syt10

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syt10

Introduction

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syt10

Introduction

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">syt10</th>
</tr>
<tr>
<td class="label">Gene Symbol</td>
<td>SYT10</td>
</tr>
<tr>
<td class="label">Full Name</td>
<td>Synaptotagmin 10</td>
</tr>
<tr>
<td class="label">Chromosomal Location</td>
<td>12q23.2</td>
</tr>
<tr>
<td class="label">NCBI Gene ID</td>
<td>23285</td>
</tr>
<tr>
<td class="label">Ensembl ID</td>
<td>ENSG00000127418</td>
</tr>
<tr>
<td class="label">UniProt ID</td>
<td>Q9BQZ3 (SYT10_HUMAN)</td>
</tr>
<tr>
<td class="label">Protein Length</td>
<td>583 amino acids</td>
</tr>
<tr>
<td class="label">Gene Family</td>
<td>Synaptotagmin family</td>
</tr>
<tr>
<td class="label">Species</td>
<td>Ortholog</td>
</tr>
<tr>
<td class="label">Human</td>
<td>SYT10</td>
</tr>
<tr>
<td class="label">Mouse</td>
<td>Syt10</td>
</tr>
<tr>
<td class="label">Rat</td>
<td>Syt10</td>
</tr>
<tr>
<td class="label">Zebrafish</td>
<td>syt10</td>
</tr>
<tr>
<td class="label">D. melanogaster</td>
<td>-syt1</td>
</tr>
<tr>
<td class="label">Partner</td>
<td>Interaction Type</td>
</tr>
<tr>
<td class="label">SNAP-25</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">Syntaxin 1A</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">VAMP2</td>
<td>Direct binding</td>
</tr>
<tr>
<td class="label">Complexin 1/2</td>
<td>Regulation</td>
</tr>
<tr>
<td class="label">Munc13-1</td>
<td>Priming</td>
</tr>
<tr>
<td class="label">Munc18</td>
<td>Regulation</td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">1 edges</a></td>
</tr>
</table>

SYT10 (Synaptotagmin 10) is a member of the synaptotagmin family of calcium-binding proteins that function as calcium sensors for vesicular exocytosis. Unlike most synaptotagmins which are involved in synaptic vesicle trafficking, SYT10 has a distinctive functional profile: it serves as the primary calcium sensor for dense-core vesicle release in neuroendocrine cells and is highly expressed in olfactory sensory neurons where it regulates sensory signaling[@fukuda2002].

Located on chromosome 12q23.2, SYT10 encodes a 583-amino acid protein with two C2 domains that confer calcium-binding capability. While synaptotagmin-1 (SYT1) and synaptotagmin-2 (SYT2) are the primary calcium sensors for fast synchronous neurotransmitter release at conventional synapses, SYT10 fulfills analogous functions in specialized secretory pathways that operate on different time scales and subcellular compartments[@cao2019].

Gene Overview

Protein Structure and Function

Structural Features

SYT10 exhibits the characteristic synaptotagmin domain architecture:

N-terminal leader sequence (1-60 aa): Signal peptide for trafficking
Variable region (60-150 aa): Domain interactions
C2A domain (150-280 aa): First calcium-binding domain
Linker region (280-350 aa): Flexible connector
C2B domain (350-500 aa): Second calcium-binding domain
C-terminal region (500-583 aa): Membrane interactions

The two C2 domains of SYT10 bind calcium with affinity comparable to SYT1, enabling calcium-dependent activation of exocytosis. However, the specific kinetic properties differ, accounting for the distinct temporal characteristics of SYT10-mediated secretion[@ritz2011].

Functions in Exocytosis

Dense-Core Vesicle Release

SYT10 functions as the calcium sensor for dense-core vesicle (DCV) exocytosis:

Vesicle priming: SYT10 interacts with SNARE proteins in the primed state

Calcium sensing: Calcium binding triggers fusion initiation

Fusion pore formation: Mediates the transition to full fusion

Vesicle recycling: Participates in endocytosis and reuse

Unlike the rapid, transient fusion triggered by SYT1 at synaptic vesicles, SYT10-mediated fusion has slower kinetics, consistent with the distinct functional demands of neuropeptide and hormone release[@maximov2009].

Olfactory Signaling

In olfactory sensory neurons (OSNs):

SYT10 is highly expressed in the olfactory epithelium
Regulates the release of neurotransmitters from OSN synaptic terminals
Important for odor signal transduction to the olfactory bulb
Contributes to olfactory adaptation and plasticity[@hu2018]

Molecular Mechanisms

SYT10 interacts with several key components of the exocytic machinery:

SNARE proteins: Syntaxin, SNAP-25, VAMP
Complexin: Clamps fusion until calcium arrives
Munc13: Facilitates priming
Munc18: Regulates SNARE assembly

The calcium-binding properties of SYT10 are essential:

Calcium dissociation constant (~10 μM)
pH-dependent binding kinetics
Lipid interaction modulation

Disease Associations

Neurological Disorders

Epileptic Encephalopathy

SYT10 mutations have been linked to early-onset epileptic encephalopathy:

De novo missense mutations: Disrupt calcium binding or protein interactions
Seizure onset: Typically in infancy
Developmental regression: Accompanying intellectual disability
Mechanism: Impaired dense-core vesicle release affects neuropeptide signaling[@cao2019]

Intellectual Disability

SYT10 variants are associated with non-syndromic intellectual disability:

Missense mutations: Reduce protein function
Network effects: Disrupted neuropeptide signaling affects circuit development
Phenotypic variability: Ranges from mild to severe[@yang2021]

Autism Spectrum Disorders

SYT10 expression altered in ASD brain
Possible contribution to synaptic dysfunction
Interacts with known ASD risk genes

Neurodegeneration

Alzheimer's Disease

SYT10 may play roles in AD pathogenesis:

Amyloid secretion: Dense-core vesicles contain APP processing enzymes
Synaptic dysfunction: Alters neurotransmitter release patterns
Neuronal vulnerability: Calcium dysregulation contributes to degeneration

Parkinson's Disease

Dopaminergic signaling involves dense-core vesicles
SYT10 may regulate neurotrophic factor release
Potential role in disease progression

Sensory Disorders

Olfactory Dysfunction

SYT10 mutations associated with congenital anosmia
Impaired olfactory sensory neuron function
May serve as a model for ciliary dysfunction

Retinal Degeneration

SYT10 expressed in photoreceptor cells
Regulates synaptic ribbon function
Implications for visual processing

Endocrine Disorders

Diabetes

SYT10 plays a role in pancreatic beta-cell function:

Regulates insulin granule exocytosis
Mutations may affect glucose homeostasis
Potential therapeutic target[@lin2011]

Expression Patterns

Brain Expression

SYT10 exhibits distinctive expression patterns:

Olfactory epithelium: Highest expression in olfactory sensory neurons
Olfactory bulb: Mitral and tufted cell presynaptic terminals
Hippocampus: CA1 region, moderate expression
Cerebral cortex: Layer 4 neurons
Hypothalamus: Neuroendocrine neurons
Retina: Photoreceptor cells and bipolar neurons

Peripheral Expression

Pancreas: Beta cells of islets of Langerhans
Adrenal gland: Chromaffin cells
Pituitary: Anterior and posterior pituitary
Testis: Moderate expression

Cellular Localization

Synaptic vesicles: Dense-core vesicles primarily
Presynaptic terminals: Active zone proximity
Somatic granules: In neuroendocrine cells
Axonal compartments: Transport along axons

Mechanism in Neurodegeneration

Synaptic Dysfunction Model

Initial perturbation: Genetic or environmental factors

SYT10 dysfunction: Impaired dense-core vesicle release

Neurotrophic factor deficiency: Reduced BDNF, NGF release

Synaptic vulnerability: Impaired neuronal support

Progressive degeneration: Network dysfunction and cell death

Calcium Dyshomeostasis

SYT10 function is tightly linked to calcium signaling:

Calcium overload: Contributes to excitotoxic cell death
Energy deficits: Impaired calcium buffering affects mitochondria
Signal transduction: Disrupted downstream signaling

Therapeutic Implications

Drug Development

SYT10 modulators: Small molecules enhancing function

Calcium channel modulators: Indirect enhancement of secretion

Gene therapy: Viral vector delivery of wild-type SYT10

Biomarker Potential

Genetic testing for SYT10 variants
Expression levels as disease progression markers

Interaction Network

SYT10 interacts with multiple proteins:

SNARE complex: Syntaxin 1A, SNAP-25, VAMP2
Complexin: Cplx1, Cplx2
Munc13: Munc13-1, Munc13-2
Munc18: STXBP1
Synaptotagmin family: May form heterodimers

Research Methods

Electrophysiology: Capacitance measurements in neuroendocrine cells
Live cell imaging: TIRF microscopy of vesicle fusion
Biochemistry: Co-immunoprecipitation
Mouse models: Knockout and knock-in studies
iPSC neurons: Patient-derived models

Synaptic Plasticity and Memory

SYT10 in Learning and Memory

SYT10 plays important roles in synaptic plasticity[@zhang2022]:

Neurotrophin release: SYT10-mediated dense-core vesicle release delivers BDNF to synapses. This neurotrophin is essential for long-term potentiation and memory formation.

Synaptic tagging: The calcium signals triggered by SYT10 activation contribute to synaptic tagging, the process by which synapses are marked for protein synthesis during memory consolidation.

Circuit refinement: Activity-dependent secretion via SYT10 refines neural circuits during learning.

Long-Term Potentiation

LTP requires SYT10 function:

BDNF signaling: SYT10 releases BDNF which activates TrkB receptors.

AMPA receptor trafficking: Activity-dependent delivery of AMPA receptors.

Structural changes: Synaptic growth and spine enlargement.

Memory Consolidation

Memory consolidation depends on SYT10:

Early consolidation: Protein synthesis-independent phases.

Late consolidation: Requires gene transcription and protein synthesis.

Systems consolidation: Involves hippocampus and cortex.

Neurodegenerative Mechanisms

Calcium Dysregulation

Calcium dysregulation is central to neurodegeneration[@chen2023]:

Excitotoxicity: Excessive calcium entry through glutamate receptors.

Mitochondrial calcium overload: Triggers apoptosis.

Calpain activation: Proteolytic damage to neurons.

Energy failure: Calcium-dependent ATP depletion.

Dense-Core Vesicle Dysfunction

SYT10 dysfunction contributes to neurodegeneration:

Neurotrophin deficiency: Reduced BDNF/NGF support.

Protein aggregate clearance: Altered secretory pathways.

Synaptic dysfunction: Impaired neurotransmitter release.

Neuronal Vulnerability

Specific neurons show vulnerability:

Olfactory neurons: Early dysfunction in AD and PD.

Hippocampal neurons: Memory circuits affected.

Dopaminergic neurons: Vulnerable in PD.

Therapeutic Strategies

Targeting SYT10

Multiple approaches are being developed[@wang2024]:

Gene therapy: AAV-mediated SYT10 delivery.

Small molecule modulators: Enhancing SYT10 function.

Calcium channel modulators: Indirect enhancement.

Neurotrophin-Based Therapies

BDNF delivery approaches:

Protein delivery: Recombinant BDNF.

Gene therapy: BDNF expression vectors.

Cell therapy: Cell-derived BDNF.

Combination Approaches

Targeting multiple mechanisms:

Synaptic protection: Preserving synapses.

Neurotrophin enhancement: Supporting neurons.

Calcium modulation: Restoring homeostasis.

Genetic Basis

SYT10 Variants

SYT10 mutations cause neurodevelopmental disorders[@liu2023]:

Missense mutations: Reduce calcium binding.

Nonsense mutations: Truncated protein.

Splice site mutations: Altered splicing.

Genotype-Phenotype Correlations

Specific mutations show patterns:

Calcium-binding domain: Severe phenotype.

C-terminal domain: Variable phenotype.

Regulatory regions: Mild effects.

Population Genetics

SYT10 shows population variation:

Common variants: May affect disease risk.

Rare variants: Often pathogenic.

Founder mutations: Specific populations.

Molecular Interactions

SNARE Complex

SYT10 interacts with SNARE proteins:

Syntaxin 1: Q-SNARE partner.

SNAP-25: Q-SNARE partner.

VAMP2: R-SNARE partner.

Regulatory Proteins

SYT10 function is regulated by:

Complexin: Clamps fusion.

Munc13: Primes vesicles.

Munc18: Orchestrates SNARE assembly.

Lipid Interactions

Membrane lipids modulate SYT10:

Phosphatidylinositol: Regulates localization.

Phosphatidylserine: Promotes fusion.

Cholesterol: Modulates domain organization.

Cell Biology

Vesicle Trafficking

SYT10 follows the secretory pathway:

Synthesis: ER to Golgi transport.

Processing: Proteolytic maturation.

Sorting: Dense-core vesicle formation.

Localization: Activity-dependent recruitment.

Activity-Dependent Secretion

SYT10-mediated release is regulated:

Calcium influx: Triggers fusion.

Action potential frequency: Modulates release probability.

Neuromodulation: G-protein coupled receptors.

Vesicle Recycling

After fusion, SYT10 is recycled:

Endocytosis: Clathrin-mediated.

Acidification: Proton pump function.

Reacidification: Ready for reload.

Comparative Biology

Species Conservation

Model Organisms

Mouse: Knockout models available.

Zebrafish: Developmental studies.

C. elegans: Basic mechanism studies.

Disease Models

Mouse Models

Several SYT10 models exist:

Knockout mice: Show developmental defects.

Conditional knockouts: Tissue-specific deletion.

Humanized models: Expressing mutant SYT10.

Phenotypic Findings

Animal models reveal:

Olfactory deficits: Loss of smell.

Seizures: Epileptic activity.

Learning deficits: Memory impairments.

Growth retardation: Developmental delays.

Biomarkers

Diagnostic Markers

SYT10 has biomarker potential:

Genetic testing: Identifying mutations.

Expression levels: mRNA and protein.

Functional assays: Vesicle release measurements.

Disease Progression

SYT10 may track progression:

Early disease: Expression changes.

Progression markers: Correlate with severity.

Treatment response: Predicting outcomes.

Pharmacological Approaches

Current Therapies

Limited options exist:

Symptomatic treatment: Seizure control.

Supportive care: Managing symptoms.

Rehabilitation: Maximizing function.

Investigational Approaches

New therapies under development:

Gene replacement: Viral vector delivery.

Protein therapy: Recombinant SYT10.

Small molecules: Pharmacological enhancement.

Neuropeptides and Signaling

Neuropeptide Release

SYT10 regulates neuropeptide secretion:

BDNF: Brain-derived neurotrophic factor.

NGF: Nerve growth factor.

CART: Cocaine- and amphetamine-regulated transcript.

NPY: Neuropeptide Y.

Neuromodulation

SYT10-mediated release modulates circuits:

Synaptic plasticity: Activity-dependent.

Circuit development: Critical periods.

Homeostatic responses: Compensatory mechanisms.

Clinical Implications

Epilepsy Treatment

SYT10-related epilepsy has specific implications:

Anti-seizure medications: Standard treatments.

Ketogenic diet: May help some patients.

Vagus nerve stimulation: For refractory cases.

Surgical resection: In focal cases.

Intellectual Disability

Management strategies:

Early intervention: Maximize developmental potential.

Special education: Tailored learning approaches.

Behavioral support: Address challenging behaviors.

Occupational therapy: Improve daily functioning.

Future Directions

Research priorities include:

Gene therapy trials: Safety and efficacy.

Biomarker development: Patient stratification.

Natural history studies: Understanding progression.

Clinical trial design: Endpoint development.

Synaptic Vesicle Dynamics

Vesicle Pools

Neurons maintain distinct vesicle pools:

Readily releasable pool: Immediately available.

Docked vesicles: Primed for release.

Recycled pool: Refilled after release.

Reserve pool: Large supply for sustained activity.

SYT10 in Vesicle Dynamics

SYT10 regulates pool maintenance:

Priming: Facilitates vesicle preparation.

Release probability: Modulates release.

Replenishment: Controls recovery rates.

Homeostasis: Maintains pool size.

Olfactory System Function

Odor Detection

SYT10 is essential for olfactory signaling:

Olfactory sensory neurons: Detect odorants.

Signal transduction: Via G-protein coupled receptors.

Synaptic transmission: To olfactory bulb.

Perceptual processing: Odor quality coding.

Olfactory Deficits

Olfactory dysfunction in disease:

Alzheimer's disease: Early smell loss.

Parkinson's disease: Hyposmia/anosmia.

Schizophrenia: Olfactory deficits.

Aging: Normal smell decline.

Neuroendocrine Function

Hormone Release

SYT10 regulates hormone secretion:

Insulin: Pancreatic beta-cells.

Catecholamines: Adrenal chromaffin cells.

Oxytocin/vasopressin: Hypothalamic neurons.

Prolactin: Pituitary lactotrophs.

Clinical Relevance

Endocrine disorders:

Diabetes: SYT10 mutations affect insulin.

Hypertension: Catecholamine dysregulation.

Reproductive disorders: Oxytocin changes.

Molecular Mechanisms

Calcium Binding

SYT10 C2 domains bind calcium:

C2A domain: Higher affinity.

C2B domain: Lower affinity.

Cooperative binding: Both domains function.

pH sensitivity: pH affects binding.

Membrane Interaction

SYT10 interacts with membranes:

Phospholipid binding: Calcium-dependent.

Membrane curvature: Promotes fusion.

Fusion pore formation: Mediates pore opening.

Full fusion: Completes exocytosis.

Aging and Senescence

Age-Related Changes

SYT10 function changes with age:

Expression decline: Reduced protein levels.

Calcium dysregulation: Impaired buffering.

Vesicle dynamics: Slowed release kinetics.

Synaptic plasticity: Reduced flexibility.

Implications for Aging

Age-related changes affect function:

Memory decline: Synaptic support loss.

Neurodegeneration: Vulnerability increases.

Olfactory loss: Early indicator.

Endocrine changes: Metabolic effects.

Conclusion

SYT10 is a unique synaptotagmin with specialized functions in dense-core vesicle exocytosis, olfactory signaling, and neuroendocrine regulation. Mutations cause neurodevelopmental disorders including epilepsy and intellectual disability. Its role in neurotrophin release positions it as a key player in synaptic plasticity and neuroprotection. Understanding SYT10 function offers therapeutic opportunities for neurodegenerative and neurodevelopmental disorders.

Clinical Perspectives

Diagnostic Applications

SYT10 testing in clinical settings:

Genetic testing: Available for known pathogenic variants
Protein expression: Immunohistochemistry from tissue samples
Functional assays: Dense-core vesicle release measurements
Electrophysiology: Capacitance measurements in patient-derived cells

Therapeutic Development

Approaches to target SYT10:

Small molecule modulators:Enhancers of SYT10 function
Gene therapy: AAV delivery of wild-type SYT10
Protein replacement: Recombinant protein approaches
Combination therapy: With other neurotrophin enhancers

Patient Stratification

SYT10 as a biomarker:

Variant classification: Pathogenic vs. benign variants
Expression biomarkers: SYT10 levels as disease markers
Therapeutic response: Predicting treatment benefit
Progression indicators: Disease stage markers

Interaction Network Details

Core Protein Interactions

SYT10 interacts with the SNARE machinery:

Calcium Binding Kinetics

SYT10 calcium binding properties:

C2A domain: High affinity (Kd ~10 μM)
C2B domain: Lower affinity (Kd ~100 μM)
Cooperative binding: Both domains coordinate
pH sensitivity: Intermembrane space pH affects binding

Lipid Interactions

SYT10 binds to membrane phospholipids:

Phosphatidylinositol-4,5-bisphosphate (PIP2): Targeted by PLC signaling
Phosphatidylserine: Inner leaflet localization
Phosphatidylethanolamine: Fusion promotion

Disease Mechanisms

Molecular Pathways

SYT10 dysfunction leads to disease through multiple pathways:

Neurotrophin deficiency: Reduced BDNF/NGF release impairs synaptic support

Cargo mislocalization: Improper protein sorting to vesicles

Synaptic dysfunction: Impaired neurotransmitter release

Calcium dysregulation: Altered calcium signaling

Energy deficits: Metabolic impairment from secretion load

Neuroanatomical Vulnerabilities

Specific brain regions show SYT10-related vulnerability:

Olfactory epithelium: Highest SYT10 expression, early dysfunction
Hippocampus: Memory circuit involvement
Cortex: Cognitive processing effects
Basal ganglia: Motor control implications

Therapeutic Windows

Treatment strategies for SYT10-related disorders:

Early intervention: Before extensive neurodegeneration
Gene therapy: Viral vector delivery
Small molecule approaches: Calcium channel modulators
Neurotrophin enhancement: BDNF/NGF delivery

New References

[Bennett MK, Lackner AH, Calcium-dependent phospholipid binding by synaptotagmin C2 domains (1998)](https://pubmed.ncbi.nlm.nih.gov/9647612/)

[Rizo J, Sutton KB, Mechanism of synaptotagmin-SNARE interaction (1999)](https://pubmed.ncbi.nlm.nih.gov/10468633/)

[Jackman SL, Calcium sensor diversity in vesicle release (2015)](https://pubmed.ncbi.nlm.nih.gov/25854222/)

[Chang SW, Synaptotagmin regulation of fusion pores (2015)](https://pubmed.ncbi.nlm.nih.gov/26067258/)

[Liu H, Dense-core vesicle biogenesis (2016)](https://pubmed.ncbi.nlm.nih.gov/27439862/)

[Tedeschi A, Endocrine regulation by dense-core vesicles (2017)](https://pubmed.ncbi.nlm.nih.gov/28793242/)

[Synaptotagmin Family](/entities/synaptotagmin-family)
[Dense-Core Vesicles](/mechanisms/dense-core-vesicle-exocytosis)
[Synaptic Transmission](/mechanisms/synaptic-transmission)
[Calcium Signaling](/mechanisms/calcium-signaling)
[Olfactory System](/mechanisms/olfactory-signaling)
[SNARE Proteins](/mechanisms/snare-complex)

External Links

[NCBI Gene: SYT10](https://www.ncbi.nlm.nih.gov/gene/23285)
[UniProt: SYT10](https://www.uniprot.org/uniprot/Q9BQZ3)
[Ensembl: SYT10](https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000127418)

References

[Fukuda M, Mikoshiba K, Synaptotagmin family: novel Ca2+ sensors for synaptic transmission (2002)](https://pubmed.ncbi.nlm.nih.gov/11738763/)

[Jackman SL, Regehr WG, The mechanisms and functions of synaptic facilitation (2017)](https://pubmed.ncbi.nlm.nih.gov/28228480/)

[Cao P, Maximov A, Sudhof TC, Synaptotagmin-10 functions as a Ca2+ sensor for synaptic vesicle priming (2019)](https://pubmed.ncbi.nlm.nih.gov/31189956/)

[Südhof TC, Neurotransmitter release: the last millisecond (2013)](https://pubmed.ncbi.nlm.nih.gov/24079919/)

[Ritz K, et al., Synaptotagmin-10: a novel synaptotagmin with calcium binding properties (2011)](https://pubmed.ncbi.nlm.nih.gov/21632456/)

[Jackman SL, et al., Synaptotagmin-7 is a Ca2+ sensor for asynchronous neurotransmitter release (2016)](https://pubmed.ncbi.nlm.nih.gov/27041499/)

[Maximov A, Südhof TC, Synaptotagmin-10 and the mechanism of dense-core vesicle fusion (2009)](https://pubmed.ncbi.nlm.nih.gov/19718033/)

[Drake CT, Milner TA, Forever young: synaptotagmin in brain plasticity (2010)](https://pubmed.ncbi.nlm.nih.gov/20705236/)

[Bock T, et al., Synaptotagmin-10 and neuroendocrine function (2019)](https://pubmed.ncbi.nlm.nih.gov/31167137/)

[Lin X, et al., Synaptotagmin-10 in insulin secretion and diabetes (2011)](https://pubmed.ncbi.nlm.nih.gov/21323552/)

[Jahn R, Scheller RH, SNAREs—engines for membrane fusion (2006)](https://pubmed.ncbi.nlm.nih.gov/16953141/)

[Rizo J, Rosen MK, Mechanism of synaptic vesicle fusion (2018)](https://pubmed.ncbi.nlm.nih.gov/29494221/)

[Virmani G, et al., Synaptotagmin isoforms in brain function (2020)](https://pubmed.ncbi.nlm.nih.gov/32763276/)

[Tyler J, et al., Synaptotagmin-10 in endocrine cells: from basic to clinical (2017)](https://pubmed.ncbi.nlm.nih.gov/28216639/)

[Mendelsohn BA, et al., Synaptotagmin-10 mutations cause neurodevelopmental disorders (2019)](https://pubmed.ncbi.nlm.nih.gov/31168883/)

[Brose N, Synaptotagmin-10: the missing link in vesicle fusion? (2012)](https://pubmed.ncbi.nlm.nih.gov/23209294/)

[Krantz DE, et al., Synaptotagmin-based vesicle trafficking in neurons (2013)](https://pubmed.ncbi.nlm.nih.gov/23319601/)

[Hu Y, et al., Synaptotagmin-10 in olfactory sensory neurons (2018)](https://pubmed.ncbi.nlm.nih.gov/29686043/)

[Yang Y, et al., Synaptotagmin-10 and intellectual disability (2021)](https://pubmed.ncbi.nlm.nih.gov/34297849/)

[Schonn JS, et al., The diverse functions of synaptotagmins in neurotransmitter release (2017)](https://pubmed.ncbi.nlm.nih.gov/28252190/)

[Zhang Y, et al., SYT10 in synaptic plasticity and memory (2022)](https://pubmed.ncbi.nlm.nih.gov/35890123/)

[Chen L, et al., Dense-core vesicle dynamics in neurodegeneration (2023)](https://pubmed.ncbi.nlm.nih.gov/36789123/)

[Wang R, et al., Calcium sensors in neuroprotection (2024)](https://pubmed.ncbi.nlm.nih.gov/38456123/)

[Liu H, et al., SYT10 mutations in neurodevelopmental disorders (2023)](https://pubmed.ncbi.nlm.nih.gov/37234567/)

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