UNC13A (Unc-13 Homolog A)

UNC13A (Unc-13 Homolog A)

title: "UNC13A \u2014 Unc-13 Homolog A"
description: "Page for UNC13A \u2014 Unc-13 Homolog A"
published: true
tags: kind:gene, section:genes, state:published

• evidence:strong

editor: markdown
pageId: 1515
dateCreated: '2026-02-27T23:21:04.661Z'
dateUpdated: '2026-03-24T01:43:54.304Z'
refs:
brown2022:
authors: Brown A-L, Wilkins OG, Keuss MJ, et al.
title: (2022). TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion
of UNC13A. Nature, 603:131-137. [DOI
year: 2022
doi: 10.1038/s41586-022-04436-3
ma2022:
authors: Ma XR, Prudencio M, Koike Y, et al.
title: (2022). TDP-43 represses cryptic exon inclusion in the FTD-ALS gene UNC13A.
Nature, 603:124-130. [DOI
year: 2022
doi: 10.1038/s41586-022-04424-7
koike2023:
authors: Koike Y, Pickles S, Estades Ayuso V, et al.
title: (2023). TDP-43 and other hnRNPs regulate cryptic exon inclusion of a key
ALS/FTD risk gene, UNC13A. PLOS Biology, 21(3):e3002028. [DOI
year: 2023
doi: 10.1371/journal.pbio.3002028
agra2024:
authors: Agra Almeida Quadros AR, Li Z, et al.
title: (2024). Cryptic splicing of stathmin-2 and UNC13A mRNAs is a pathological
hallmark of TDP-43-associated Alzheimer's Disease. Acta Neuropathologica,
147:9. [DOI
year: 2024
doi: 10.1007/s00401-023-02655-0
augustin1999:
title: "Augustin I, Rosenmund C, S\xFCdhof TC, Brose N. (1999). Munc13-1 is essential\
\ for fusion competence of glutamatergic synaptic vesicles.

...

UNC13A (Unc-13 Homolog A)

title: "UNC13A \u2014 Unc-13 Homolog A"
description: "Page for UNC13A \u2014 Unc-13 Homolog A"
published: true
tags: kind:gene, section:genes, state:published

• evidence:strong

editor: markdown
pageId: 1515
dateCreated: '2026-02-27T23:21:04.661Z'
dateUpdated: '2026-03-24T01:43:54.304Z'
refs:
brown2022:
authors: Brown A-L, Wilkins OG, Keuss MJ, et al.
title: (2022). TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion
of UNC13A. Nature, 603:131-137. [DOI
year: 2022
doi: 10.1038/s41586-022-04436-3
ma2022:
authors: Ma XR, Prudencio M, Koike Y, et al.
title: (2022). TDP-43 represses cryptic exon inclusion in the FTD-ALS gene UNC13A.
Nature, 603:124-130. [DOI
year: 2022
doi: 10.1038/s41586-022-04424-7
koike2023:
authors: Koike Y, Pickles S, Estades Ayuso V, et al.
title: (2023). TDP-43 and other hnRNPs regulate cryptic exon inclusion of a key
ALS/FTD risk gene, UNC13A. PLOS Biology, 21(3):e3002028. [DOI
year: 2023
doi: 10.1371/journal.pbio.3002028
agra2024:
authors: Agra Almeida Quadros AR, Li Z, et al.
title: (2024). Cryptic splicing of stathmin-2 and UNC13A mRNAs is a pathological
hallmark of TDP-43-associated Alzheimer's Disease. Acta Neuropathologica,
147:9. [DOI
year: 2024
doi: 10.1007/s00401-023-02655-0
augustin1999:
title: "Augustin I, Rosenmund C, S\xFCdhof TC, Brose N. (1999). Munc13-1 is essential\
\ for fusion competence of glutamatergic synaptic vesicles. Nature, 400:457-461.\
\ [DOI"
year: 1999
doi: 10.1038/22012
rhee2002:
authors: Rhee JS, Betz A, Bhola S, et al.
title: (2002). Beta phorbol ester- and diacylglycerol-induced augmentation of
transmitter release is mediated by Munc13s and not by PKCs. Cell, 108(1):121-133
year: 2002
doi: 10.1016/S0092-8674(02
van2009:
authors: van Es MA, Veldink JH, Saris CG, et al.
title: (2009). Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2
as susceptibility loci for sporadic amyotrophic lateral sclerosis. Nature Genetics,
41(10):1083-1087. [DOI
year: 2009
doi: 10.1038/ng.442
bhatt2025:
authors: Bhatt DK, et al.
title: (2025). Pathogenic UNC13A variants cause a neurodevelopmental syndrome
by impairing synaptic function. Nature Genetics. [DOI:10.1038/s41588-025-02361-5
year: 2025
doi: 10.1038/s41588-025-02361-5
deng2023:
authors: Deng L, et al.
title: (2023). Unc13A dynamically stabilizes vesicle priming at synaptic release
sites for short-term facilitation and homeostatic potentiation. Cell Reports,
42(5):112577. [DOI
year: 2023
doi: 10.1016/j.celrep.2023.112577
zhou2013:
authors: Zhou K, Bhargava A, Bhatt T, et al.
title: (2013). Position of UNC-13 in the active zone regulates synaptic vesicle
release probability and release kinetics. eLife, 2:e01180. [DOI
year: 2013
doi: 10.7554/eLife.01180
allen:
authors: '-'
title: Allen Brain Atlas
url: https://brain-map.org
allena:
authors: '-'
title: 'Allen Human Brain Atlas: UNC13A search'
url: https://human.brain-map.org/microarray/search/show?search_term=UNC13A
allenb:
authors: '-'
title: 'Allen Mouse Brain Atlas: UNC13A search'
url: https://mouse.brain-map.org/search/index.html?query=UNC13A
allenc:
authors: '-'
title: Allen Cell Type Atlas
url: https://portal.brain-map.org/atlases-and-data/rnaseq
brainspan:
authors: '-'
title: BrainSpan Developmental Transcriptome
url: https://www.brainspan.org
stmn:
title: "- stmn2 \u2014 The other major TDP-43 cryptic splicing target in ALS/FTD"
tardbp:
title: "- tardbp \u2014 Gene encoding TDP-43, the key regulator of UNC13A splicing"
tdp:
title: "- tdp-43 \u2014 Protein whose nuclear loss drives UNC13A cryptic exon\
\ inclusion"
tdpproteinopathy:
title: "- tdp-43-proteinopathy \u2014 Mechanism page on TDP-43 pathology"
als:
title: "- als \u2014 Disease where UNC13A risk variants are among strongest GWAS\
\ signals"
ftd:
title: "- ftd \u2014 Disease linked to UNC13A risk variants"
synapticdysfunction:
title: "- synaptic-dysfunction \u2014 Mechanism page on synaptic pathology"
motor:
title: ""- Motor Neurons/cell-types/motor-neurons \u2014 Cell type expressing\"
\ UNC13A at synapses## See Also"
genes:
title: ''- Genes Index''
alzheimers:
title: '- alzheimers'
parkinsons:
title: '- parkinsons'
alsa:
title: '- als'
ncbi:
authors: '-'
title: 'NCBI Gene: UNC13A'
url: https://www.ncbi.nlm.nih.gov/gene/23025
omim:
authors: '-'
title: 'OMIM: 609894'
url: https://www.omim.org/entry/609894
uniprot:
authors: '-'
title: 'UniProt: Q9UPW8'
url: https://www.uniprot.org/uniprot/Q9UPW8
ensembl:
authors: '-'
title: 'Ensembl: ENSG00000130477'
url: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000130477
genecards:
authors: '-'
title: 'GeneCards: UNC13A'
url: https://www.genecards.org/cgi-bin/carddisp.pl?gene=UNC13A
allend:
authors: '-'
title: 'Allen Brain Atlas: UNC13A'
url: https://human.brain-map.org/microarray/search/show?search_term=UNC13A

<table class="infobox infobox-gene">
<tr>
<th class="infobox-header" colspan="2">UNC13A — Unc-13 Homolog A</th>
</tr>
<tr> [@augustin1999]
<td class="label">Symbol</td> [@rhee2002]
<td><strong>UNC13A</strong></td> [@van2009]
</tr> [@bhatt2025]
<tr> [@deng2023]
<td class="label">Full Name</td> [@zhou2013]
<td>Unc-13 Homolog A (Munc13-1)</td> [@allen]
</tr> [@allena]
<tr> [@allenb]
<td class="label">Chromosome</td> [@allenc]
<td>19p13.11</td> [@brainspan]
</tr> [@stmn]
<tr> [@tardbp]
<td class="label">NCBI Gene</td> [@tdp]
<td><a href="https://www.ncbi.nlm.nih.gov/gene/23025" target="_blank">23025</a></td> [@tdpproteinopathy]
</tr> [@als]
<tr> [@ftd]
<td class="label">Ensembl</td> [@synapticdysfunction]
<td><a href="https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000130477" target="_blank">ENSG00000130477</a></td> [@motor]
</tr> [@genes]
<tr> [@alzheimers]
<td class="label">OMIM</td> [@parkinsons]
<td><a href="https://www.omim.org/entry/609894" target="_blank">609894</a></td> [@alsa]
</tr> [@ncbi]
<tr> [@omim]
<td class="label">UniProt</td> [@uniprot]
<td><a href="https://www.uniprot.org/uniprot/Q9UPW8" target="_blank">Q9UPW8</a></td> [@ensembl]
</tr> [@genecards]
<tr> [@allend]
<td class="label">Diseases</td>
<td>[ALS](/diseases/als), [FTD](/diseases/ftd), [Alzheimer's Disease](/diseases/alzheimers), [TDP-43 Proteinopathies](/mechanisms/tdp-43-proteinopathy)</td>
</tr>
<tr>
<td class="label">Expression</td>
<td>Presynaptic terminals, [Motor Neurons](/cell-types/motor-neurons), Cortical [Neurons](/entities/neurons), [Hippocampus](/brain-regions/hippocampus)</td>
</tr>
<tr>
<td class="label">Associated Diseases</td>
<td><a href="/wiki/alzheimer" style="color:#ef9a9a">ALZHEIMER</a>, <a href="/wiki/als" style="color:#ef9a9a">Als</a>, <a href="/wiki/alzheimer" style="color:#ef9a9a">Alzheimer</a>, <a href="/wiki/amyotrophic-lateral-sclerosis" style="color:#ef9a9a">Amyotrophic Lateral Sclerosis</a>, <a href="/wiki/dementia" style="color:#ef9a9a">Dementia</a></td>
</tr>
<tr>
<td class="label">KG Connections</td>
<td><a href="/atlas" style="color:#4fc3f7">83 edges</a></td>
</tr>
</table>

UNC13A (Unc-13 Homolog A)

Introduction

Unc13A — Unc 13 Homolog A is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.

Overview

UNC13A (Unc-13 Homolog A, also known as Munc13-1) is a gene on chromosome 19p13.11 encoding a presynaptic protein essential for synaptic vesicle priming and neurotransmitter release. The UNC13A protein is a critical component of the synaptic release machinery, acting downstream of vesicle docking to render synaptic vesicles fusion-competent at active zones ([Augustin et al., 1999](https://doi.org/10.1038/22012)). UNC13A has become one of the most important genes in [als](/diseases/als) and [ftd](/diseases/ftd) research following the discovery that common risk variants in UNC13A directly potentiate cryptic exon inclusion upon [tdp-43](/proteins/tdp-43) loss, providing the first mechanistic link between a GWAS risk locus and [tdp-43](/proteins/tdp-43) pathology ([Brown et al., 2022](https://pubmed.ncbi.nlm.nih.gov/35197626/); [Ma et al., 2022](https://doi.org/10.1038/s41586-022-04436-3)).

Together with [stmn2](/proteins/stmn2-protein), UNC13A represents one of the two most disease-relevant targets of [tdp-43](/proteins/tdp-43)-mediated cryptic splicing, and therapeutic strategies targeting UNC13A cryptic exon inclusion are under active development.

Function

Synaptic Vesicle Priming

UNC13A (Munc13-1) is the predominant Munc13 isoform at excitatory synapses in the mammalian brain. It functions as an essential synaptic vesicle priming factor by catalyzing the conformational transition of syntaxin-1 from a closed to an open state, enabling SNARE complex assembly between the vesicle membrane (VAMP2/synaptobrevin) and the presynaptic plasma membrane (syntaxin-1, SNAP-25). Without UNC13A, synaptic vesicles can dock at the active zone but cannot become fusion-competent ([Brose et al., 2000](https://doi.org/10.1016/S0896-6273(00)00038-8)).

Regulation of Neurotransmitter Release

UNC13A directly determines the size of the readily releasable pool (RRP) of synaptic vesicles and the probability of neurotransmitter release at individual synapses. Higher UNC13A levels correlate with larger RRP sizes and stronger synaptic transmission. During high-frequency stimulation, UNC13A supports rapid vesicle replenishment, sustaining synaptic transmission under conditions of heavy demand. UNC13A is regulated by diacylglycerol (DAG) through its C1 domain, linking it to the DAG/PKC second messenger pathway and providing a mechanism for activity-dependent potentiation of release ([Rhee et al., 2002](https://doi.org/10.1016/S0092-8674(02)00803-9)).

Short-Term Synaptic Plasticity

UNC13A is a key determinant of short-term [long-term-potentiation](/mechanisms/long-term-potentiation), particularly short-term facilitation. It dynamically stabilizes vesicle priming at release sites, and its activity-dependent modulation contributes to presynaptic forms of plasticity including post-tetanic potentiation and homeostatic potentiation ([Deng et al., 2023](https://doi.org/10.1016/j.celrep.2023.112577)).

Active Zone Organization

Within the active zone, the precise positioning of UNC13A molecules relative to calcium channels determines release probability and kinetics. UNC13A positioned closer to voltage-gated calcium channels supports fast, synchronous release with high probability, while more distally positioned molecules contribute to slower, asynchronous release ([Zhou et al., 2013](https://doi.org/10.7554/eLife.01180)).

Disease Associations

Genetic Risk for ALS and FTD

UNC13A harbors common intronic polymorphisms (rs12608932 and rs12973192) that are among the strongest genetic risk factors for sporadic [als](/diseases/als) and [ftd](/diseases/ftd), originally identified through genome-wide association studies (GWAS). The risk alleles confer approximately 1.2-1.3-fold increased odds of disease. Despite robust GWAS signals, the mechanism by which these non-coding variants contribute to disease remained mysterious until 2022.

TDP-43-Dependent Cryptic Exon Inclusion

Two landmark studies published simultaneously in 2022 revealed that [tdp-43](/proteins/tdp-43) normally represses a cryptic exon in UNC13A, and that the ALS/FTD risk SNPs overlap with [tdp-43](/proteins/tdp-43) binding sites within this region. When [tdp-43](/proteins/tdp-43) is depleted from the nucleus—as occurs in the majority of ALS and ~45% of FTD cases—a cryptic exon is included in UNC13A mRNA, leading to nonsense-mediated decay and loss of UNC13A protein ([Brown et al., 2022](https://pubmed.ncbi.nlm.nih.gov/35197626/); [Ma et al., 2022](https://doi.org/10.1038/s41586-022-04436-3)).

Critically, the ALS/FTD risk alleles potentiate this cryptic exon inclusion. Carriers of the risk haplotype show stronger cryptic exon inclusion upon [TDP-43](/mechanisms/tdp-43-proteinopathy) loss, both in cultured cells and in patient brain and spinal cord tissue. This elegant mechanism provides the first example of a GWAS risk variant acting through a TDP-43-dependent gain of cryptic splicing, directly linking genetic risk to the core molecular pathology of disease.

Regulatory Redundancy with hnRNPs

Beyond TDP-43, several heterogeneous nuclear ribonucleoproteins (hnRNPs) also repress UNC13A cryptic exon inclusion, including hnRNP L, hnRNP A1, and hnRNP A2B1. [These factors bind UNC13A RNA independently of TDP-43 and provide partial redundancy. Higher hnRNP L protein levels in patient brains correlate with lower UNC13A cryptic exon burden, suggesting that individual variation in hnRNP levels may modulate disease severity ([Koike et al., 2023](https://pubmed.ncbi.nlm.nih.gov/36930682/)).

Alzheimer's Disease

Like [stmn2](/proteins/stmn2-protein), UNC13A cryptic splicing has been detected in [alzheimers](/diseases/alzheimers-disease) brains with TDP-43 co-pathology. The levels of UNC13A cryptic exon RNA correlate with TDP-43 pathology burden but not with [Amyloid-Beta](/proteins/amyloid-beta) or [tau](/proteins/tau)[/proteins/[tau-protein](/proteins/tau) deposits, indicating that TDP-43-mediated UNC13A loss may contribute to synaptic dysfunction independently of classical AD pathology ([Agra Almeida Quadros et al., 2024](https://pubmed.ncbi.nlm.nih.gov/38175301/)).

Neurodevelopmental Syndromes

Rare pathogenic variants in UNC13A (missense and truncating mutations) cause a neurodevelopmental syndrome characterized by severe intellectual disability, epilepsy, and dyskinesia. These variants impair UNC13A's synaptic vesicle priming function, leading to profoundly reduced neurotransmitter release. This demonstrates that both gain of cryptic splicing (in neurodegeneration) and direct loss-of-function mutations (in neurodevelopment) converge on reduced UNC13A activity at synapses ([Bhatt et al., 2025](https://doi.org/10.1038/s41588-025-02361-5)).

Expression

UNC13A is expressed predominantly at excitatory presynaptic terminals throughout the mammalian brain:

• [cortex](/brain-regions/cortex) — excitatory glutamatergic synapses across all layers
• [hippocampus](/brain-regions/hippocampus) — CA3 mossy fiber terminals, CA1 Schaffer collateral synapses
• [motor-neurons](/cell-types/motor-neurons) — neuromuscular junction and spinal cord synapses
• [cerebellum](/brain-regions/cerebellum) — parallel fiber-Purkinje cell synapses
• [basal-ganglia](/brain-regions/basal-ganglia) — corticostriatal terminals

UNC13A expression is largely absent from inhibitory synapses, which instead express the related isoform UNC13B (Munc13-2). This differential expression pattern means that UNC13A loss preferentially affects excitatory neurotransmission.

Therapeutic Targeting

Antisense Oligonucleotides

ASOs targeting the UNC13A cryptic exon are in preclinical development. By blocking the cryptic splice site, these ASOs aim to prevent UNC13A mRNA degradation and restore UNC13A protein levels at synapses, even in the context of TDP-43 depletion. This approach is complementary to STMN2-targeting ASOs and may provide additive therapeutic benefit in combination.

Dual-Target Approaches

Because both STMN2 and UNC13A are major functional targets of TDP-43 loss, combination strategies targeting both cryptic exons simultaneously are under investigation. The rationale is that restoring both axonal maintenance (STMN2) and synaptic function (UNC13A) would address two distinct pathogenic consequences of TDP-43 dysfunction.

Brain Atlas Resources

• [Allen Brain Atlas](https://brain-map.org)
• [Allen Human Brain Atlas: UNC13A search](https://human.brain-map.org/microarray/search/show?search_term=UNC13A)
• [Allen Mouse Brain Atlas: UNC13A search](https://mouse.brain-map.org/search/index.html?query=UNC13A)
• [Allen Cell Type Atlas](https://portal.brain-map.org/atlases-and-data/rnaseq)
• [BrainSpan Developmental Transcriptome](https://www.brainspan.org)

See Also

• [Genes Index](/genes)
• [Amyotrophic Lateral Sclerosis](/diseases/als)
• [RNA Metabolism](/mechanisms/rna-metabolism)
• [Synaptic Transmission](/mechanisms/synaptic-transmission)

External Links

• [PubMed](https://pubmed.ncbi.nlm.nih.gov/)
• [NCBI Gene: UNC13A](https://www.ncbi.nlm.nih.gov/gene)
• [UniProt: UNC13A](https://www.uniprot.org)
• [OMIM: UNC13A](https://www.omim.org)

Background

The study of Unc13A — Unc 13 Homolog A has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.

Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.

References

[Brown A-L, Wilkins OG, Keuss MJ, et al., (2022). TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A. Nature, 603:131-137. [DOI (2022)](https://doi.org/10.1038/s41586-022-04436-3)

[Ma XR, Prudencio M, Koike Y, et al., (2022). TDP-43 represses cryptic exon inclusion in the FTD-ALS gene UNC13A. Nature, 603:124-130. [DOI (2022)](https://doi.org/10.1038/s41586-022-04424-7)

[Koike Y, Pickles S, Estades Ayuso V, et al., (2023). TDP-43 and other hnRNPs regulate cryptic exon inclusion of a key ALS/FTD risk gene, UNC13A. PLOS Biology, 21(3):e3002028. [DOI (2023)](https://doi.org/10.1371/journal.pbio.3002028)

[Agra Almeida Quadros AR, Li Z, et al., (2024). Cryptic splicing of stathmin-2 and UNC13A mRNAs is a pathological hallmark of TDP-43-associated Alzheimer's Disease. Acta Neuropathologica, 147:9. [DOI (2024)](https://doi.org/10.1007/s00401-023-02655-0)

[Unknown, Augustin I, Rosenmund C, Südhof TC, Brose N. (1999). Munc13-1 is essential for fusion competence of glutamatergic synaptic vesicles. Nature, 400:457-461. [DOI (1999)](https://doi.org/10.1038/22012)

[Rhee JS, Betz A, Bhola S, et al., (2002). Beta phorbol ester- and diacylglycerol-induced augmentation of transmitter release is mediated by Munc13s and not by PKCs. Cell, 108(1):121-133 (2002)](https://doi.org/10.1016/S0092-8674(02)

[van Es MA, Veldink JH, Saris CG, et al., (2009). Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis. Nature Genetics, 41(10):1083-1087. [DOI (2009)](https://doi.org/10.1038/ng.442)

[Bhatt DK, et al., (2025). Pathogenic UNC13A variants cause a neurodevelopmental syndrome by impairing synaptic function. Nature Genetics. [DOI:10.1038/s41588-025-02361-5 (2025)](https://doi.org/10.1038/s41588-025-02361-5)

[Deng L, et al., (2023). Unc13A dynamically stabilizes vesicle priming at synaptic release sites for short-term facilitation and homeostatic potentiation. Cell Reports, 42(5):112577. [DOI (2023)](https://doi.org/10.1016/j.celrep.2023.112577)

[Zhou K, Bhargava A, Bhatt T, et al., (2013). Position of UNC-13 in the active zone regulates synaptic vesicle release probability and release kinetics. eLife, 2:e01180. [DOI (2013)](https://doi.org/10.7554/eLife.01180)

-, Allen Brain Atlas (n.d.)

-, Allen Human Brain Atlas: UNC13A search (n.d.)

-, Allen Mouse Brain Atlas: UNC13A search (n.d.)

-, Allen Cell Type Atlas (n.d.)

-, BrainSpan Developmental Transcriptome (n.d.)

Unknown, - stmn2 — The other major TDP-43 cryptic splicing target in ALS/FTD (n.d.)

Unknown, - tardbp — Gene encoding TDP-43, the key regulator of UNC13A splicing (n.d.)

Unknown, - tdp-43 — Protein whose nuclear loss drives UNC13A cryptic exon inclusion (n.d.)

Unknown, - tdp-43-proteinopathy — Mechanism page on TDP-43 pathology (n.d.)

Unknown, - als — Disease where UNC13A risk variants are among strongest GWAS signals (n.d.)

Unknown, - ftd — Disease linked to UNC13A risk variants (n.d.)

Unknown, - synaptic-dysfunction — Mechanism page on synaptic pathology (n.d.)

Unknown, - Motor [Neurons/cell-types/[motor-neurons — Cell type expressing UNC13A at synapses## See Also (n.d.)

Unknown, - [Genes Index (n.d.)

Unknown, - alzheimers (n.d.)

Unknown, - parkinsons (n.d.)

Unknown, - als (n.d.)

-, NCBI Gene: UNC13A (n.d.)

-, OMIM: 609894 (n.d.)

-, UniProt: Q9UPW8 (n.d.)

-, Ensembl: ENSG00000130477 (n.d.)

-, GeneCards: UNC13A (n.d.)

-, Allen Brain Atlas: UNC13A (n.d.)

Pathway Diagram

The following diagram shows the key molecular relationships involving unc13a discovered through SciDEX knowledge graph analysis:

Pathway Diagram

The following diagram shows the key molecular relationships involving UNC13A (Unc-13 Homolog A) discovered through SciDEX knowledge graph analysis: