Affinage

SCFD1

Sec1 family domain-containing protein 1 · UniProt Q8WVM8

Length
642 aa
Mass
72.4 kDa
Annotated
2026-04-28
43 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SCFD1 (Sly1) is a Sec1/Munc18-family SNARE chaperone that orchestrates membrane fusion at multiple stations of the endomembrane system, including ER-to-Golgi, intra-Golgi, and autophagosome–lysosome fusion. It binds the conserved N-terminal peptide motif of syntaxins 5 and 18, loosens their closed conformation to permit productive trans-SNARE complex assembly, and additionally tethers incoming vesicles at close range via an ALPS-like helix that senses high membrane curvature, thereby coupling vesicle docking to SNAREpin nucleation (PMID:11879635, PMID:25189771, PMID:38478018, PMID:38478017). SCFD1 bridges tethering and fusion machinery by interacting with the COG complex subunit Cog4 for intra-Golgi transport and with TANGO1 at ER exit sites for export of bulky ECM cargoes such as procollagens via a specific SCFD1–syntaxin 18 pathway (PMID:19536132, PMID:24842878, PMID:27851892). In autophagy, SCFD1 localizes to autolysosomes where it is required for STX17–SNAP29–VAMP8 SNARE complex formation; this function is positively regulated by mTORC1-controlled dephosphorylation of VAMP8 and by AMPK-dependent suppression of KAT2B-mediated acetylation of SCFD1 at K126/K515 (PMID:34785650, PMID:35465820).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1996 High

    Identifying SCFD1 as a syntaxin 5 partner established that a Sec1/Munc18-family protein operates in the early secretory pathway and positively regulates ER-to-Golgi transport.

    Evidence Co-immunoprecipitation from rat liver membranes and overexpression rescue of dominant-negative syntaxin 5

    PMID:8647468 PMID:8663406

    Open questions at the time
    • Mechanism of positive regulation unknown
    • Whether Sly1 acts on syntaxin 5 conformation or SNARE complex assembly not resolved
  2. 2002 High

    Discovery that Sly1 binds a short N-terminal peptide motif of syntaxins 5 and 18, and that this binding promotes assembly of cognate SNARE complexes while suppressing non-cognate pairings, defined the dual role of SM proteins as catalysts and specificity factors for SNARE-mediated fusion.

    Evidence Biochemical pulldowns and in vitro SNARE complex reconstitution with purified proteins and truncation/temperature-sensitive mutants in yeast and mammalian systems

    PMID:11879635 PMID:11994317 PMID:12186954

    Open questions at the time
    • Whether Sly1 also engages the closed conformation of its syntaxin was unresolved
    • The mechanism coupling Rab GTPase signaling to Sly1 activation was unknown
  3. 2007 Medium

    Mapping gain-of-function SLY1-20 mutations to a single regulatory α-helix (α-20) revealed a built-in autoinhibitory element that gates Rab/Ypt-controlled activation of Sly1.

    Evidence Site-directed mutagenesis and yeast genetic suppressor analysis across fungal and mammalian homologues

    PMID:18036347

    Open questions at the time
    • How the α-20 helix senses Rab status mechanistically was unknown
    • No structural model of the autoinhibited state existed
  4. 2009 High

    Demonstrating that the COG tethering complex subunit Cog4 binds Sly1 directly provided the first physical link between a vesicle-tethering complex and SM-protein-driven SNARE assembly for intra-Golgi transport.

    Evidence GST pulldown with purified proteins, co-immunoprecipitation, and siRNA knockdown with retrograde transport assays in mammalian cells

    PMID:19536132

    Open questions at the time
    • Whether Cog4 allosterically activates Sly1 or simply recruits it was not determined
    • Structural basis of Cog4–Sly1 interaction unknown
  5. 2014 High

    Two advances resolved how Sly1 handles syntaxin conformation and cargo specificity: quantitative binding assays showed Sly1 simultaneously engages both the N-peptide and the closed conformation of Sed5, loosening rather than locking it; and siRNA studies identified a specific SCFD1–TANGO1–syntaxin 18 pathway required for ER export of bulky procollagens.

    Evidence Fluorescence anisotropy and analytical ultracentrifugation with purified proteins; siRNA knockdown of SLY1 and STX18 with procollagen VII retention and COPII/retrograde transport controls

    PMID:24842878 PMID:25189771

    Open questions at the time
    • Whether syntaxin 18 vs. syntaxin 5 engagement involves distinct Sly1 conformations was unresolved
    • Whether TANGO1 directly recruits Sly1 or acts through syntaxin 18 was unclear
  6. 2016 High

    In vivo genetic loss of scfd1 in zebrafish demonstrated that the SCFD1–STX18 pathway is essential for ECM protein secretion during vertebrate chondrogenesis and that its disruption triggers the unfolded protein response.

    Evidence Zebrafish forward genetic screen, CRISPR knockdown, collagen trafficking immunofluorescence, and UPR reporter assays conserved in mammalian chondrocytes

    PMID:27851892

    Open questions at the time
    • Whether SCFD1 loss causes UPR as a secondary consequence of cargo retention or has a direct role in ER homeostasis was not distinguished
  7. 2021 High

    Establishing that SCFD1 is recruited to autolysosomes to promote STX17–SNAP29–VAMP8 SNARE complex formation extended SCFD1 function beyond the secretory pathway to autophagy, and showed this step is negatively regulated by mTORC1 phosphorylation of VAMP8.

    Evidence In vitro autophagosome–lysosome fusion reconstitution, siRNA knockdown, phosphomimetic mutants, live-cell imaging, and mouse hepatocyte lipid droplet assays

    PMID:34785650

    Open questions at the time
    • How SCFD1 is physically recruited to the autolysosomal membrane was not fully defined
    • Whether other SM proteins can substitute for SCFD1 in autophagy was untested
  8. 2022 High

    Identification of KAT2B-mediated acetylation at K126/K515 and SIRT4-mediated deacetylation of SCFD1, with AMPK phosphorylation suppressing acetylation, revealed a nutrient-sensing post-translational code that tunes SCFD1 activity in autophagy.

    Evidence Mass spectrometry, acetylation-site mutagenesis, co-immunoprecipitation with KAT2B/SIRT4, SNARE complex pull-down, autophagic flux assays

    PMID:35465820

    Open questions at the time
    • Structural mechanism by which acetylation blocks SNARE complex formation unknown
    • Whether acetylation also regulates SCFD1 function in the secretory pathway was not tested
  9. 2023 High

    Genetic null studies in zebrafish and Drosophila knockdown extended the physiological requirement for SCFD1/Slh to cardiac development and neuromuscular function, with loss causing ER stress, Golgi fragmentation, and motor deficits.

    Evidence CRISPR null zebrafish with cardiomyocyte ultrastructure and echocardiography; Drosophila RNAi with behavioral and NMJ phenotyping; RNA-seq

    PMID:36944290 PMID:37887855

    Open questions at the time
    • Whether cardiac and neuronal phenotypes reflect general secretory pathway failure or tissue-specific SCFD1 functions is not resolved
    • No mammalian knockout model reported
  10. 2024 High

    Chemically defined reconstitution revealed that Sly1 promotes fusion through three parallel mechanisms — opening the syntaxin closed conformation, close-range vesicle tethering via an ALPS-like helix, and trans-SNARE complex nucleation — and that the Habc domain of syntaxin is required for Sly1-dependent lipid mixing.

    Evidence Chemically defined in vitro ER–Golgi fusion, high-curvature liposome binding, split-Sed5 reconstitution in vitro and in vivo, genetic epistasis with tethering-loop mutants

    PMID:38478017 PMID:38478018

    Open questions at the time
    • Whether the ALPS-like tethering function operates similarly at autolysosomes is untested
    • Structural visualization of Sly1 bound simultaneously to membrane and SNARE complex is lacking
  11. 2024 High

    The finding that the intracellular pathogen Anaplasma phagocytophilum hijacks SCFD1 via its T4SS effector EgeA to redirect the TANGO1–SCFD1 complex from ERES to pathogen inclusions revealed an unexpected host–pathogen interface exploiting SCFD1-dependent trafficking.

    Evidence Yeast two-hybrid and pulldown confirming direct EgeA–SCFD1 binding; siRNA knockdown reducing infection; immunofluorescence of SCFD1 redistribution

    PMID:39106308

    Open questions at the time
    • Whether EgeA mimics the TANGO1 binding interface on SCFD1 is unknown
    • In vivo relevance in animal infection models not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of the ALPS-like tethering loop interacting with both curved membranes and SNAREs, whether the autophagy and secretory functions of SCFD1 are regulated by distinct or overlapping post-translational codes, and whether mammalian knockout phenotypes recapitulate the cardiac and skeletal defects seen in zebrafish.
  • No mammalian genetic knockout model reported
  • No high-resolution structure of full-length mammalian SCFD1 in complex with its SNARE and membrane
  • Whether acetylation/phosphorylation codes regulate SCFD1 in the secretory pathway is untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 6 GO:0060090 molecular adaptor activity 2 GO:0008289 lipid binding 1
Localization
GO:0005794 Golgi apparatus 4 GO:0005783 endoplasmic reticulum 3 GO:0031410 cytoplasmic vesicle 2 GO:0005764 lysosome 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 7 R-HSA-1474244 Extracellular matrix organization 2 R-HSA-9609507 Protein localization 2 R-HSA-9612973 Autophagy 2
Partners
COG4KAT2BSNAP29STX17STX18STX5TANGO1VAMP8
Complex memberships
SNARE complex (STX17-SNAP29-VAMP8)SNARE complex (STX5-containing)TANGO1-SCFD1 ERES complex

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 Mammalian Sly1 (SCFD1) forms a native complex with syntaxin 5 on ER-Golgi membranes, and overexpression of rat Sly1 neutralizes the dominant-negative effects of excess syntaxin 5 on ER-to-Golgi transport, establishing that Sly1 positively regulates syntaxin 5 function in the early secretory pathway. Co-immunoprecipitation from rat liver membranes; transient overexpression rescue assay The Journal of biological chemistry High 8663406
1996 Rat Sly1 (SCFD1/RA410) is a member of the Sec1/Munc18 family and is expressed ubiquitously in all rat tissues examined, consistent with a general role in vesicular transport. cDNA cloning, sequence analysis, Northern blotting Gene Medium 8647468
1997 RA410 (rat Sly1/SCFD1) protein localizes predominantly to the plasma membrane fraction and to large vesicles associated with the Golgi (but not in the Golgi itself) by sucrose gradient fractionation and immunoelectron microscopy, consistent with a role in post-Golgi vesicular transport; it is also induced as an immediate-early gene in astrocytes upon reoxygenation. Sucrose gradient fractionation, immunoelectron microscopy, Western blotting The Journal of biological chemistry Medium 9195952
2002 Sly1 binds to a short, evolutionarily conserved N-terminal peptide motif of syntaxins 5 and 18 (vertebrates) and their yeast orthologues Sed5p and Ufe1p, a binding mode distinct from the closed-conformation interaction of Munc18 with syntaxin 1, suggesting a general peptide-based SM–syntaxin interaction mechanism. Biochemical pulldown with purified proteins; sequence analysis; binding assays with truncation mutants Developmental cell High 11879635
2002 Sly1p bound to the Golgi syntaxin Sed5p permits assembly of ER-to-Golgi SNARE fusion complexes (Sed5p-Bos1p-Sec22p-Bet1p) in vitro; Sly1p also joins preassembled SNARE complexes and is present in SNARE complexes immunoprecipitated from yeast lysates. Crucially, Sly1p-bound Sed5p suppresses formation of non-physiological SNARE complexes, demonstrating that the SM protein contributes to SNARE pairing specificity. In vitro SNARE complex assembly with purified proteins; co-immunoprecipitation from yeast lysates The Journal of cell biology High 11994317
2002 In yeast, Sly1p binding to Sed5p enhances formation of the trans-SNARE complex (Sed5p–Bet1p) in vitro in yeast lysates; a temperature-sensitive Sly1p mutant with reduced Sed5p binding shows reduced complex formation, and recombinant Sly1p added back rescues complex assembly. Co-immunoprecipitation; in vitro SNARE complex formation in yeast lysates; temperature-sensitive mutant analysis Journal of cell science High 12186954
2003 Sly1p cooperates with Sec18/NSF in disassembly of cis-SNARE complexes: a Sly1p temperature-sensitive mutant defective in Sed5p binding shows retarded cis-SNARE complex disassembly, and sec18-1/sly1-ts double mutants are synthetically lethal, placing Sly1 upstream of NSF-mediated SNARE recycling. Temperature-sensitive mutant analysis; synthetic lethality genetic epistasis; in vitro SNARE disassembly assay Bioscience, biotechnology, and biochemistry Medium 12729020
2005 In yeast, the Sly1-20 gain-of-function allele bypasses GTPase requirements for ER-Golgi vesicle tethering by allowing an alternative Rab (Ypt6) to substitute for Ypt1p; Uso1p-dependent vesicle tethering is not bypassed, establishing that Sly1-20 does not circumvent the requirement for tethering per se but shifts Rab dependency. Co-immunoprecipitation; in vitro tethering and fusion assays with ypt1Δ/SLY1-20 membranes; Rab GDP dissociation inhibitor sensitivity assay Molecular biology of the cell High 15689495
2005 RA410/Sly1 (SCFD1) protects dopaminergic SH-SY5Y cells from MPP+- and 6-OHDA-induced cell death; antisense knockdown accelerates ER disruption and increases caspase-2, -3, and -9 activation, while sense overexpression suppresses caspase activation, indicating a cytoprotective role linked to ER integrity. Antisense/sense RNA stable transfection; electron microscopy of ER morphology; caspase activity assays; cell viability assay Neurobiology of disease Medium 15649705
2007 All gain-of-function SLY1-20-type mutations in yeast Sly1p that bypass Ypt/Rab GTPase requirements map to or cause deletion of a conserved short α-helix (α-20); deletion of α-20 alone is sufficient for GTPase bypass, identifying this helix as a regulatory element mediating Ypt/Rab-controlled Sly1 function in membrane fusion. Site-directed mutagenesis; yeast genetic suppressor analysis; complementation assays with fungal and mammalian Sly1 homologues FEBS letters Medium 18036347
2009 The SM protein Sly1 interacts directly with the COG tethering complex via the Cog4 subunit; Cog4 binds Syntaxin 5 through a different site. Disruption of the Cog4–Sly1 interaction impairs SNARE pairing for intra-Golgi transport and markedly attenuates Golgi-to-ER retrograde transport, linking tethering to SNAREpin assembly. Co-immunoprecipitation; GST pulldown with purified proteins; siRNA knockdown with retrograde transport assays The EMBO journal High 19536132
2014 Sly1 binds both the closed conformation and the N-peptide of Sed5 simultaneously (in contrast to Munc18, which only engages the closed conformation of syntaxin 1); unlike Munc18, Sly1 facilitates SNARE complex formation by loosening the closed conformation of Sed5 rather than locking it. Fluorescence anisotropy binding assays; analytical ultracentrifugation; in vitro SNARE complex assembly kinetics with purified proteins Proceedings of the National Academy of Sciences of the United States of America High 25189771
2014 SLY1 (SCFD1) interacts with the cytoplasmic domain of TANGO1 at ER exit sites and is required specifically for procollagen VII export from the ER; siRNA knockdown of SLY1 arrests procollagen VII in the ER without affecting COPII recruitment, general secretion, or retrograde KDEL-receptor transport. Of the two ER SNAREs that interact with SLY1 (syntaxins 17 and 18), only syntaxin 18 is required for this cargo. siRNA knockdown; co-immunoprecipitation; fluorescence microscopy of ER cargo retention; COPII/retrograde transport controls eLife High 24842878
2016 Loss of Scfd1 in zebrafish impairs ER-to-Golgi transport of ECM proteins (type II collagen) in chondrocytes and activates the unfolded protein response; knockdown of either SCFD1 or its partner STX18 in mammalian chondrocytes severely impairs type II collagen transport, establishing a conserved SCFD1–STX18 pathway for secretion of large ECM proteins during chondrogenesis. Zebrafish forward genetic screen; morpholino/CRISPR knockdown; immunofluorescence of collagen trafficking; UPR reporter assays; mammalian chondrocyte siRNA knockdown Developmental biology High 27851892
2021 mTORC1 inhibits autophagosome–lysosome fusion by phosphorylating VAMP8, which blocks SCFD1 recruitment to autolysosomes; dephosphorylated VAMP8 promotes SCFD1 localization to autolysosomes where SCFD1 is required for STX17–SNAP29–VAMP8 SNARE complex formation and autophagosome–lysosome fusion. A phosphomimetic VAMP8 mutant fails to support fusion in vitro and causes lipid droplet accumulation in mouse liver. In vitro autophagosome–lysosome fusion assay; siRNA knockdown; phosphomimetic/phosphoresistant mutant overexpression; live-cell imaging of SCFD1 localization; hepatocyte lipid droplet assay in vivo Nature communications High 34785650
2022 SCFD1 is acetylated at K126 and K515 by the acetyltransferase KAT2B/PCAF, and deacetylated by SIRT4; acetylation of these residues inhibits autophagic flux by blocking STX17–SNAP29–VAMP8 SNARE complex formation. AMPK-mediated phosphorylation of SCFD1 disrupts its interaction with KAT2B, keeping acetylation levels low under autophagy-stimulating conditions. Mass spectrometry identification of acetylation sites; co-immunoprecipitation of SCFD1 with KAT2B and SIRT4; acetylation-site mutagenesis; SNARE complex pull-down; autophagic flux assays Autophagy High 35465820
2023 Loss of scfd1 in zebrafish causes severe cardiac defects (reduced myofibril density, dilated cardiomyopathy) and craniofacial abnormalities accompanied by ER stress (upregulation of UPR and apoptosis markers) and Golgi fragmentation in cardiomyocytes, establishing that scfd1 is required for ER/Golgi membrane trafficking in cardiac development. CRISPR/Cas9 null mutant generation; electron microscopy of cardiomyocyte ultrastructure; qPCR for ER stress markers; echocardiography of adult heterozygotes Journal of cardiovascular development and disease High 37887855
2023 Moderate knockdown of Slh (Drosophila orthologue of SCFD1) in adult flies causes climbing and flight defects; severe knockdown causes larval immobility, neuromuscular junction deficits, and lethality before metamorphosis; RNA-seq reveals downregulation of chaperone genes mediating protein folding downstream of Slh ablation. RNAi-mediated knockdown; climbing/flight behavioral assays; NMJ morphology analysis; RNA-seq transcriptomics Neurobiology of aging Medium 36944290
2024 Sly1 contains an amphipathic lipid-packing sensor (ALPS)-like helix within its regulatory loop that directly binds high-curvature membranes; this binding both relieves autoinhibition of Sly1 and enables Sly1 to tether incoming vesicles to the Qa-SNARE on the target organelle at close range. The SLY1-20 gain-of-function mutation loses its bypass activity when tethering is additionally impaired, placing close-range tethering as an essential step before trans-SNARE assembly. Chemically defined in vitro ER-Golgi fusion reconstitution; membrane-binding assays with high-curvature liposomes; genetic epistasis (SLY1-20 combined with tethering loop mutations); SNARE mutant analysis The Journal of cell biology High 38478018
2024 Sly1 promotes fusion through three parallel mechanisms: (i) opening the closed conformation of Sed5 (Qa-SNARE), (ii) close-range vesicle tethering via its regulatory loop, and (iii) nucleation of productive trans-SNARE complexes. The autoinhibitory Habc domain of Sed5 additionally promotes Sly1-dependent fusion by facilitating events leading to lipid mixing and is required for correct Sed5 localization. Chemically defined in vitro fusion assays with SNARE and Sly1 mutants; 'split Sed5' reconstitution in vitro and in vivo; lipid mixing assays The Journal of cell biology High 38478017
2024 The Anaplasma phagocytophilum T4SS effector EgeA directly binds SCFD1 (by yeast two-hybrid), and both TANGO1 and SCFD1 are redistributed from ER-Golgi exit sites to pathogen-occupied inclusions during infection; knockdown of either TANGO1 or SCFD1 significantly reduces Anaplasma infection, establishing that the pathogen hijacks the TANGO1–SCFD1 ERES complex to acquire nutrients and reduce ER stress. Yeast two-hybrid (EgeA-C / SCFD1 direct binding); pulldown assay (EgeA-GFP / TANGO1); siRNA knockdown of TANGO1 and SCFD1; immunofluorescence localization to inclusion surface; ER stress marker qPCR Proceedings of the National Academy of Sciences of the United States of America High 39106308

Source papers

Stage 0 corpus · 43 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Sly1 binds to Golgi and ER syntaxins via a conserved N-terminal peptide motif. Developmental cell 166 11879635
2002 Sly1 protein bound to Golgi syntaxin Sed5p allows assembly and contributes to specificity of SNARE fusion complexes. The Journal of cell biology 125 11994317
2009 Direct interaction between the COG complex and the SM protein, Sly1, is required for Golgi SNARE pairing. The EMBO journal 83 19536132
1999 SlY1, the first active gene cloned from a plant Y chromosome, encodes a WD-repeat protein. The EMBO journal 83 10428956
1996 Mammalian Sly1 regulates syntaxin 5 function in endoplasmic reticulum to Golgi transport. The Journal of biological chemistry 76 8663406
2014 SLY1 and Syntaxin 18 specify a distinct pathway for procollagen VII export from the endoplasmic reticulum. eLife 70 24842878
2021 mTOR-mediated phosphorylation of VAMP8 and SCFD1 regulates autophagosome maturation. Nature communications 58 34785650
2015 E3 SUMO ligase AtSIZ1 positively regulates SLY1-mediated GA signalling and plant development. The Biochemical journal 52 26008766
2003 Positional cloning of a temperature-sensitive mutant emmental reveals a role for sly1 during cell proliferation in zebrafish fin regeneration. Developmental biology 49 12798289
2022 Acetylation of SCFD1 regulates SNARE complex formation and autophagosome-lysosome fusion. Autophagy 39 35465820
2016 The Sec domain protein Scfd1 facilitates trafficking of ECM components during chondrogenesis. Developmental biology 35 27851892
2014 The SM protein Sly1 accelerates assembly of the ER-Golgi SNARE complex. Proceedings of the National Academy of Sciences of the United States of America 33 25189771
2002 Binding of Sly1 to Sed5 enhances formation of the yeast early Golgi SNARE complex. Journal of cell science 29 12186954
2005 Impaired immune responses and prolonged allograft survival in Sly1 mutant mice. Molecular and cellular biology 28 16227612
2014 The roles of the GA receptors GID1a, GID1b, and GID1c in sly1-independent GA signaling. Plant signaling & behavior 23 24521922
1997 Cloning of a putative vesicle transport-related protein, RA410, from cultured rat astrocytes and its expression in ischemic rat brain. The Journal of biological chemistry 22 9195952
2005 A Rab requirement is not bypassed in SLY1-20 suppression. Molecular biology of the cell 21 15689495
2021 SCFD1 expression quantitative trait loci in amyotrophic lateral sclerosis are differentially expressed. Brain communications 19 34708205
2005 RA410/Sly1 suppresses MPP+ and 6-hydroxydopamine-induced cell death in SH-SY5Y cells. Neurobiology of disease 19 15649705
2001 Multicopy suppressors of the sly1 temperature-sensitive mutation in the ER-Golgi vesicular transport in Saccharomyces cerevisiae. Yeast (Chichester, England) 19 11481671
2015 SLy1 regulates T-cell proliferation during Listeria monocytogenes infection in a Foxo1-dependent manner. European journal of immunology 18 26306874
2009 The orphan adapter protein SLY1 as a novel anti-apoptotic protein required for thymocyte development. BMC immunology 15 19604361
2008 Reduced notch activity is associated with an impaired marginal zone B cell development and function in Sly1 mutant mice. Molecular immunology 15 18950867
2019 Structure of the SLy1 SAM homodimer reveals a new interface for SAM domain self-association. Scientific reports 14 30631134
2019 Does SCFD1 rs10139154 Polymorphism Decrease Alzheimer's Disease Risk? Journal of molecular neuroscience : MN 14 31267315
2023 Loss of amyotrophic lateral sclerosis risk factor SCFD1 causes motor dysfunction in Drosophila. Neurobiology of aging 12 36944290
2017 Transcriptional mechanisms associated with seed dormancy and dormancy loss in the gibberellin-insensitive sly1-2 mutant of Arabidopsis thaliana. PloS one 11 28628628
2023 Loss of Sec-1 Family Domain-Containing 1 (scfd1) Causes Severe Cardiac Defects and Endoplasmic Reticulum Stress in Zebrafish. Journal of cardiovascular development and disease 9 37887855
2016 Deficiency of the adaptor protein SLy1 results in a natural killer cell ribosomopathy affecting tumor clearance. Oncoimmunology 9 28123874
2017 An association study between SCFD1 rs10139154 variant and amyotrophic lateral sclerosis in a Chinese cohort. Amyotrophic lateral sclerosis & frontotemporal degeneration 6 29260601
2007 Mutations of the SM protein Sly1 resulting in bypass of GTPase requirement in vesicular transport are confined to a short helical region. FEBS letters 6 18036347
2003 Cooperation of Sly1/SM-family protein and sec18/NSF of Saccharomyces cerevisiae in disassembly of cis-SNARE membrane-protein complexes. Bioscience, biotechnology, and biochemistry 6 12729020
2024 Anaplasma phagocytophilum effector EgeA facilitates infection by hijacking TANGO1 and SCFD1 from ER-Golgi exit sites to pathogen-occupied inclusions. Proceedings of the National Academy of Sciences of the United States of America 5 39106308
1996 A mammalian homologue of SLY1, a yeast gene required for transport from endoplasmic reticulum to Golgi. Gene 5 8647468
2025 Reenacting a mouse genetic evolutionary arms race in yeast reveals that SLXL1/SLX compete with SLY1/2 for binding to Spindlins. Proceedings of the National Academy of Sciences of the United States of America 4 39928872
2024 SNARE chaperone Sly1 directly mediates close-range vesicle tethering. The Journal of cell biology 4 38478018
2022 Lack of an association between SCFD1 rs10139154 polymorphism and amyotrophic lateral sclerosis. Molecular medicine reports 4 35234271
2024 Arabidopsis retromer subunit AtVPS29 is involved in SLY1-mediated gibberellin signaling. Plant cell reports 3 38315261
2024 SM protein Sly1 and a SNARE Habc domain promote membrane fusion through multiple mechanisms. The Journal of cell biology 1 38478017
2026 MsDUF3700 regulates plant growth via SLY1-mediated DELLA degradation in alfalfa and Arabidopsis. Plant physiology and biochemistry : PPB 0 41775168
2026 Structure-guided optimization of SLY1 expression and purification in Escherichia coli. Protein science : a publication of the Protein Society 0 42010839
2024 Reenacting a mouse genetic evolutionary arms race in yeast reveals SLXL1/SLX compete with SLY1/2 for binding to Spindlins. bioRxiv : the preprint server for biology 0 39484540
2022 Knockout of SLy1 decreases double-negative thymocyte proliferation and protects mice from p53-induced tumor formation. European journal of immunology 0 36401605