and lipid-kinase machinery.

    Evidence Dominant-negative ΔNTD/GFP-tagged STX17 with autophagosome purification, plus Pacer Co-IP and loss-of-function flux assays

    PMID:28306502 PMID:28598244

    Open questions at the time
    • Molecular role of the N-terminal domain at the fusion step not mechanistically resolved
    • How Pacer site-specificity is achieved unclear
  3. 2019 High

    Revealed STX17 functions beyond autophagosome fusion, shuttling between ER and mitochondria under Fis1 control to gate a non-canonical mitophagy pathway, and identified ER-resident regulators of its activity.

    Evidence SR-SIM, proteomics, Co-IP and Fis1 depletion for the mitochondrial pathway; BAP31 and DIPK2A Co-IP/functional assays for fusion regulation

    PMID:31053718 PMID:31251111 PMID:31671609

    Open questions at the time
    • Signal triggering ER-to-mitochondria redistribution unknown
    • Relationship between the mitochondrial and autophagosomal pools of STX17 unresolved
  4. 2020 High

    Showed that PTM of the SNARE domain by acetylation/deacetylation (CREBBP vs HDAC2) acts as a nutrient-responsive switch controlling SNAP29 and HOPS engagement, separating recruitment from complex assembly.

    Evidence Mass spectrometry PTM mapping, Co-IP, GST pulldown, and KO cells with flux assays

    PMID:32264736

    Open questions at the time
    • Quantitative stoichiometry of acetylation under physiological conditions not defined
    • Interplay with other STX17 PTMs unaddressed
  5. 2022 High

    Identified STING as a sequestering brake on STX17 that couples energy and innate-immune signaling to autophagy, with TBK1 phosphorylation releasing STX17 pools.

    Evidence Reciprocal Co-IP, Drosophila genetics, STING KO mice, and exercise-induced autophagy assays

    PMID:35510944

    Open questions at the time
    • Structural basis of STING-STX17 sequestration not defined
    • Which STX17 pool is released under each stimulus incompletely resolved
  6. 2023 High

    Mapped the recruitment logic of STX17 onto kinase and adaptor control — ULK phosphorylation at S289 driving FLNA-ATG8-mediated autophagosomal targeting — and defined RUNDC1 as a negative regulator that traps the pre-fusion complex.

    Evidence In vitro kinase assay, phospho-mutagenesis, Co-IP and rescue (FLNA); reciprocal Co-IP and zebrafish/human cell validation (RUNDC1)

    PMID:37389864 PMID:37684417

    Open questions at the time
    • Hierarchy among S289 phosphorylation, PtdIns4P binding, and acetylation not ordered
    • How RUNDC1 phosphorylation is regulated unknown
  7. 2024 High

    Provided the biophysical and staged-assembly basis of STX17 action: PtdIns4P binding via C-terminal basic residues for membrane recruitment, and a YKT6 priming complex that precedes the fusogenic VAMP8 complex.

    Evidence In vitro liposome recruitment, MD simulation, Ala-substitution rescue (PtdIns4P); Co-IP and reconstituted lipid/content-mixing assays (YKT6)

    PMID:38340317 PMID:38411137

    Open questions at the time
    • How PtdIns4P generation is spatially restricted to autophagosomes unclear
    • Trigger for YKT6-to-VAMP8 exchange not defined
  8. 2024 Medium

    Connected STX17 to transcriptional and stability control and to disease contexts, with BMAL1 driving STX17 transcription for amyloid-beta clearance and SLC34A2 stabilizing STX17 against ubiquitin-mediated degradation in cancer.

    Evidence Luciferase, Co-IP, and TEM (BMAL1); Co-IP/MS, cycloheximide chase, and ubiquitination assays (SLC34A2)

    PMID:38720472 PMID:39687016

    Open questions at the time
    • E3 ligase targeting STX17 for degradation not identified
    • Direct causal contribution to disease pathology beyond correlation incompletely established
  9. 2026 High

    Added GCN5/SIRT1 acetylation at K254 as a starvation-responsive PTM coupling STX17 to a myosin VI motor for autophagosomal translocation.

    Evidence Mass spectrometry PTM mapping, K254 mutagenesis, GCN5/SIRT1/myosin VI knockdown, and flux assays

    PMID:42062288

    Open questions at the time
    • Relationship between K254 acetylation and SNARE-domain acetylation not integrated
    • Spatial coordination of myosin VI transport with PtdIns4P-dependent docking unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the many recruitment cues (PtdIns4P, S289 phosphorylation, K254 and SNARE-domain acetylation, FLNA, myosin VI) are temporally ordered into a single coherent maturation program, and how the autophagosomal versus mitochondrial pools of STX17 are physically partitioned, remain unresolved.
  • No integrated kinetic model of STX17 recruitment
  • Mechanism partitioning ER/mitochondrial/autophagosomal pools undefined
  • Structural basis of the priming-to-fusion SNARE transition not solved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0005198 structural molecule activity 2 GO:0060090 molecular adaptor activity 2 GO:0008289 lipid binding 1
Localization
GO:0005739 mitochondrion 2 GO:0005783 endoplasmic reticulum 2 GO:0031410 cytoplasmic vesicle 2 GO:0005764 lysosome 1 GO:0005829 cytosol 1
Pathway
R-HSA-9612973 Autophagy 5 R-HSA-1643685 Disease 3 R-HSA-5653656 Vesicle-mediated transport 2
Partners
ATG14FIS1FLNARUNDC1SNAP29STINGVAMP8YKT6
Complex memberships
ATG14-STX17-SNAP29 complexSTX17-SNAP29-VAMP8 SNARE complexYKT6-STX17-SNAP29 priming complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2013 STX17 (syntaxin 17) forms a SNARE complex with SNAP29 and the endosomal/lysosomal VAMP8 (or VAMP7 in Drosophila) to mediate autophagosome fusion with endosomes and lysosomes; this role is evolutionarily conserved from Drosophila to human cells. Genetic loss-of-function (Drosophila Syx17 mutants), cell culture knockdown, autophagy flux assays Autophagy High 24113031
2019 STX17 dynamically shuttles between the ER and mitochondria, controlled by the outer mitochondrial membrane protein Fis1. Loss of Fis1 causes aberrant STX17 accumulation on mitochondria, exposes its N-terminus, promotes self-oligomerization, and triggers PINK1/Parkin-independent mitophagy. Mitochondrial STX17 interacts with ATG14, recruits core autophagy proteins to form the mitophagosome, and Rab7-dependent mitophagosome-lysosome fusion follows. Structured illumination microscopy (SR-SIM), proteomics, co-immunoprecipitation, loss-of-function (Fis1 depletion) Nature communications High 31053718
2020 STX17 is acetylated at its SNARE domain by the acetyltransferase CREBBP/CBP; HDAC2 acts as the deacetylase. Upon starvation or MTORC1 inhibition, CREBBP inactivation leads to STX17 deacetylation, which promotes its interaction with SNAP29 and formation of the STX17-SNAP29-VAMP8 SNARE complex, and also enhances STX17 interaction with the HOPS tethering complex, thereby promoting autophagosome-lysosome fusion. Deacetylation does not affect STX17 recruitment to autophagosomal membranes. Mass spectrometry (PTM identification), Co-immunoprecipitation, GST pulldown, KO cell lines, autophagy flux assays Autophagy High 32264736
2017 STX17 on autophagosomes serves as an anchor for the Pacer protein, which recruits both the PI3KC3 complex and the HOPS complex to the autophagosome, enabling site-specific activation and tethering for autophagosome-lysosome fusion. Pacer antagonizes Rubicon to stimulate Vps34 kinase activity at this step. Co-immunoprecipitation, loss-of-function, autophagy flux assays Molecular cell High 28306502
2022 STING physically interacts with STX17 and sequesters it, preventing its translocation to phagophores and mature autophagosomes. Energy crisis or TBK1-mediated phosphorylation disrupts the STING-STX17 interaction, releasing different pools of STX17 to promote autophagic flux. Loss of STING in cells and mice enhances starvation-induced autophagy. Co-immunoprecipitation, Drosophila genetic loss-of-function, STING KO mice, exercise-induced autophagy assay The Journal of cell biology High 35510944
2019 DIPK2A, a late endosome- and lysosome-localized protein, binds VAMP7B (a SNARE-domain-disrupted isoform), inhibiting VAMP7B's competitive interaction with STX17. This allows STX17 to preferentially bind the functional isoform VAMP7A, thereby enhancing autophagosome-lysosome fusion. Co-immunoprecipitation, overexpression/knockdown, autophagy flux assays Autophagy Medium 31251111
2019 The small molecule EACC blocks autophagosome-lysosome fusion by preventing STX17 and SNAP29 loading onto autophagosomes and reducing the interaction of STX17 with HOPS subunit VPS33A and lysosomal R-SNARE VAMP8; this effect is reversible and does not impair lysosomal properties or endocytic degradation. Small molecule treatment, immunofluorescence, Co-immunoprecipitation, autophagy flux assays Molecular biology of the cell Medium 31188703
2017 STX17 carrying a deletion of the N-terminal domain (ΔNTD) or N-terminally tagged with GFP acts as a dominant-negative, causing accumulation of undegraded autophagosomes devoid of lysosomal markers. The N-terminal domain is required for STX17's function in promoting autophagosome-lysosome fusion. Dominant-negative overexpression, inducible cell line, density-gradient centrifugation, immunoprecipitation purification of autophagosomes Autophagy Medium 28598244
2023 ULK kinase phosphorylates STX17 at residue S289, which is required for STX17 localization specifically to autophagosomes. Phosphorylation of S289 promotes STX17 interaction with the actin-binding protein FLNA; FLNA acts as a linker between ATG8 family proteins and STX17 to recruit STX17 to autophagosomes and facilitate autophagosome-lysosome fusion. Disease-causing mutations in FLNA's ATG8- and STX17-binding regions disrupt these interactions and inhibit fusion. In vitro kinase assay, phospho-site mutagenesis, Co-immunoprecipitation, autophagy flux assays, disease mutation analysis The Journal of cell biology High 37389864
2024 PtdIns4P generated on autophagosomes is required for STX17 recruitment to autophagosomal membranes. Recombinant STX17 is recruited to negatively charged liposomes containing PtdIns4P, mediated by C-terminal positively charged (Lys/Arg) residues. Alanine substitution of these residues abolishes membrane binding and autophagosomal recruitment, and fails to rescue autophagosome-lysosome fusion in STX17 loss-of-function cells. In vitro liposome recruitment assay, molecular dynamics simulation, mutagenesis (Ala substitution), cell-based rescue experiments, co-localization imaging Autophagy High 38411137
2024 YKT6 forms a priming complex with STX17 and SNAP29 on autophagosomes via its SNARE domain, enhancing autophagy flux. VAMP8 subsequently displaces YKT6 from this complex to form the fusogenic STX17-SNAP29-VAMP8 complex. The YKT6-SNAP29-STX17 complex facilitates both lipid and content mixing driven by the STX17-SNAP29-VAMP8 complex. Co-immunoprecipitation, in vitro lipid/content mixing assays, autophagy flux assays Cell reports High 38340317
2023 RUNDC1 negatively regulates autophagy by binding ATG14 and stimulating its homo-oligomerization to trap the ATG14-STX17-SNAP29 complex, thereby preventing VAMP8 from binding STX17-SNAP29 and blocking STX17-SNAP29-VAMP8 complex assembly and autophagosome-lysosome fusion. Phosphorylation of RUNDC1 at Ser379 is required for this inhibitory activity. Gain/loss-of-function (human cells and zebrafish model), Co-immunoprecipitation, phospho-site mutagenesis, autophagy flux assays Cell death and differentiation High 37684417
2023 PRRSV nonstructural protein nsp5 directly interacts with STX17 (via the N-terminal motif and SNARE motif of STX17) and inhibits STX17-SNAP29 interaction, thereby blocking autophagosome-lysosome fusion and inducing incomplete autophagy. Co-immunoprecipitation, overexpression, autophagy flux assays, domain mapping Microbiology spectrum Medium 36815765
2019 The ER membrane protein BAP31 interacts with STX17 to suppress autophagy induction; loss of BAP31 stimulates autophagy and tumor growth under metabolic stress, identifying the BAP31-STX17 complex as a regulatory node coupling ER stress to autophagy. Co-immunoprecipitation, KO/KD, in vivo tumor growth assays Cells Medium 31671609
2023 During Neisseria gonorrhoeae infection, IRGM directly recruits STX17 to pathogen-containing endosomes. This IRGM-STX17 interaction is enhanced by LC3, enabling STX17 tethering to lysosomes and directing bacterial degradation. Interaction was still detected at reduced levels in LC3-KO cells. Co-immunoprecipitation, LC3 KO cell line, immunofluorescence, infection assays The Journal of infectious diseases Medium 37926090
2022 STX17 has different localization and function across species: fly Syx17 expressed in mammalian cells localizes to the cytosol and translocates to autophagosomes upon starvation; nematode SYX-17 localizes mainly to mitochondria and promotes mitochondrial fission but does not participate in autophagy. In vivo, fly Syx17 is not involved in mitochondrial fission and nematode SYX-17 is not involved in autophagy. The C-terminal hydrophobic domain (CHD) is conserved, but the C-terminal tail differs substantially across species. Ectopic expression in mammalian cells, in vivo genetic studies in flies and nematodes, subcellular fractionation/localization Autophagy reports Medium 40396044
2024 STX17 interacts with STING, and reducing STX17 expression increases STING levels; further knockdown of STING enhances autophagy flux. This interaction between STX17 and STING plays a role in STX17-mediated regulation of autophagosome degradation and the inflammatory response in atherosclerosis models. Co-immunoprecipitation, shRNA knockdown, autophagy flux assays in HUVEC cells and ApoE KO mice Journal of cellular and molecular medicine Medium 39008328
2025 STX17 colocalizes with the mitochondrial outer membrane marker TOM20; STX17 knockdown impairs mitochondrial transfer from astrocytes to dopaminergic neurons. Drp1 interacts with STX17, and LRRK2 G2019S mutation increases Drp1 Ser616 phosphorylation, reducing STX17-TOM20 colocalization and mitochondrial transfer. Inhibiting Drp1 Ser616 phosphorylation with DUSP6 restores STX17-TOM20 colocalization and mitochondrial transfer efficiency. Co-immunoprecipitation (Drp1-STX17), immunofluorescence colocalization, KD, iPSC-derived co-culture system, Drp1 phosphorylation inhibitor Translational neurodegeneration Medium 41354840
2024 BMAL1 directly binds to the STX17 promoter (confirmed by luciferase assay) and upregulates STX17 transcription. Increased STX17 promotes its interaction with SNAP29 and VAMP8 (confirmed by Co-IP) to form SNARE complexes, facilitating autophagosome-lysosome fusion and autophagic clearance of amyloid-β in hippocampal neurons. Luciferase reporter assay, Co-immunoprecipitation, KD/OE, transmission electron microscopy, RT-PCR iScience Medium 39687016
2026 Upon starvation, STX17 is acetylated at lysine 254 (K254) by the acetyltransferase GCN5, and this modification is reversed by the deacetylase SIRT1. K254 acetylation promotes autophagosomal translocation of STX17, mediated by myosin VI (an F-actin-based motor protein), and is required for subsequent autophagosome-lysosome fusion. Mass spectrometry (PTM identification), mutagenesis (K254 substitution), Co-immunoprecipitation, KD of GCN5/SIRT1/myosin VI, autophagy flux assays Nature communications High 42062288
2025 Legionella SidE effectors mediate phosphoribosyl ubiquitination (PR-Ub) of STX17. PR-Ub modification of STX17 alters its interaction with ATG14L and drives recruitment of STX17+ ER membranes to Legionella-containing phagosomes in a PI3K-dependent manner, forming replicative vacuoles that do not fuse with lysosomes. Proximity labeling (BioID), mass spectrometry (identification of PR-Ub sites), mutagenesis, Legionella infection assays, biochemistry bioRxivpreprint Medium bio_10.1101_2025.05.19.654886
2024 SLC34A2 interacts with STX17 (identified by immunoprecipitation and mass spectrometry) and promotes autophagy and cell proliferation in esophageal squamous cell carcinoma by inhibiting the ubiquitination and degradation of STX17, thereby stabilizing STX17 protein levels. Co-immunoprecipitation, mass spectrometry, cycloheximide chase assay, ubiquitination assay Thoracic cancer Medium 38720472

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 STX17 dynamically regulated by Fis1 induces mitophagy via hierarchical macroautophagic mechanism. Nature communications 114 31053718
2020 Acetylation of STX17 (syntaxin 17) controls autophagosome maturation. Autophagy 106 32264736
2018 MALAT1 modulates the autophagy of retinoblastoma cell through miR-124-mediated stx17 regulation. Journal of cellular biochemistry 81 29073720
2017 Pacer Mediates the Function of Class III PI3K and HOPS Complexes in Autophagosome Maturation by Engaging Stx17. Molecular cell 81 28306502
2022 STING controls energy stress-induced autophagy and energy metabolism via STX17. The Journal of cell biology 61 35510944
2019 DIPK2A promotes STX17- and VAMP7-mediated autophagosome-lysosome fusion by binding to VAMP7B. Autophagy 47 31251111
2019 A reversible autophagy inhibitor blocks autophagosome-lysosome fusion by preventing Stx17 loading onto autophagosomes. Molecular biology of the cell 45 31188703
2018 O-GlcNAc-modified SNAP29 inhibits autophagy-mediated degradation via the disturbed SNAP29-STX17-VAMP8 complex and exacerbates myocardial injury in type I diabetic rats. International journal of molecular medicine 41 30221662
2013 Evolutionarily conserved role and physiological relevance of a STX17/Syx17 (syntaxin 17)-containing SNARE complex in autophagosome fusion with endosomes and lysosomes. Autophagy 40 24113031
2012 Copy number expansion of the STX17 duplication in melanoma tissue from Grey horses. BMC genomics 38 22857264
2017 Accumulation of undegraded autophagosomes by expression of dominant-negative STX17 (syntaxin 17) mutants. Autophagy 35 28598244
2021 Long non-coding RNA Xist regulates oocyte loss via suppressing miR-23b-3p/miR-29a-3p maturation and upregulating STX17 in perinatal mouse ovaries. Cell death & disease 27 34035229
2024 Human YKT6 forms priming complex with STX17 and SNAP29 to facilitate autophagosome-lysosome fusion. Cell reports 26 38340317
2019 BAP31 Inhibits Cell Adaptation to ER Stress Conditions, Negatively Regulating Autophagy Induction by Interaction with STX17. Cells 23 31671609
2023 Porcine Reproductive and Respiratory Syndrome Virus nsp5 Induces Incomplete Autophagy by Impairing the Interaction of STX17 and SNAP29. Microbiology spectrum 21 36815765
2020 Circular RNA circ_0000034 upregulates STX17 level to promote human retinoblastoma development via inhibiting miR-361-3p. European review for medical and pharmacological sciences 20 33336726
2023 RUNDC1 inhibits autolysosome formation and survival of zebrafish via clasping ATG14-STX17-SNAP29 complex. Cell death and differentiation 19 37684417
2023 S670, an amide derivative of 3-O-acetyl-11-keto-β-boswellic acid, induces ferroptosis in human glioblastoma cells by generating ROS and inhibiting STX17-mediated fusion of autophagosome and lysosome. Acta pharmacologica Sinica 15 37749236
2024 PtdIns4P is required for the autophagosomal recruitment of STX17 (syntaxin 17) to promote lysosomal fusion. Autophagy 14 38411137
2020 The Long Noncoding RNA LOC441461 (STX17-AS1) Modulates Colorectal Cancer Cell Growth and Motility. Cancers 14 33126743
2023 ULK phosphorylation of STX17 controls autophagosome maturation via FLNA. The Journal of cell biology 13 37389864
2020 Hyperoxia reduces STX17 expression and inhibits the autophagic flux in alveolar type II epithelial cells in newborn rats. International journal of molecular medicine 12 32467992
2020 Long non-coding RNA XIST confers aggressive progression via miR-361-3p/STX17 in retinoblastoma cells. European review for medical and pharmacological sciences 12 33155266
2023 Inhibition of STX17-SNAP29-VAMP8 complex formation by costunolide sensitizes ovarian cancer cells to cisplatin via the AMPK/mTOR signaling pathway. Biochemical pharmacology 11 37060961
2021 Acinetobacter baumannii up-regulates LncRNA-GAS5 and promotes the degradation of STX17 by blocking the activation of YY1. Virulence 10 34304694
2025 STX17-DT facilitates axitinib resistance in renal cell carcinoma by inhibiting mitochondrial ROS accumulation and ferroptosis. Cell death & disease 9 39988631
2021 The equine graying with age mutation of the STX17 gene: A copy number study using droplet digital PCR reveals a new pattern. Animal genetics 8 33550611
2024 SLC34A2 promotes cell proliferation by activating STX17-mediated autophagy in esophageal squamous cell carcinoma. Thoracic cancer 6 38720472
2024 BMAL1 upregulates STX17 levels to promote autophagosome-lysosome fusion in hippocampal neurons to ameliorate Alzheimer's disease. iScience 5 39687016
2024 Exacerbation of atherosclerosis by STX17 knockdown: Unravelling the role of autophagy and inflammation. Journal of cellular and molecular medicine 4 39008328
2025 Edaravone dexborneol attenuates cerebral Ischemia-Reperfusion injury via cGAS-STING inhibition, STX17-Mediated autophagic flux restoration, and NLRP3 inflammasome suppression. European journal of pharmacology 3 41202962
2023 Epithelial Cell NOD1/IRGM Recruits STX17 to Neisseria gonorrhoeae-Containing Endosomes to Initiate Lysosomal Degradation. The Journal of infectious diseases 2 37926090
2025 LRRK2 G2019S mutation contributes to mitochondrial transfer dysfunction in a Drp1-STX17-dependent manner. Translational neurodegeneration 1 41354840
2026 Acetylation of STX17 promotes its autophagosomal translocation. Nature communications 0 42062288
2026 Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17. Frontiers in pharmacology 0 42131811
2025 Corrigendum to "STING guides the STX17-SNAP29-VAMP8 complex assembly to control autophagy" [Cell Insight 3 (2024) 100147]. Cell insight 0 40256202
2024 RETRACTED: Clinical study on the role of LncRNA STX17-AS1 in wound healing and hypertrophic scar formation. International wound journal 0 42052922
2022 STX17: an ancient SNARE protein whose roles have not been conserved. Autophagy reports 0 40396044

Missed literature

Know a paper Affinage missed for STX17? Flag it for the maintainers and the community.

No submissions yet.