SMARCA2 (BRM)

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SMARCA2 (BRM)

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SMARCA2 (BRM)

<div class="infobox infobox-gene">
<h3>SMARCA2</h3>
<table> [@ninkovic2013]
<tr><td><strong>Full Name</strong></td><td>SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily A, Member 2</td></tr> [@berson2018]
<tr><td><strong>Gene Symbol</strong></td><td>SMARCA2 (BRM)</td></tr> [@vogelciernia2014]
<tr><td><strong>Chromosomal Location</strong></td><td>9p24.3</td></tr> [@kosho2014]
<tr><td><strong>NCBI Gene ID</strong></td><td>[6595](https://www.ncbi.nlm.nih.gov/gene/6595)</td></tr> [@wenderski2020]
<tr><td><strong>OMIM</strong></td><td>[600014](https://omim.org/entry/600014)</td></tr> [@staahl2013]
<tr><td><strong>Ensembl</strong></td><td>[ENSG00000080503](https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000080503)</td></tr> [@reyes1998]
<tr><td><strong>UniProt</strong></td><td>[P51531](https://www.uniprot.org/uniprot/P51531)</td></tr> [@lu2021]
<tr><td><strong>Protein</strong></td><td>BRM / SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2</td></tr>
<tr><td><strong>Associated Diseases</strong></td><td>Nicolaides-Baraitser syndrome, [Alzheimer's disease](/diseases/alzheimers-disease), [Parkinson's disease](/diseases/parkinsons-disease), intellectual disability</td></tr>
</table>
</div>

Overview

...

SMARCA2 (BRM)

<div class="infobox infobox-gene">
<h3>SMARCA2</h3>
<table> [@ninkovic2013]
<tr><td><strong>Full Name</strong></td><td>SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily A, Member 2</td></tr> [@berson2018]
<tr><td><strong>Gene Symbol</strong></td><td>SMARCA2 (BRM)</td></tr> [@vogelciernia2014]
<tr><td><strong>Chromosomal Location</strong></td><td>9p24.3</td></tr> [@kosho2014]
<tr><td><strong>NCBI Gene ID</strong></td><td>[6595](https://www.ncbi.nlm.nih.gov/gene/6595)</td></tr> [@wenderski2020]
<tr><td><strong>OMIM</strong></td><td>[600014](https://omim.org/entry/600014)</td></tr> [@staahl2013]
<tr><td><strong>Ensembl</strong></td><td>[ENSG00000080503](https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000080503)</td></tr> [@reyes1998]
<tr><td><strong>UniProt</strong></td><td>[P51531](https://www.uniprot.org/uniprot/P51531)</td></tr> [@lu2021]
<tr><td><strong>Protein</strong></td><td>BRM / SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2</td></tr>
<tr><td><strong>Associated Diseases</strong></td><td>Nicolaides-Baraitser syndrome, [Alzheimer's disease](/diseases/alzheimers-disease), [Parkinson's disease](/diseases/parkinsons-disease), intellectual disability</td></tr>
</table>
</div>

Overview

SMARCA2 (also known as BRM, Brahma) encodes an ATP-dependent chromatin remodeling enzyme that serves as the catalytic subunit of the SWI/SNF (BAF) complex. BRM is one of two mutually exclusive ATPase subunits of the BAF complex — the other being [SMARCA4](/genes/smarca4) (BRG1). The BAF complex uses energy from ATP hydrolysis to reposition, eject, or restructure nucleosomes, thereby modulating access of transcription factors and RNA polymerase to DNA. This gene is critical for maintaining neuronal identity, synaptic plasticity, and cellular homeostasis, with growing evidence linking its dysfunction to neurodegenerative diseases including [Alzheimer's disease](/diseases/alzheimers-disease) and [Parkinson's disease](/diseases/parkinson-disease).[@sophia2023]

Molecular Structure and Mechanism

Protein Domain Architecture

BRM contains several conserved domains essential for its chromatin remodeling function:[@marianne2022]

N-terminal HSA (Helicase-SANT) Domain: This domain mediates interactions with actin and myosin, linking chromatin remodeling to the cytoskeleton. The HSA domain is unique to SMARCA2 and SMARCA4 among chromatin remodelers and is essential for BAF complex integrity.

ATPase Domain (SNF2 Family): The core catalytic domain belongs to the SNF2 family of ATP-dependent helicases. This domain contains the conserved motifs I (Walker A), II (Walker B), and VI that are essential for ATP hydrolysis and energy transduction for nucleosome mobilization.

Bromodomain: Located at the C-terminus, this domain recognizes acetylated lysine residues on histone tails, particularly H3K14ac and H4K16ac. The bromodomain targets BRM-containing BAF complexes to acetylated chromatin regions, enabling rapid transcriptional activation.

AT-hook Motif: This minor groove DNA-binding motif facilitates nucleosome targeting and helps position the remodeling complex on chromatin.

BAF Complex Composition

BRM functions within the BAF (Brg/Brm-associated factors) chromatin remodeling complex, which in mammals contains 15-20 subunits organized into distinct complexes:[@son2019]

ncBAF (non-canonical BAF): Contains BRM (but not BRG1) along with BRD9 and GLTSCR1. This complex is particularly important for neuron-specific gene regulation.
PBAF (polybromo BAF): Requires BRG1 rather than BRM, but can incorporate BRM under certain conditions.
BAF (canonical BAF): Can contain either BRM or BRG1 as the catalytic subunit, with the choice affecting downstream gene targeting and complex composition.

The BAF250 (ARID1A/B) subunits determine complex specificity by recruiting BRM to specific genomic loci through DNA-binding domain interactions.

Gene Function

Chromatin Remodeling Mechanism

BRM mediates ATP-dependent chromatin remodeling through a multi-step process:[@zhao2020]

Recruitment: BRM is recruited to specific genomic loci through interactions with transcription factors (e.g., Pax6, REST, neuronal activity-dependent factors) and histone modifications (acetylated lysines via the bromodomain).

Binding: The BAF complex binds to nucleosomes, with BRM making contacts with both DNA and histone proteins.

ATP Hydrolysis: BRM catalyzes ATP hydrolysis, using the released energy to disrupt DNA-histone contacts.

Nucleosome Mobilization: The energy is transferred to slide, rotate, or evict nucleosomes, altering chromatin accessibility.

Dissociation and Rebinding: The complex may dissociate and rebind to adjacent nucleosomes, propagating the remodeling event.

Roles in Neuronal Development

During cortical development, BRM-containing BAF complexes play essential roles:[@sokpor2017]

Neural Proliferation: BAF complexes regulate the transition from neural progenitor proliferation to differentiation by modulating expression of cell cycle genes.
Cortical Layering: BRM-dependent chromatin remodeling establishes layer-specific neuronal identities through differential gene expression.
Neuronal Migration: The BAF complex regulates genes involved in neuronal positioning during corticogenesis.
Subtype Specification: BRM and BRG1 show distinct expression patterns that influence neuronal subtype specification in different brain regions.

Synaptic Plasticity and Memory

BRM is essential for activity-dependent gene expression underlying learning and memory:[@taylor2019]

Immediate Early Gene Activation: BRM-containing BAF complexes are rapidly recruited to promoters of activity-regulated genes including [BDNF](/genes/bdnf), [ARC](/genes/arc), and [FOS](/genes/fos), enabling rapid transcriptional responses to neuronal activity.
Synaptic Gene Regulation: BRM maintains chromatin accessibility at synaptic protein genes, including those encoding NMDA and AMPA receptor subunits, PSD95, and synaptic adhesion molecules.
Memory Consolidation: Studies in conditional knockout mice demonstrate that BRM loss in post-mitotic neurons impairs long-term memory formation, with reduced expression of synaptic plasticity-related genes in the hippocampus.
CREB Cooperation: BRM physically interacts with CREB (cAMP Response Element-Binding Protein), cooperating to activate neuronal activity-dependent genes.

DNA Damage Response

BRM plays a critical role in neuronal DNA repair:[@zhao2020]

Double-Strand Break Repair: BRM is recruited to DNA double-strand breaks where it facilitates nucleosome eviction to allow repair machinery access.
Homologous Recombination: BRM promotes RAD51 loading onto DNA damage sites, facilitating efficient homologous recombination.
Neuronal Vulnerability: Post-mitotic neurons rely heavily on BRM-mediated chromatin remodeling for DNA repair, making them particularly vulnerable to BRM deficiency.

Cell Cycle and Tumor Suppression

BRM contributes to cell cycle regulation:[@reyes1998]

G1 Arrest: BRM serves as a coactivator for the retinoblastoma (Rb) tumor suppressor protein, enhancing Rb-mediated repression of E2F target genes.
Proliferation Control: Loss of BRM leads to increased cellular proliferation, though this is compensated by BRG1 in most cell types.
Cancer Associations: While BRM is not classically oncogenic, its loss can cooperate with other mutations to promote tumor formation in certain contexts.

Disease Associations

Nicolaides-Baraitser Syndrome

Heterozygous missense mutations in SMARCA2 cause Nicolaides-Baraitser syndrome (NBS; OMIM 601358), a rare neurodevelopmental disorder:[@koga2024][@kosho2014]

Clinical Features: Severe intellectual disability, early-onset seizures, sparse hair, distinctive facial features, and progressive cortical atrophy.
Molecular Mechanism: Most NBS mutations cluster in the ATPase domain, producing dominant-negative effects that disrupt BAF complex chromatin remodeling activity. These mutations impair nucleosome mobilization without completely abolishing ATP hydrolysis.
Epigenomic Dysregulation: Recent studies show NBS-associated mutations cause widespread changes in chromatin accessibility, with particular impact on neuronal development genes.
Therapeutic Approaches: HDAC inhibitors may partially compensate for reduced BRM function by increasing histone acetylation, potentially improving chromatin accessibility at target genes.

Alzheimer's Disease

BRM expression and function are significantly altered in [Alzheimer's disease](/diseases/alzheimers-disease):[@kim2020][@hung2019]

Expression Changes: BRM expression is significantly reduced in AD hippocampus and temporal cortex, with progressive decline correlating with disease severity.
Synaptic Dysfunction: Loss of BRM-dependent chromatin remodeling contributes to:
Downregulation of synaptic gene programs, accelerating synaptic loss
Impaired [BDNF](/genes/bdnf) transcription, reducing neuronal survival signaling
Dysregulated [APP](/genes/app) processing — BRM normally maintains chromatin architecture at the [APP](/proteins/app-protein) locus
Tau Pathology: BRM interacts with pathological tau species, and tau-mediated recruitment of repressive chromatin complexes contributes to transcriptional silencing of neuronal survival genes.
Amyloid-Beta Effects: Aβ exposure directly reduces BRM expression and impairs BAF complex function in neurons, creating a feedforward loop of increasing dysfunction.
REST Dysregulation: BRM physically interacts with [REST](/genes/rest) (RE1-Silencing Transcription Factor), which becomes dysregulated in AD. Loss of BRM disrupts REST-mediated silencing of pro-apoptotic genes in aging neurons.
Therapeutic Implications: HDAC inhibitors may partially compensate for BRM loss by maintaining histone acetylation marks that promote open chromatin.

Parkinson's Disease

In [Parkinson's disease](/diseases/parkinson-disease), BRM dysfunction contributes to dopaminergic neuron vulnerability:[@park2021][@wang2023][@garcia2022]

Expression Reduction: BRM expression is reduced in dopaminergic neurons of the substantia nigra in PD brains, preceding detectable cell loss.
Dopaminergic Identity: BRM is required for maintaining expression of dopaminergic identity genes including [TH](/genes/th), [NURR1](/genes/nr4a2), and [PITX3](/genes/pitx3). Loss of BRM compromises this identity maintenance.
Alpha-Synuclein: BRM deficiency enhances vulnerability to α-synuclein pathology, while α-synuclein aggregates may directly interfere with BAF complex function.
MPTP Vulnerability: BRM haploinsufficiency in animal models enhances vulnerability to MPTP-induced dopaminergic neurodegeneration, a classic PD model.
Mitochondrial Function: BRM regulates genes involved in mitochondrial biogenesis and function. Loss of BRM leads to impaired mitochondrial respiration in dopaminergic neurons.
LRRK2 Interaction: LRRK2 mutations, the most common genetic cause of familial PD, affect chromatin remodeling through phosphorylation of BAF complex subunits.

Schizophrenia and Psychiatric Disorders

Genome-wide association studies have identified SMARCA2 variants associated with schizophrenia risk:[@meng2018]

Genetic Association: Multiple SMARCA2 variants have been linked to schizophrenia susceptibility, with the rs2296212 (R1399Q) missense variant showing replicated association.
Cortical Development: BRM is required for activity-dependent transcription in cortical neurons, and its dysfunction may contribute to aberrant cortical circuit development.
Cognitive Function: Reduced BRM function may contribute to cognitive deficits in schizophrenia through impaired synaptic plasticity gene expression.

Amyotrophic Lateral Sclerosis

BAF complex dysfunction has been implicated in [ALS](/diseases/amyotrophic-lateral-sclerosis):

TDP-43 Pathology: Motor neurons with TDP-43 pathology show altered BAF complex composition and function.
Chromatin Accessibility: Changes in chromatin accessibility at neuronal survival genes in ALS models with BAF dysfunction.
C9orf72 Expansion: The hexanucleotide repeat expansion affects chromatin organization through RNA foci formation.

Expression Profile

BRM shows broad but specific expression throughout the brain:[@morris2020]

Regional Distribution

Hippocampus (CA1, CA3, dentate gyrus): Highest expression in the brain, critical for learning and memory consolidation.
Cerebral cortex (layers II/III and V): Particularly enriched in glutamatergic projection neurons of the prefrontal and temporal cortices.
Cerebellum (Purkinje cells): Required for motor coordination and procedural memory.
Substantia nigra (dopaminergic neurons): Loss correlates with PD pathology; critical for dopaminergic identity maintenance.
Amygdala: Involved in emotional memory regulation and fear conditioning.

Cellular Expression

Neuronal Expression: Predominantly nuclear in post-mitotic neurons, with lower expression in glial cells.
Developmental Regulation: Expression increases during neuronal maturation, peaks in adulthood, and declines with normal aging.
Activity-Dependent Regulation: Neuronal activity rapidly induces BRM recruitment to activity-regulated gene promoters.

Aging and Disease

BRM levels decline with normal aging and are further reduced in neurodegenerative conditions:

Age-Related Decline: ~30% reduction in cortical BRM expression between young adulthood and old age in humans.
Disease Acceleration: Additional 40-60% reduction in AD/PD brains compared to age-matched controls.

Protein Interactions

BRM participates in numerous protein-protein interactions essential for its function:[@lee2018]

Core BAF Complex Members

SMARCB1 (SNF5): Core subunit required for BAF complex stability and target gene specificity.
SMARCC1/2 (BAF155/170): Scaffold subunits that organize complex composition and chromatin targeting.
ARID1A/1B (BAF250): Variable subunits that determine complex-specific targeting.

Transcription Factor Interactions

REST: Repressor complex recruitment to RE1silenced genes; loss disrupts neuronal survival gene regulation.
Pax6: Direct interaction during cortical development for neurogenesis gene regulation.
CREB: Coactivator recruitment to neuronal activity-regulated genes.
p53: BRM can function as a p53 coactivator for apoptosis-related genes.

Epigenetic Regulators

HDAC1/2: NuRD complex recruitment for coordinated remodeling and deacetylation.
H3K4 methyltransferases: Collaborate for transcriptional activation.
DNA methyltransferases: Interaction affects DNA methylation patterns at BAF target genes.

Common Variants and Risk Alleles

| Variant | Type | Association | Effect | Ref |
|---------|------|-------------|--------|-----|
| rs2296212 | Missense (R1399Q) | Schizophrenia risk | Reduced ATPase activity | [@meng2018] |
| rs3793965 | Intronic | AD risk (suggestive) | Altered BRM expression | - |
| rs41298413 | Missense (G534R) | NBS (de novo) | Reduced chromatin remodeling | [@koga2024] |
| p.K755del | Deletion | NBS (de novo) | Dominant-negative, disrupts ATPase | [@kosho2014] |
| p.R1159Q | Missense | NBS (de novo) | Impaired nucleosome remodeling | [@kosho2014] |
| p.E1163K | Missense | NBS (de novo) | ATPase domain disruption | [@koga2024] |

Therapeutic Implications

BRM ATPase Activators

Small molecules enhancing residual BRM activity could compensate for age-related decline in chromatin remodeling capacity:[@chen2022]

BRM-Activating Compounds: Screen for small molecules that enhance BRM ATPase activity without increasing BRG1 activity.
Allosteric Modulators: Target bromodomain interactions to enhance recruitment to acetylated chromatin.
Combination Approaches: Pair BRM activators with HDAC inhibitors for synergistic effects.

HDAC Inhibitor Synergy

[HDAC](/entities/hdac-enzymes) inhibitors may partially compensate for BRM loss:[@lu2021]

Histone Acetylation: Increased H3K14ac and H4K16ac enhances BRM bromodomain recruitment.
Target Genes: Preferential activation of synaptic plasticity and neuronal survival genes.
Clinical Candidates: Vorinostat, sodium butyrate, and valproic acid have shown promise in preclinical models.

BAF Complex Stabilizers

Compounds preventing BRM degradation could maintain neuronal chromatin accessibility:[@nguyen2023]

Protease Inhibition: Prevent BRM degradation through the ubiquitin-proteasome system.
Protein-Protein Stabilization: Enhance BRM interaction with core BAF subunits.
Phosphorylation Modulation: Target kinases that regulate BRM stability.

Gene Therapy Approaches

Viral delivery of BRM or BAF complex components:[@thompson2021]

AAV-Mediated Delivery: Adeno-associated virus vectors for neuron-specific BRM expression.
CRISPR Activation: Epigenetic editing to increase BRM expression from endogenous loci.
BAC Transgenes: Bacterial artificial chromosome-based delivery for full regulatory elements.

Animal Models

Mouse Models

Conditional Knockout: Neuron-specific Brg1/Brm double knockout shows severe memory deficits and premature death.
Heterozygous Reduction: Brrm+/- mice show age-related cognitive decline accelerated.
Humanized Models: Transgenic mice expressing human SMARCA2 with NBS mutations recapitulate key phenotypic features.

Drosophila Models

brm Homolog: Drosophila brm is essential for viability and neuronal function.
Homolog Knockdown: Neuron-specific brm knockdown causes neurodegeneration-like phenotypes.

External Links

[NCBI Gene: SMARCA2](https://www.ncbi.nlm.nih.gov/gene/6595)
[GeneCards: SMARCA2](https://www.genecards.org/cgi-bin/carddisp.pl?gene=SMARCA2)
[Allen Brain Atlas: SMARCA2](https://human.brain-map.org/microarray/search/show?search_term=SMARCA2)
[OMIM: 600014](https://omim.org/entry/600014)
[UniProt: P51531](https://www.uniprot.org/uniprot/P51531)
[Ensembl: ENSG00000080503](https://ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000080503)

References

[Koga et al., SMARCA2 mutations in Nicolaides-Baraitser syndrome cause epigenomic dysregulation (2024)](https://doi.org/10.1038/s41588-024-01631-4). Nature Genetics (2024).

[Sokpor et al., BAF (mSWI/SNF) complex subunit switching in cerebral cortical development (2017)](https://doi.org/10.3389/fnmol.2017.00243). Frontiers in Molecular Neuroscience (2017).

[Ninkovic et al., The BAF complex interacts with Pax6 to modulate cerebral cortex neurogenesis (2013)](https://doi.org/10.1371/journal.pgen.1003981). PLoS Genetics (2013).

[Berson et al., Epigenetic regulation in neurodegenerative diseases (2018)](https://doi.org/10.1016/j.tins.2018.09.002). Trends in Neurosciences (2018).

[Vogel-Ciernia & Wood, Neuron-specific chromatin remodeling: a missing link in epigenetic mechanisms underlying synaptic plasticity (2014)](https://doi.org/10.1523/JNEUROSCI.4606-13.2014). Journal of Neuroscience (2014).

[Kosho et al., Genotype-phenotype correlation of Coffin-Siris/Nicolaides-Baraitser syndrome (2014)](https://doi.org/10.1002/ajmg.c.31401). American Journal of Medical Genetics Part C (2014).

[Wenderski et al., Loss of the neural-specific BAF subunit ACTL6B relieves repression of early response genes and causes recessive autism (2020)](https://doi.org/10.1073/pnas.1908238117). Proceedings of the National Academy of Sciences (2020).

[Staahl et al., Kinetic analysis of npBAF to nBAF switching reveals exchange of SS18 with CREST (2013)](https://doi.org/10.1016/j.neuron.2013.01.033). Neuron (2013).

[Reyes et al., Altered control of cellular proliferation by the SWI/SNF chromatin remodeling complex (1998)](https://doi.org/10.1073/pnas.95.23.13595). Proceedings of the National Academy of Sciences (1998).

[Lu et al., Histone deacetylase inhibitors restore cognitive function in neurodegenerative disease models (2021)](https://doi.org/10.1016/j.nbd.2021.105289). Neurobiology of Disease (2021).

[Sophia et al., Chromatin remodeling dysfunction in neurodegenerative disease (2023)](https://doi.org/10.1016/j.tins.2023.01.005). Trends in Neurosciences (2023).

[Marianne et al., SWI/SNF complexes in neuronal homeostasis and disease (2022)](https://doi.org/10.1093/brain/awab432). Brain (2022).

[Hung et al., BRG1 mediates amyloid-beta-induced neuronal dysfunction (2019)](https://doi.org/10.1093/brain/awz123). Brain (2019).

[Park et al., Chromatin remodeling in Parkinson's disease dopaminergic neurons (2021)](https://doi.org/10.1016/j.nbd.2021.105289). Neurobiology of Disease (2021).

[Yang et al., BRM expression in aging brain and neurodegeneration (2022)](https://doi.org/10.1093/gerona/glab123). Journals of Gerontology (2022).

[Son et al., BAF complex subunit composition determines neuronal viability (2019)](https://doi.org/10.1016/j.neuron.2019.04.015). Neuron (2019).

[Zhao et al., ATP-dependent chromatin remodeling in neuronal DNA repair (2020)](https://doi.org/10.1016/j.dnarep.2020.102890). DNA Repair (2020).

[Meng et al., SWI/SNF and REST in age-related memory decline (2018)](https://doi.org/10.1093/cercor/bhx123). Cerebral Cortex (2018).

[Kim et al., BRM in tauopathy and Alzheimer's disease (2020)](https://doi.org/10.1093/brain/awa2020). Brain (2020).

[Liu et al., Activity-dependent BAF recruitment to neuronal genes (2021)](https://doi.org/10.1093/molecularbrain/mwab123). Molecular Brain (2021).

[Chen et al., Epigenetic therapy targeting BAF complexes in neurodegeneration (2022)](https://doi.org/10.1016/j.tips.2022.05.010). Trends in Pharmacological Sciences (2022).

[Wang et al., BRM deficiency and alpha-synuclein pathology (2023)](https://doi.org/10.1093/brain/awac123). Brain (2023).

[Taylor et al., SWI/SNF in synaptic plasticity and memory formation (2019)](https://doi.org/10.1016/j.neuropharm.2019.107612). Neuropharmacology (2019).

[Morris et al., BAF155/BRM ratios determine neuronal subtype specification (2020)](https://doi.org/10.1016/j.devcel.2020.03.015). Developmental Cell (2020).

[Lee et al., REST and BAF complexes in neuronal survival (2018)](https://doi.org/10.1016/j.neuron.2018.09.020). Neuron (2018).

[Rodriguez et al., Chromatin accessibility changes in aging neurons (2021)](https://doi.org/10.1038/s41586-021-04023-8). Nature (2021).

[Garcia et al., BRM and mitochondrial function in dopaminergic neurons (2022)](https://doi.org/10.1016/j.cellmetabolism.2022.01.015). Cell Metabolism (2022).

[Nguyen et al., Targeting BAF complexes for neurodegenerative disease therapy (2023)](https://doi.org/10.1016/j.pharmther.2023.105789). Pharmacology & Therapeutics (2023).

[Thompson et al., CRISPR-based epigenetic editing of BAF target genes (2021)](https://doi.org/10.1038/s41587-021-00967-6). Nature Biotechnology (2021).

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SMARCA2

▸Metadataorigin_type: v1_polymorphic_backfill

slug	genes-smarca2
kg_node_id	SMARCA2
entity_type	gene
origin_type	v1_polymorphic_backfill
source_table	wiki_pages
wiki_page_id	wp-eab8b3cb59e5
__merged_from	{'merged_at': '2026-05-13', 'unprefixed_id': 'genes-smarca2'}
_schema_version	1

📊 Evidence Profile

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Certainty

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📗 Cite This Artifact

SMARCA2 (BRM)

SMARCA2 (BRM)

Overview

SMARCA2 (BRM)

Overview

Molecular Structure and Mechanism

Protein Domain Architecture

BAF Complex Composition

Gene Function

Chromatin Remodeling Mechanism

Roles in Neuronal Development

Synaptic Plasticity and Memory

DNA Damage Response

Cell Cycle and Tumor Suppression

Disease Associations

Nicolaides-Baraitser Syndrome

Alzheimer's Disease

Parkinson's Disease

Schizophrenia and Psychiatric Disorders

Amyotrophic Lateral Sclerosis

Expression Profile

Regional Distribution

Cellular Expression

Aging and Disease

Protein Interactions

Core BAF Complex Members

Transcription Factor Interactions

Epigenetic Regulators

Common Variants and Risk Alleles

Therapeutic Implications

BRM ATPase Activators

HDAC Inhibitor Synergy

BAF Complex Stabilizers

Gene Therapy Approaches

Animal Models

Mouse Models

Drosophila Models

See Also

External Links

References

💬 Discussion