Affinage

Showing SCFD1 — SLY1 is a alias.

SCFD1

Sec1 family domain-containing protein 1 · UniProt Q8WVM8

Length
642 aa
Mass
72.4 kDa
Annotated
2026-06-10
40 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SCFD1 (Sly1/RA410) is a Sec1/Munc18-family SM protein that orchestrates SNARE-mediated membrane fusion in the early secretory pathway and in autophagy (PMID:8663406, PMID:11879635). Unlike Munc18's closed-conformation clamp on syntaxin 1, SCFD1 engages ER/Golgi Qa-SNAREs (Syntaxin 5, Syntaxin 18, yeast Sed5 and Ufe1) through a short conserved N-terminal peptide motif while also binding the closed conformation, an interaction that loosens the closed state and licenses SNARE assembly (PMID:11879635, PMID:25189771). Through this engagement it confers specificity on SNARE pairing by supporting cognate complex formation while preventing non-physiological complexes, and it enhances productive trans-SNARE assembly (PMID:11994317, PMID:12186954). Mechanistic reconstitution resolves three parallel contributions to ER-Golgi fusion: opening the Qa-SNARE, nucleating trans-SNARE complexes, and close-range vesicle tethering via an ALPS-like amphipathic helix in a regulatory loop that binds high-curvature membranes and relieves SCFD1 autoinhibition, downstream of Rab-dependent long-range tethering (PMID:38478018, PMID:38478017, PMID:15689495). SCFD1 couples tethering to fusion by directly binding the Cog4 subunit of the COG complex, an interaction required for intra-Golgi SNARE pairing and Golgi-to-ER retrograde transport (PMID:19536132). In vivo, a SCFD1–Syntaxin 18 pathway is specifically required for ER export of bulky cargo such as procollagen VII and type II collagen, and its loss causes chondrogenesis, craniofacial, and cardiac defects with ER stress in zebrafish (PMID:24842878, PMID:27851892, PMID:37887855). Independently, SCFD1 localizes to autolysosomes where it is required for STX17–SNAP29–VAMP8 SNARE complex assembly and autophagosome–lysosome fusion; this autophagic function is gated by mTORC1 phosphorylation of VAMP8 (controlling SCFD1 recruitment) and by KAT2B/SIRT4-mediated acetylation of SCFD1 at K126/K515, itself disrupted by AMPK phosphorylation of SCFD1 (PMID:34785650, PMID:35465820).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1996 Medium

    Established that mammalian SCFD1 is a positive regulator of syntaxin 5-dependent ER-to-Golgi transport, placing the SM protein in the early secretory pathway.

    Evidence Native complex co-purification with syntaxin 5 from rat liver membranes and dominant-negative rescue in cells

    PMID:8663406

    Open questions at the time
    • Binding mode to syntaxin 5 not defined
    • No reconstitution of the fusion step
  2. 1997 Medium

    Identified SCFD1 as a Sec1/Unc18-family protein and localized it to vesicles associated with the Golgi, framing it as a vesicle transport factor.

    Evidence Subcellular fractionation and immunoelectron microscopy with peptide antibody

    PMID:9195952

    Open questions at the time
    • Localization without functional mutagenesis
    • Plasma membrane fraction signal unexplained mechanistically
  3. 2002 High

    Defined the distinctive binding mode of SCFD1: it recognizes a conserved N-terminal peptide motif of ER/Golgi syntaxins, mechanistically separating it from Munc18 closed-syntaxin binding, and showed it supports SNARE pairing specificity.

    Evidence In vitro binding and domain mapping with purified yeast and vertebrate syntaxins; in vitro SNARE assembly and co-IP

    PMID:11879635 PMID:11994317 PMID:12186954

    Open questions at the time
    • How peptide binding mechanistically promotes assembly not yet resolved
    • Role of the syntaxin closed conformation not addressed
  4. 2003 Medium

    Connected SCFD1's syntaxin binding to upstream SNARE recycling and to an essential organismal proliferation requirement, broadening its functional importance.

    Evidence Yeast genetic epistasis with sec18/NSF plus disassembly assays; zebrafish temperature-sensitive mutant with proliferation phenotype

    PMID:12729020 PMID:12798289

    Open questions at the time
    • Mechanistic link between Sed5 binding and cis-SNARE disassembly not defined
    • Whether fin regeneration defect is cell-autonomous secretory failure unclear
  5. 2005 Medium

    Showed SCFD1's fusion function operates downstream of, and still depends on, Rab-mediated tethering, and linked it to ER integrity and cytoprotection.

    Evidence Cell-free tethering/fusion assays with Rab GDI sensitivity and genetic epistasis; gain/loss-of-function in neuronal cells with ER morphology and caspase readouts

    PMID:15649705 PMID:15689495

    Open questions at the time
    • Direct molecular handoff from Rab tethering to SCFD1 not shown
    • Cytoprotection mechanism downstream of ER integrity unresolved
  6. 2007 Medium

    Mapped the Rab-regulated function of SCFD1 to a short conserved alpha-helix (alpha-20), identifying the structural element that couples Rab signaling to fusion.

    Evidence Mutagenesis screen and domain deletion with genetic bypass phenotypes in yeast

    PMID:18036347

    Open questions at the time
    • Biochemical activity of alpha-20 not defined at this stage
    • Membrane interaction not yet demonstrated
  7. 2009 High

    Linked SCFD1 tethering to fusion mechanistically by demonstrating a direct interaction with the Cog4 subunit of the COG tethering complex required for intra-Golgi SNARE pairing and retrograde transport.

    Evidence Purified-protein pulldowns, co-IP, siRNA, and Golgi-to-ER retrograde transport assay

    PMID:19536132

    Open questions at the time
    • Structural basis of Cog4-SCFD1 interface not resolved
    • Whether COG binding competes with syntaxin engagement unknown
  8. 2014 High

    Resolved the mechanism of Qa-SNARE activation (dual N-peptide plus closed-conformation binding that loosens the closed state) and defined an in vivo SCFD1–Syntaxin 18 pathway dedicated to bulky collagen export.

    Evidence Fluorescence anisotropy and SNARE assembly kinetics with purified proteins; siRNA with cargo-specific pulse-chase secretion assays

    PMID:24842878 PMID:25189771

    Open questions at the time
    • Why bulky cargo selectively requires this pathway not fully explained
    • Structural model of loosened Sed5 absent
  9. 2016 High

    Established the conserved physiological consequence of the SCFD1–STX18 pathway in ECM secretion, showing chondrocyte collagen transport failure and UPR activation across species.

    Evidence Zebrafish mutagenesis and mammalian chondrocyte siRNA with ER-to-Golgi transport and UPR markers

    PMID:27851892

    Open questions at the time
    • Tissue specificity of cargo dependence not mechanistically resolved
  10. 2021 High

    Extended SCFD1 function beyond the secretory pathway to autophagy, showing it drives autophagosome-lysosome fusion via STX17-SNAP29-VAMP8 assembly under mTORC1 control of VAMP8 phosphorylation.

    Evidence mTORC1 kinase assay, phospho-site mutagenesis, in vitro fusion reconstitution, siRNA, imaging, mouse liver

    PMID:34785650

    Open questions at the time
    • How dephospho-VAMP8 recruits SCFD1 at the molecular level not detailed
    • Relationship to its secretory role at the same locus unclear
  11. 2022 High

    Defined an acetylation/phosphorylation regulatory code on SCFD1 itself that gates its autophagic SNARE-assembly activity.

    Evidence MS site mapping, KAT2B/SIRT4 writer/eraser manipulation, acetyl- and phospho-mimetic mutants, autophagic flux assays

    PMID:35465820

    Open questions at the time
    • Whether the same PTMs regulate secretory-pathway function untested
    • Structural impact of K126/K515 acetylation unknown
  12. 2024 High

    Provided the unified fusion mechanism: SCFD1 opens the Qa-SNARE, nucleates trans-SNARE complexes, and tethers vesicles at close range via an ALPS-like helix that senses curvature and relieves autoinhibition, completing a tethering-to-fusion handoff model.

    Evidence Chemically defined in vitro ER-Golgi fusion reconstitution with separation-of-function and ALPS-helix mutants, liposome binding, split-Sed5 complementation

    PMID:38478017 PMID:38478018

    Open questions at the time
    • Whether the ALPS-like tethering activity operates in the autophagic fusion context untested
    • Structural snapshot of the tethered intermediate absent
  13. 2024 Medium

    Showed SCFD1's ERES function is hijacked by a bacterial pathogen, identifying a direct effector interaction that redirects SCFD1 and TANGO1.

    Evidence Yeast two-hybrid, GFP-fusion localization, and siRNA infection assays with Anaplasma EgeA effector

    PMID:39106308

    Open questions at the time
    • Y2H interaction not validated by reciprocal pulldown in mammalian cells
    • Mechanism by which EgeA binding relocalizes SCFD1 unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SCFD1 is partitioned between its secretory (ER-Golgi/ERES) and autophagic (autolysosome) fusion roles, and whether its tethering and PTM-regulatory mechanisms are shared across both, remains unresolved.
  • No structural model of SCFD1 bound to closed Sed5/syntaxin
  • Spatial/temporal control switching SCFD1 between compartments unknown
  • No human disease mutation directly evaluated in the corpus

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 3 GO:0140096 catalytic activity, acting on a protein 3 GO:0008289 lipid binding 1
Localization
GO:0005783 endoplasmic reticulum 3 GO:0005794 Golgi apparatus 2 GO:0031410 cytoplasmic vesicle 2 GO:0005764 lysosome 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9609507 Protein localization 3 R-HSA-1474244 Extracellular matrix organization 2 R-HSA-9612973 Autophagy 2
Partners
COG4SED5STX18STX5TANGO1UFE1VAMP8
Complex memberships
ER-Golgi (Sed5/Syntaxin 5) SNARE complexSTX17-SNAP29-VAMP8 SNARE complex

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 Mammalian Sly1 (RA410/SCFD1) forms a native complex with syntaxin 5 in rat liver membranes, and overexpression of rSly1 neutralizes the dominant-negative effects of excess syntaxin 5 on ER-to-Golgi transport, establishing a positive regulatory role for SCFD1 in syntaxin 5-dependent early secretory pathway transport. Biochemical co-purification from rat liver membranes, dominant-negative rescue by transient overexpression in mammalian cells The Journal of biological chemistry Medium 8663406
1997 RA410 (SCFD1), cloned from reoxygenated rat astrocytes, encodes a Sec1/Unc18-family vesicle transport protein that localizes predominantly to the plasma membrane fraction and, by immunoelectron microscopy, to large vesicles associated with the Golgi apparatus (but not the Golgi itself), consistent with a role in post-Golgi transport. Subcellular fractionation on sucrose gradients, immunoelectron microscopy, polyclonal antibody against synthetic peptide The Journal of biological chemistry Medium 9195952
2002 Sly1 binds to a short, evolutionarily conserved N-terminal peptide motif of the syntaxins Sed5p and Ufe1p (yeast) and syntaxins 5 and 18 (vertebrates); this binding site is upstream of the autonomously folded N-terminal domain of these syntaxins, defining a distinct peptide-based interaction mode for this SM protein that differs from the closed-conformation binding of Munc18 to syntaxin 1. Biochemical binding assays with purified proteins, peptide competition, domain mapping Developmental cell High 11879635
2002 Sly1p can bind simultaneously to the ER-to-Golgi core SNARE fusion complex assembled on syntaxin Sed5p; Sly1p-bound Sed5p supports assembly of the cognate SNARE complex without significantly altering kinetics, but prevents formation of several non-physiological SNARE complexes, demonstrating that this SM protein contributes to the specificity of SNARE pairing. In vitro SNARE complex assembly with purified yeast proteins, co-immunoprecipitation from yeast lysates The Journal of cell biology High 11994317
2002 In yeast, Sly1 binding to the t-SNARE Sed5 enhances trans-SNARE complex formation with the v-SNARE Bet1; a temperature-sensitive sly1 mutant with reduced Sed5 binding shows reduced presence in the Sed5-Bet1 complex, directly linking Sly1-Sed5 interaction to productive SNARE complex assembly. Co-immunoprecipitation, in vitro SNARE complex formation with recombinant proteins added to yeast lysate Journal of cell science Medium 12186954
2003 In zebrafish, the orthologue of yeast sly1 (SCFD1) is required for blastema formation and cell proliferation during caudal fin regeneration; a temperature-sensitive point mutation in sly1 blocks regeneration by reducing proliferation in the proximal blastema, demonstrating an essential in vivo role for this SM protein in cell proliferation during tissue regeneration. Positional cloning of temperature-sensitive zebrafish mutant (emmental), histology, BrdU proliferation assay, molecular analysis Developmental biology Medium 12798289
2003 In yeast, the binding of Sly1 to the t-SNARE Sed5 cooperates with Sec18/NSF ATPase to promote disassembly of cis-SNARE complexes; a sly1(ts) mutant defective in Sed5 binding retards cis-SNARE disassembly, and the sly1(ts) and sec18-1 mutations show synthetic lethality. Genetic epistasis (synthetic lethality), temperature-sensitive yeast mutants, SNARE disassembly assay Bioscience, biotechnology, and biochemistry Medium 12729020
2005 The gain-of-function SLY1-20 allele in yeast does not bypass the requirement for vesicle tethering mediated by Uso1p; rather, an alternative Rab GTPase (Ypt6) substitutes for Ypt1p in tethering when SLY1-20 is expressed, and tethering/fusion remain sensitive to Rab GDI, indicating that SLY1-20 suppression still requires Rab-dependent tethering. Co-immunoprecipitation, cell-free tethering and fusion assays, Rab GDI sensitivity, genetic epistasis Molecular biology of the cell Medium 15689495
2005 RA410/Sly1 (SCFD1) overexpression in SH-SY5Y cells protects against MPP+- and 6-OHDA-induced cell death by suppressing caspase-2, -3, and -9 activation, and antisense knockdown of RA410/Sly1 accelerates ER disruption upon MPP+ treatment, demonstrating a cytoprotective role linked to ER integrity. Antisense and sense RNA stable transformants, cell viability assay, electron microscopy of ER morphology, caspase activation assays Neurobiology of disease Medium 15649705
2007 Gain-of-function mutations in the SM protein Sly1 that bypass Ypt/Rab GTPase requirements for ER-to-Golgi vesicular transport all map to a short conserved alpha-helix (α-20); deletion of this helix also causes bypass suppression, identifying α-20 as the domain mediating Rab-regulated Sly1 function in membrane fusion. Mutagenesis screen, genetic complementation, domain deletion analysis in yeast FEBS letters Medium 18036347
2009 The SM protein Sly1 (SCFD1) directly interacts with the Cog4 subunit of the conserved oligomeric Golgi (COG) tethering complex; Cog4 also independently interacts with Syntaxin 5 through a distinct binding site, and disruption of the Cog4-Sly1 interaction impairs SNARE pairing for intra-Golgi transport and markedly attenuates Golgi-to-ER retrograde transport. Co-immunoprecipitation, pulldown assays with purified proteins, siRNA knockdown, Golgi-to-ER retrograde transport assay The EMBO journal High 19536132
2014 The yeast SM protein Sly1 binds to both the N-peptide and the closed conformation of the Qa-SNARE Sed5, and this dual engagement facilitates SNARE complex formation by loosening the closed conformation of Sed5, in contrast to Munc18 which locks syntaxin 1 in a closed state incompatible with SNARE assembly. Biochemical binding assays with purified proteins, fluorescence anisotropy, in vitro SNARE complex formation kinetics Proceedings of the National Academy of Sciences of the United States of America High 25189771
2014 SLY1 (SCFD1) is required for ER export of Procollagen VII but not Procollagen I; knockdown of SLY1 arrests Procollagen VII in the ER without affecting COPII recruitment, general secretion, or retrograde transport; among SLY1-interacting SNAREs, only Syntaxin 18 (not Syntaxin 17) is specifically required for Procollagen VII export, defining a TANGO1-SLY1-Syntaxin 18 pathway for bulky collagen export. siRNA knockdown, pulse-chase secretion assays, immunofluorescence colocalization, rescue experiments eLife High 24842878
2016 Loss of scfd1 in zebrafish causes craniofacial defects due to failure of chondrogenesis; scfd1 mutation hinders ER-to-Golgi transport of ECM proteins and activates the unfolded protein response in chondrocytes; knockdown of either SCFD1 or STX18 (a SLY1-interacting t-SNARE) in mammalian chondrocytes severely impairs type II collagen transport, demonstrating a conserved SCFD1-STX18 pathway for large ECM protein secretion. Zebrafish forward mutagenesis screen, siRNA knockdown in mammalian chondrocytes, ER-to-Golgi transport assay, UPR activation markers Developmental biology High 27851892
2021 mTORC1 phosphorylates VAMP8 to block autophagosome-lysosome fusion; dephosphorylated VAMP8 promotes recruitment of SCFD1 to autolysosomes; SCFD1 localizes to the autolysosome and is required for formation of the STX17-SNAP29-VAMP8 SNARE complex and for autophagosome-lysosome fusion; VAMP8 phosphorylation mimic or SCFD1 depletion blocks this fusion in vitro. mTORC1 kinase assay, phosphorylation site mutagenesis, siRNA knockdown, in vitro fusion assay, live-cell imaging, immunofluorescence co-localization, mouse liver overexpression Nature communications High 34785650
2022 SCFD1 is acetylated at residues 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 SCFD1 interaction with KAT2B, keeping SCFD1 acetylation low during autophagy stimulation. Mass spectrometry identification of acetylation sites, acetyltransferase/deacetylase co-expression and knockdown, acetylation-mimetic and phospho-mimetic mutants, co-immunoprecipitation, autophagic flux assay Autophagy High 35465820
2023 Moderate silencing of Slh (Drosophila orthologue of SCFD1) causes climbing and flight motor defects in adult flies; severe knockdown causes larval mobility reduction, neuromuscular junction deficits, and lethality before metamorphosis; RNA-seq downstream of Slh ablation reveals downregulation of chaperone genes mediating protein folding. RNAi-mediated gene silencing in Drosophila, behavioral assays (climbing, flight), NMJ morphology analysis, RNA-seq transcriptomic profiling Neurobiology of aging Medium 36944290
2023 Loss of scfd1 in zebrafish (nonsense mutation or CRISPR knockout) causes severe cardiac and craniofacial defects with ER stress; electron microscopy of scfd1-depleted cardiomyocytes shows reduced myofibril width, sarcomere density reduction, and Golgi fragmentation; qPCR confirms upregulation of ER stress response and apoptosis markers, linking scfd1 to ER/Golgi membrane transport in cardiomyocytes. Positional cloning, CRISPR/Cas9 knockout, electron microscopy, qPCR for ER stress markers, cardiac phenotype analysis Journal of cardiovascular development and disease Medium 37887855
2024 Sly1 contains an ALPS (amphipathic lipid packing sensor)-like helix within a conserved regulatory loop that directly binds high-curvature membranes; this membrane binding both relieves Sly1 autoinhibition and allows Sly1 to tether incoming vesicles to the Qa-SNARE on the target organelle (close-range tethering); the SLY1-20 gain-of-function allele loses its bypass-tethering ability when this tethering activity is impaired, supporting a handoff model from long-range to Sly1-mediated close-range tethering. Chemically defined in vitro reconstitution of ER-Golgi fusion, genetic analyses with Sly1 loop mutants, liposome binding assay, gain-of-function allele analysis The Journal of cell biology High 38478018
2024 Sly1 promotes ER-Golgi SNARE-mediated membrane fusion through three parallel mechanisms: (i) opening the closed conformation of Qa-SNARE Sed5, (ii) close-range vesicle tethering via its regulatory loop, and (iii) nucleating productive trans-SNARE complexes; additionally, the autoinhibitory Habc domain of Sed5 has positive activities—required for correct Sed5 localization and directly promoting Sly1-dependent lipid mixing. Chemically defined in vitro fusion assays with SNARE and Sly1 mutants, 'split Sed5' in vitro and in vivo complementation, lipid mixing assays The Journal of cell biology High 38478017
2024 The T4SS effector EgeA of Anaplasma phagocytophilum directly binds SCFD1 (via its C-terminal half, confirmed by yeast two-hybrid), redirecting SCFD1 and its binding partner TANGO1 from ER-Golgi exit sites (ERES) to pathogen-occupied inclusions; knockdown of either TANGO1 or SCFD1 significantly reduces Anaplasma infection, demonstrating that SCFD1 function at ERES is exploited by the pathogen. Yeast two-hybrid (EgeA-C vs SCFD1), GFP-fusion localization, siRNA knockdown infection assay, pulldown for TANGO1 binding Proceedings of the National Academy of Sciences of the United States of America Medium 39106308

Source papers

Stage 0 corpus · 40 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 60 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 40 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 30 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 25 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
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
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 6 39106308
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 SNARE chaperone Sly1 directly mediates close-range vesicle tethering. The Journal of cell biology 5 38478018
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
2022 Lack of an association between SCFD1 rs10139154 polymorphism and amyotrophic lateral sclerosis. Molecular medicine reports 4 35234271
2024 SM protein Sly1 and a SNARE Habc domain promote membrane fusion through multiple mechanisms. The Journal of cell biology 3 38478017
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

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