Affinage

SYT4

Synaptotagmin-4 · UniProt Q9H2B2

Length
425 aa
Mass
48.0 kDa
Annotated
2026-06-10
55 papers in source corpus 20 papers cited in narrative 20 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SYT4 is a vesicle-associated C2-domain protein that functions as a non-canonical, largely Ca2+-insensitive synaptotagmin paralog modulating regulated secretion and intercellular signaling (PMID:20688915, PMID:29656931). In mammals its C2A domain carries a conserved Asp-to-Ser substitution that abolishes Ca2+ binding, converting it into an inhibitor of SNARE-catalyzed membrane fusion; reverting this substitution restores Ca2+-stimulated fusion, whereas the Drosophila ortholog instead stimulates fusion through a Ca2+-sensing C2B domain (PMID:20688915). In pancreatic β cells SYT4 localizes to insulin granules, rises ~8-fold during β-cell maturation under repression by Myt transcription factors, and inversely scales with the readily releasable pool to suppress basal secretion and tune glucose-stimulated insulin secretion (PMID:29656931, PMID:22939844). SYT4 trafficking is actively regulated: JNK phosphorylation at serine 135 uncouples it from the kinesin Kif1A, shifting dense-core-vesicle transport from microtubule-based long-range delivery to activity-dependent actin-based capture at presynaptic boutons (PMID:29166604). At the Drosophila NMJ SYT4 mediates Ca2+-dependent retrograde signaling, with its synaptic membrane levels set by the t-SNARE Syntaxin 4 alongside Neuroligin 1, by retromer- and Rab11-balanced sorting, and by endocytic machinery (Nwk, dynamin, AP-2) that maintains a release-competent pool (PMID:27223326, PMID:34019080, PMID:35320349). SYT4 binds partners including ARMS through its C2A/C2B domains and SNAP25, links that connect it to control of BDNF secretion and vesicle efflux (PMID:38069318, PMID:38889208). Functionally it supports somatodendritic dopamine release together with Syt7 (PMID:21576241) and is required for axonal sprouting and recovery after spinal cord injury (PMID:39266302). Across non-neuronal contexts SYT4 has been linked to BDNF–TrkB-dependent stress susceptibility in the mPFC, Wnt/β-catenin signaling in gastric cancer, melanogenesis, and GLUT1-mediated glucose uptake in diabetic retinopathy (PMID:38297157, PMID:41281742, PMID:31743468, PMID:38766439).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2010 High

    Established the core biochemical identity of mammalian SYT4 as an inhibitory fusion clamp rather than a stimulatory Ca2+ sensor, resolving why this isoform diverges functionally from canonical synaptotagmins.

    Evidence Reconstituted in vitro SNARE-catalyzed fusion assay with C2-domain chimeras and point mutagenesis of Ca2+-coordinating residues

    PMID:20688915

    Open questions at the time
    • Does not establish the in vivo fusion target or vesicle context in mammalian cells
    • Divergent stimulatory behavior of Drosophila SYT4 leaves the conserved physiological role ambiguous
  2. 2011 Medium

    Showed SYT4 has compartment-specific secretory roles, supporting somatodendritic dopamine release in concert with Syt7 distinct from terminal release driven by Syt1.

    Evidence siRNA knockdown of Syt isoforms in cultured dopaminergic neurons with amperometric dopamine measurement and Ca2+-channel pharmacology

    PMID:21576241

    Open questions at the time
    • Does not define whether SYT4 acts as a direct Ca2+ sensor or modulator in this context
    • Knockdown specificity and compensation by other Syt isoforms not fully excluded
  3. 2012 Medium

    Linked SYT4 to insulin secretion and human disease relevance by showing knockdown reduces glucose-stimulated insulin secretion and that SYT4 protein is decreased in type 2 diabetes islets.

    Evidence siRNA knockdown in INS1-832/13 β cells with GSIS assay and Western blotting of human T2D islets

    PMID:22939844

    Open questions at the time
    • Correlative protein-level association in human tissue does not establish causality
    • Mechanism of how SYT4 sets secretory competence not resolved here
  4. 2013 High

    Revealed that SYT4 is transferred between cells via anterograde exosome release, redefining how a postsynaptic retrograde signaling component is supplied by the presynaptic neuron.

    Evidence Exosome isolation, live imaging, and genetic loss-of-function at the Drosophila NMJ

    PMID:23522040

    Open questions at the time
    • Whether mammalian SYT4 uses analogous intercellular transfer not addressed
    • Molecular machinery sorting SYT4 into exosomes not defined here
  5. 2016 High

    Identified the t-SNARE Syntaxin 4 as a controller of synaptic SYT4 membrane levels, placing SYT4, Syx4, and Neuroligin 1 in convergent pathways governing retrograde signaling and synaptic growth.

    Evidence pHluorin-tagged Syt4 trafficking screen and genetic epistasis with live NMJ imaging in Drosophila

    PMID:27223326

    Open questions at the time
    • Direct physical interaction between Syx4 and Syt4 not demonstrated
    • Conservation in mammalian synapses untested
  6. 2017 High

    Defined an activity-dependent switch governing SYT4 vesicle trafficking, where JNK phosphorylation at S135 uncouples SYT4 from Kif1A and redirects dense-core vesicles to actin-based boutonic capture.

    Evidence S135A/S135E phospho-site mutagenesis, Syt4-Kif1A co-immunoprecipitation, and live DCV imaging in hippocampal neurons

    PMID:29166604

    Open questions at the time
    • Identity of the actin-based capture machinery not defined
    • Whether captured DCVs preferentially undergo fusion or proteostatic turnover unresolved
  7. 2018 High

    Established SYT4 as a developmentally regulated brake on basal secretion, with Myt-repressed expression rising during β-cell maturation to suppress basal insulin release and set Ca2+ sensitivity, conserved in human cells.

    Evidence Syt4 knockout/overexpression mice, insulin-granule immunolocalization, RRP capacitance measurements, human β-cell line knockdown, and Myt ChIP

    PMID:29656931

    Open questions at the time
    • Mechanism by which non-Ca2+-binding SYT4 sets vesicle pool size not fully resolved
    • Relationship between maturation role and acute secretory clamp unclear
  8. 2020 Medium

    Connected SYT4 expression to activity- and metabolism-dependent transcription, showing CREB drives SYT4 transcription and that glucose excess suppresses this to impair synaptic transmission.

    Evidence ChIP for CREB at the SYT4 promoter with electrophysiology (mEPSC, NMDAR currents) in autaptic hippocampal neurons and a diabetic mouse model

    PMID:32974347

    Open questions at the time
    • Whether reduced SYT4 is causal for the electrophysiological deficits not isolated
    • Direct postsynaptic vs presynaptic locus of SYT4 action unresolved
  9. 2020 Medium

    Tested the necessity of SYT4 for fast exocytosis in vestibular hair cells, establishing it is dispensable for readily releasable pool kinetics but may shape the secondary releasable pool.

    Evidence Patch-clamp capacitance measurements in control vs Syt4-knockout mouse Type II vestibular hair cells

    PMID:32691536

    Open questions at the time
    • SRP role is a weak positive requiring confirmation
    • Limited to a single electrophysiological method
  10. 2022 Medium

    Resolved the trafficking logic that maintains synaptic SYT4, showing endocytic machinery (Nwk, dynamin, AP-2) sustains a release-competent cargo pool upstream of retromer-dependent removal.

    Evidence Drosophila endocytic mutants with Syt4 cargo imaging, nwk-syt4 and nwk-retromer epistasis, and synaptic plasticity assays

    PMID:35320349

    Open questions at the time
    • Direct cargo-recognition step for SYT4 endocytosis not identified
    • Mammalian relevance untested
  11. 2021 Medium

    Defined retromer and Rab11 as opposing regulators of SYT4 sorting into extracellular vesicles, framing synaptic EV traffic as a recycling-versus-removal balance.

    Evidence Drosophila retromer and rab mutants with Syt4 immunofluorescence, EV cargo quantification, and rab11 suppression epistasis

    PMID:34019080

    Open questions at the time
    • Whether EV-released SYT4 has signaling significance left open
    • Direct binding of SYT4 to sorting machinery not shown
  12. 2023 Medium

    Identified ARMS as a specific direct partner of SYT4 engaged through both C2A and C2B domains, providing a molecular link to BDNF secretion control.

    Evidence Co-IP, GST pull-down, AlphaFold2-guided point mutagenesis, and domain-deletion mapping

    PMID:38069318

    Open questions at the time
    • Functional consequence of the SYT4-ARMS interaction for fusion not directly measured
    • Single-lab biochemistry without cellular validation of the mapped residues
  13. 2024 Medium

    Dissociated SYT4's signaling activity from its EV-mediated transfer, showing ESCRT-dependent EV release is dispensable for SYT4 signaling and may instead serve proteostasis.

    Evidence ESCRT depletion in Drosophila motor neurons with EV cargo quantification, signaling readouts, and phagocytosis imaging

    PMID:38842573

    Open questions at the time
    • Reconciliation with earlier exosome-transfer model not fully resolved
    • Proteostatic interpretation inferred rather than directly demonstrated
  14. 2024 Medium

    Extended SYT4 function into disease and developmental contexts, implicating it in mPFC BDNF-TrkB-dependent stress susceptibility, gastric cancer Wnt/β-catenin signaling, prostate cancer vesicle efflux, melanogenesis, GLUT1-driven glucose uptake in retinopathy, and axonal sprouting after spinal cord injury.

    Evidence Gain/loss-of-function in mPFC with behavioral assays; Co-IP/IP-MS, GST pull-down and reporter assays for PSMC6 and SNAP25; overexpression with pathway readouts in melanocytes and ARPE-19 cells; loss-of-function with SCI tracing and behavior

    PMID:31743468 PMID:38297157 PMID:38766439 PMID:38889208 PMID:39266302 PMID:41281742

    Open questions at the time
    • Many contexts rely on single-lab overexpression or knockdown without reconstitution
    • Whether these effects share a common SYT4 fusion/trafficking mechanism is unclear
    • Direct SYT4-ERK and SYT4-GLUT1 interactions not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the conserved non-Ca2+-binding biochemistry of mammalian SYT4 maps onto its diverse cellular roles, and whether a single fusion-clamp mechanism unifies its actions across neurons, β cells, and cancer.
  • No structural model of SYT4 engaged with its native SNARE complex
  • No unifying account linking inhibitory fusion activity to its disease and developmental phenotypes
  • Mammalian counterpart of the Drosophila EV/retrograde-signaling program untested

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 2 GO:0140313 molecular sequestering activity 1
Localization
GO:0005886 plasma membrane 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-162582 Signal Transduction 3 R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9609507 Protein localization 3
Partners
ARMS/KIDINS220KIF1ANLG1PSMC6SNAP25STX4SYT7

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2010 Rat SYT4 inhibits SNARE-catalyzed membrane fusion in both the absence and presence of Ca2+, functioning as a negative/inhibitory isoform. This is due to a conserved Asp-to-Ser substitution in the C2A domain that abolishes Ca2+ binding; reverting this substitution restores Ca2+-stimulated fusion. In contrast, Drosophila SYT4 stimulates SNARE-mediated membrane fusion in response to Ca2+, with its C2B domain sensing Ca2+ and being sufficient to stimulate fusion. In vitro SNARE-catalyzed membrane fusion assay, C2 domain chimera analysis, point mutagenesis of Ca2+-coordinating residues The Journal of biological chemistry High 20688915
2013 Presynaptic cells deliver Synaptotagmin 4 (Syt4) to the postsynaptic cell via anterograde exosome release, thereby enabling Ca2+-dependent retrograde signaling at the Drosophila NMJ. Thus, the presynaptic cell supplies an essential component of postsynaptic retrograde signaling machinery. Exosome isolation and characterization, live imaging, genetic loss-of-function at Drosophila NMJ Neuron High 23522040
2016 The postsynaptic t-SNARE Syntaxin 4 (Syx4) controls membrane levels of Syt4 and the transsynaptic adhesion protein Neuroligin 1 (Nlg1) at Drosophila NMJs, regulating retrograde signaling, synaptic bouton number, and activity-dependent plasticity. Genetic interaction experiments placed Syx4, Syt4, and Nlg1 in overlapping and parallel pathways controlling synaptic growth. pHluorin-tagged Syt4 trafficking screen, genetic epistasis (double mutant analysis), live imaging of Syt4 membrane levels at NMJ eLife High 27223326
2017 JNK phosphorylates Syt4 at serine 135, which destabilizes the Syt4–Kif1A interaction and shifts DCV (dense core vesicle) trafficking from microtubule-dependent long-range transport to actin-based capture at presynaptic boutons. Neuronal activity increases DCV capture via this JNK-S135 phosphorylation mechanism. Phospho-site mutagenesis (S135A/S135E), co-immunoprecipitation (Syt4-Kif1A interaction), live imaging of DCV trafficking in hippocampal neurons, activity-dependent capture assays Cell reports High 29166604
2011 Syt4 and Syt7 are expressed in dopaminergic neuron dendrites and their knockdown severely reduces somatodendritic (STD) dopamine release, whereas terminal release requires Syt1. Ca2+ influx through N- and P/Q-type voltage-gated channels (not intracellular Ca2+ stores) is required to trigger STD DA release through Syt4/Syt7. siRNA knockdown of Syt isoforms in cultured dopaminergic neurons, amperometric/electrochemical measurement of dopamine release, pharmacological block of Ca2+ channel subtypes The Journal of biological chemistry Medium 21576241
2018 Syt4 is a non-Ca2+-binding paralog of Syt7 that localizes on insulin granules in pancreatic β cells. Syt4 levels increase ~8-fold during β cell maturation and inversely correlate with the number of readily releasable vesicles. Syt4 ablation increases basal insulin secretion and impairs GSIS; precocious expression represses basal secretion but impairs islet morphogenesis. Myt transcription factors repress Syt4 transcription. Human SYT4 similarly regulates GSIS in EndoC-βH1 cells. Syt4 knockout and transgenic overexpression in mice, immunolocalization on insulin granules, capacitance/patch-clamp measurement of readily releasable pool, siRNA knockdown in human β cell line, ChIP for Myt binding Developmental cell High 29656931
2012 Silencing SYT4 in INS1-832/13 β cells reduces glucose-stimulated insulin secretion (GSIS). SYT4 and STX1A protein levels are correspondingly decreased in human type 2 diabetes islets. siRNA knockdown of SYT4 in INS1-832/13 cells, insulin secretion assay (GSIS), Western blotting of human T2D islets, microarray expression profiling Molecular and cellular endocrinology Medium 22939844
2023 ARMS (ankyrin repeat-rich membrane spanning protein) directly interacts with Syt4 through its N-terminal ankyrin repeats 1–8; both the C2A and C2B domains of Syt4 are required for binding. Residues E15 and W72 of ARMS are essential for complex formation. ARMS does not interact with Syt1 or Syt3, indicating specificity for Syt4. This interaction was previously shown to negatively regulate BDNF secretion. Co-immunoprecipitation, GST pull-down, point mutagenesis guided by AlphaFold2 structural predictions, domain deletion mapping International journal of molecular sciences Medium 38069318
2024 SYT4 promotes vesicle efflux by binding to SNAP25, contributing to exosomal secretion and enzalutamide resistance in prostate cancer cells. BRD4 mediates transcriptional upregulation of SYT4 in enzalutamide-resistant cells. Co-immunoprecipitation (SYT4-SNAP25 binding), siRNA knockdown of SYT4 combined with enzalutamide treatment, BRD4 inhibitor experiments, antisense oligonucleotide (ASO) targeting SYT4 Cancer science Medium 38889208
2024 Syt4 overexpression in the medial prefrontal cortex (mPFC) promotes stress susceptibility (anhedonia), while Syt4 knockdown promotes resilience. The pro-susceptible effects of Syt4 are mediated through reduction in BDNF–TrkB signaling in the mPFC. Viral overexpression and shRNA knockdown of Syt4 in mPFC, FosTRAP/optogenetics for circuit identification, RNA-seq with WGCNA, sucrose preference and social reward behavioral assays Experimental & molecular medicine Medium 38297157
2024 SYT4 directly interacts with PSMC6 via its C2B domain (amino acids 288–423), stabilizes PSMC6 protein, and thereby activates Wnt/β-catenin signaling to drive gastric cancer proliferation and suppress apoptosis. Immunoprecipitation-mass spectrometry (IP-MS), Co-IP, GST pull-down, TOP/FOP luciferase reporter assay for Wnt/β-catenin activity, in vitro and in vivo (xenograft) functional assays, domain deletion mapping International journal of biological sciences Medium 41281742
2024 SYT4 promotes melanogenesis and dendrite extension in melanocytes by interacting with ERK to decrease p-ERK activity, which upregulates CREB. CREB upregulation leads to increased MITF and melanogenic enzymes (TYR, TYRP1, DCT) and TRPM1. SYT4 regulates Ca2+ influx via TRPM1 channels; intracellular Ca2+ activates CAMK4, which phosphorylates CREB to further drive MITF transcription. SYT4 overexpression in alpaca melanocytes and B16-F10 cells, Western blotting for ERK/p-ERK/CREB/MITF/melanogenic enzymes, intracellular Ca2+ imaging, tyrosinase activity assay Cell biochemistry and function Medium 31743468
2020 Glucose excess inhibits activity-dependent CREB phosphorylation and CREB-mediated transcription of SYT4 in hippocampal neurons. This reduces SYT4 protein expression and impairs miniature excitatory postsynaptic current frequency and NMDA receptor-mediated currents. ChIP for CREB binding at SYT4 promoter, Western blotting, electrophysiology (mEPSC and NMDAR currents) in autaptic hippocampal neurons, diabetic mouse model Frontiers in cell and developmental biology Medium 32974347
2021 Loss of retromer complex leads to accumulation of Syt4 (and other EV cargoes) at Drosophila presynaptic terminals and increased release of Syt4 in extracellular vesicles. Rab11 suppresses Syt4 cargo accumulation in retromer mutants, indicating that EV traffic at synapses reflects a balance between Rab4/Rab11 recycling and retromer-dependent removal from EV precursor compartments. Drosophila genetics (retromer and rab mutants), immunofluorescence of Syt4 at presynaptic terminals, EV isolation and cargo quantification, genetic epistasis (rab11 suppression of retromer mutant) The Journal of cell biology Medium 34019080
2022 Endocytic machinery (including Nwk/nervous wreck, dynamin/shibire, and AP-2) promotes local maintenance of a release-competent pool of EV cargoes including Syt4 at Drosophila presynaptic terminals. Loss of nwk phenocopies synaptic plasticity defects caused by loss of Syt4, and nwk acts upstream of retromer-dependent removal and retrograde axonal transport of EV cargoes. Drosophila endocytic mutants, fluorescence imaging of Syt4 cargo levels, genetic epistasis (nwk-syt4 double mutant, nwk-retromer epistasis), synaptic plasticity assays (bouton formation) The Journal of cell biology Medium 35320349
2024 Loss of ESCRT machinery disrupts release of Syt4 in extracellular vesicles from Drosophila motor neurons, but ESCRT depletion does not affect the signaling activities of Syt4. EVs containing Syt4 are phagocytosed by glia and muscles. These data suggest Syt4 may not require EV-mediated intercellular transfer for its signaling function and that synaptic EV release may serve primarily as a proteostatic mechanism for Syt4. ESCRT component depletion in Drosophila motor neurons, EV cargo quantification, signaling readout assays, phagocytosis imaging The Journal of cell biology Medium 38842573
2024 Syt4 is required for axon elongation and spontaneous axonal sprouting after spinal cord injury. Silencing Syt4 in primary cortical neurons inhibits neurite elongation and alters expression of genes in neuronal development signaling pathways. In vivo, Syt4 inhibition in cortical neurons prevents corticospinal tract axonal sprouting and impairs neurological recovery after spinal cord injury. Loss-of-function genetic screen in cortical neurons, siRNA/shRNA-mediated Syt4 silencing, neurite elongation assay, RNA-seq of gene expression changes, spinal cord injury model with anterograde tracing of corticospinal tract, behavioral recovery assessment The Journal of neuroscience Medium 39266302
2024 In diabetic retinopathy, SYT4 overexpression manipulates Ca2+ influx to induce GLUT1 fusion with the plasma membrane, promotes abnormal GLUT1 expression and excessive glucose uptake, and induces ARPE-19 cell apoptosis. Parkin deficiency inhibits proteasomal degradation of SYT4, causing SYT4 accumulation and enhanced GLUT1 membrane fusion. Myt1 transcription factor dysregulation further activates SYT4-mediated stimulus-secretion coupling. Parkin overexpression or Myt1 overexpression blocked these effects. SYT4 overexpression/knockdown in ARPE-19 cells, Ca2+ imaging, flow cytometry for GLUT1 membrane localization and apoptosis, Parkin overexpression rescue, Western blotting, streptozotocin mouse model World journal of diabetes Medium 38766439
2020 Exocytosis in Type II vestibular hair cells displays a high-order Ca2+ dependence that is independent of Syt4; the Ca2+ dependence and release kinetics of the readily releasable pool (RRP) are not affected by Syt4 knockout. However, Syt4 may play a role in regulating the secondary releasable pool (SRP) in these cells. Patch-clamp capacitance measurements of exocytosis in control vs. Syt4 knockout mouse Type II vestibular hair cells, analysis of RRP and SRP kinetics Physiological reports Medium 32691536
2011 Astrocytes endogenously express Syt4 (not Syt1). Exogenous expression of Syt1 in astrocytes (which express endogenous Syt4) increased the proportion of transient fusion events upon bradykinin stimulation and reduced fusion pore dwell time, indicating that Syt4 and Syt1 have distinct roles in regulating fusion pore dynamics in glial exocytosis. TIRFM imaging of synapto-pHluorin fusion events in cultured astrocytes, exogenous Syt1 expression, pharmacological stimulation (bradykinin, mechanical) The Journal of physiology Low 21746780

Source papers

Stage 0 corpus · 55 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Regulation of postsynaptic retrograde signaling by presynaptic exosome release. Neuron 205 23522040
2020 Environment and Gene Association With Obesity and Their Impact on Neurodegenerative and Neurodevelopmental Diseases. Frontiers in neuroscience 112 32982666
2012 Reduced insulin secretion correlates with decreased expression of exocytotic genes in pancreatic islets from patients with type 2 diabetes. Molecular and cellular endocrinology 107 22939844
2018 Synaptotagmin 4 Regulates Pancreatic β Cell Maturation by Modulating the Ca2+ Sensitivity of Insulin Secretion Vesicles. Developmental cell 75 29656931
2007 Brain regions and genes affecting postural control. Progress in neurobiology 63 17222959
2011 Temporal characteristics of vesicular fusion in astrocytes: examination of synaptobrevin 2-laden vesicles at single vesicle resolution. The Journal of physiology 60 21746780
2011 Somatodendritic dopamine release requires synaptotagmin 4 and 7 and the participation of voltage-gated calcium channels. The Journal of biological chemistry 58 21576241
1996 Two synaptotagmin genes, Syt1 and Syt4, are differentially regulated in adult brain and during postnatal development following kainic acid-induced seizures. Brain research. Molecular brain research 54 8872307
2011 Profiling trait anxiety: transcriptome analysis reveals cathepsin B (Ctsb) as a novel candidate gene for emotionality in mice. PloS one 50 21897848
2017 Capture of Dense Core Vesicles at Synapses by JNK-Dependent Phosphorylation of Synaptotagmin-4. Cell reports 45 29166604
2016 The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling. eLife 40 27223326
2018 Gene Co-expression Analysis Indicates Potential Pathways and Regulators of Beef Tenderness in Nellore Cattle. Frontiers in genetics 37 30344530
2017 Molecular Mechanisms for the Coupling of Endocytosis to Exocytosis in Neurons. Frontiers in molecular neuroscience 35 28348516
2021 Opposing functions for retromer and Rab11 in extracellular vesicle traffic at presynaptic terminals. The Journal of cell biology 32 34019080
2010 Rat and Drosophila synaptotagmin 4 have opposite effects during SNARE-catalyzed membrane fusion. The Journal of biological chemistry 28 20688915
1999 Variations of synaptotagmin I, synaptotagmin IV, and synaptophysin mRNA levels in rat hippocampus during the estrous cycle. Experimental neurology 28 10506530
2020 Significance of achaete-scute complex homologue 1 (ASCL1) in pulmonary neuroendocrine carcinomas; RNA sequence analyses using small cell lung cancer cells and Ascl1-induced pulmonary neuroendocrine carcinoma cells. Histochemistry and cell biology 27 32170367
2019 Synaptotagmin-4 promotes dendrite extension and melanogenesis in alpaca melanocytes by regulating Ca2+ influx via TRPM1 channels. Cell biochemistry and function 27 31743468
2010 A 5.3Mb deletion in chromosome 18q12.3 as the smallest region of overlap in two patients with expressive speech delay. European journal of medical genetics 26 21145994
2014 Risk of false positive genetic associations in complex traits with underlying population structure: a case study. Veterinary journal (London, England : 1997) 24 25278384
2017 Dynamin regulates the fusion pore of endo- and exocytotic vesicles as revealed by membrane capacitance measurements. Biochimica et biophysica acta. General subjects 20 28669852
2023 Lactate promotes neuronal differentiation of SH-SY5Y cells by lactate-responsive gene sets through NDRG3-dependent and -independent manners. The Journal of biological chemistry 18 37172727
2022 Local regulation of extracellular vesicle traffic by the synaptic endocytic machinery. The Journal of cell biology 18 35320349
2009 Novel SYT-SSX fusion transcript variants in synovial sarcoma. Cancer genetics and cytogenetics 18 19837269
2012 Identification of differentially expressed genes in SHSY5Y cells exposed to okadaic acid by suppression subtractive hybridization. BMC genomics 17 22284234
2015 Age-related obesity and type 2 diabetes dysregulate neuronal associated genes and proteins in humans. Oncotarget 16 26337083
2024 ESCRT disruption provides evidence against trans-synaptic signaling via extracellular vesicles. The Journal of cell biology 13 38842573
2024 Single-cell multiomics analysis reveals cell/tissue-specific associations in bipolar disorder. Translational psychiatry 13 39107272
2013 Inducible protein traps with dominant phenotypes for functional analysis of the Drosophila genome. Genetics 13 24172131
2020 Glucose Overload Inhibits Glutamatergic Synaptic Transmission: A Novel Role for CREB-Mediated Regulation of Synaptotagmins 2 and 4. Frontiers in cell and developmental biology 12 32974347
2018 The orphan nuclear receptor TLX regulates hippocampal transcriptome changes induced by IL-1β. Brain, behavior, and immunity 12 29518529
2011 Genetic ablation of a candidate tumor suppressor gene, Rest, does not promote mouse colon carcinogenesis. Cancer science 12 21668584
2020 Exocytosis in mouse vestibular Type II hair cells shows a high-order Ca2+ dependence that is independent of synaptotagmin-4. Physiological reports 9 32691536
2024 Synaptotagmin-4 induces anhedonic responses to chronic stress via BDNF signaling in the medial prefrontal cortex. Experimental & molecular medicine 8 38297157
2024 Amlodipine inhibits Synaptotagmin-4's oncogenic activity on gastric cancer proliferation by targeting calcium signaling. Functional & integrative genomics 8 38632140
2015 Hippocampal synaptotagmin-4 is correlated with impaired spatial learning and memory in SAMP8 mice. Neuroscience letters 8 26365408
2020 Genetic locus responsible for diabetic phenotype in the insulin hyposecretion (ihs) mouse. PloS one 7 32502168
2020 Glucosamine potentiates the differentiation of adipose-derived stem cells into glucose-responsive insulin-producing cells. Annals of translational medicine 7 32775362
2024 FLRT3 and TGF-β/SMAD4 signalling: Impacts on apoptosis, autophagy and ion channels in supraventricular tachycardia. Journal of cellular and molecular medicine 6 38509727
2024 SYT4 binds to SNAP25 to facilitate exosomal secretion and prostate cancer enzalutamide resistance. Cancer science 5 38889208
2023 The role of ferroptosis-related genes in airway epithelial cells of asthmatic patients based on bioinformatics. Medicine 5 36862916
2023 Behavioral and Transcriptome Profiling of Heterozygous Rab10 Knock-Out Mice. eNeuro 5 37156612
2025 Discovery of Novel Pain Regulators Through Integration of Cross-Species High-Throughput Data. CNS neuroscience & therapeutics 4 39924344
2024 Environmental enrichment improves social isolation-induced memory impairment: The possible role of ITSN1-Reelin-AMPA receptor signaling pathway. PloS one 4 38241230
2024 Alterations in Synaptic Connectivity and Synaptic Transmission in Alzheimer's Disease with High Physical Activity. Journal of Alzheimer's disease : JAD 4 38759013
2024 Synaptotagmins family affect glucose transport in retinal pigment epithelial cells through their ubiquitination-mediated degradation and glucose transporter-1 regulation. World journal of diabetes 3 38766439
2024 Synaptotagmin 4 Supports Spontaneous Axon Sprouting after Spinal Cord Injury. The Journal of neuroscience : the official journal of the Society for Neuroscience 3 39266302
2023 Role of SNAP25 on the occurrence and development of eosinophilic gastritis. Medicine 2 37478220
2023 Neuronal Scaffold Protein ARMS Interacts with Synaptotagmin-4 C2AB through the Ankyrin Repeat Domain with an Unexpected Mode. International journal of molecular sciences 1 38069318
2021 A pH-eQTL Interaction at the RIT2-SYT4 Parkinson's Disease Risk Locus in the Substantia Nigra. Frontiers in aging neuroscience 1 34305570
2025 Divergence in expression of a singing-related neuroplasticity gene in the brains of 2 Ficedula flycatchers and their hybrids. G3 (Bethesda, Md.) 0 39670717
2025 SYT4 Interacts with PSMC6 to Facilitate Malignant Progression in Gastric Carcinoma via Activating Wnt/β-catenin Signaling. International journal of biological sciences 0 41281742
2025 Chromothriptic Translocation t(1;18): A Paradigm of Genomic Complexity in a Child with Normal Intellectual Development and Pyridoxine-Dependent Epilepsy. Genes 0 41300786
2024 ESCRT disruption provides evidence against transsynaptic signaling functions for extracellular vesicles. bioRxiv : the preprint server for biology 0 38746182
2024 Conserved expression of the zebrafish syt4 gene in GABAergic neurons in the cerebellum of adult fishes revealed by mammalian SYT4 immunoreactive-like signals. Heliyon 0 38765140

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