Affinage

SMARCA2

SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2 · UniProt P51531

Length
1590 aa
Mass
181.3 kDa
Annotated
2026-06-10
100 papers in source corpus 41 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCA2 (BRM/hBRM) is the DNA-dependent ATPase catalytic subunit of a class of human SWI/SNF chromatin-remodeling complexes that uses ATP hydrolysis to remodel nucleosomal arrays and govern transcription during differentiation, cell-cycle control, and tumor suppression (PMID:11238380, PMID:7739891). Purified hBRM-containing complexes increase restriction-enzyme accessibility on nucleosomal arrays and hydrolyze ATP in a DNA-dependent manner, though they are markedly less active than BRG1/SMARCA4-containing complexes, and they incorporate the co-repressor mSin3A (PMID:11238380). Chromatin targeting is multivalent: an AT-hook-like domain tethers BRM to chromatin and is required for cooperation with the glucocorticoid receptor, while the bromodomain shows modest H3K14ac preference and, with the adjacent AT-hook, binds AT-rich DNA, contributing to stable promoter occupancy (PMID:10330133, PMID:28706277). BRM acts as a cofactor that is recruited by, and confers specificity through, partners distinct from those used by BRG1 — including the pRB family, which bridges BRM to E2F1 to repress proliferative genes and impose growth arrest, and a series of sequence-specific factors (SHP, STAT1, Notch-associated ankyrin proteins, Cdx2, Sp1, NF-κB p52 via the REQ/DPF2 adaptor) that direct it to specific promoters and enhancers for either activation or repression, frequently via recruitment of co-repressors such as HDAC1 (PMID:9326598, PMID:8657132, PMID:19805516, PMID:21079652, PMID:19371634, PMID:20460684, PMID:19144648, PMID:30946989). BRM activity and abundance are regulated post-translationally and epigenetically — it is cleaved during apoptosis by cathepsin G to release it from the nuclear matrix, phosphorylated and excluded from chromosomes during mitosis, and silenced in many cancers through HDAC/MEF2-dependent promoter polymorphisms and PRC2-mediated H3K27me3 despite an intact, mutation-free gene (PMID:11259672, PMID:8670841, PMID:21478907, PMID:29087303, PMID:16007216). In SMARCA4-mutant cancers, residual SMARCA2-containing SWI/SNF complexes become essential for proliferation, defining a synthetic-lethal dependency exploitable by selective SMARCA2 PROTAC degraders and allosteric ATPase inhibitors (PMID:24421395, PMID:24520176, PMID:36216795, PMID:30339381). Genetic variants reducing SMARCA2 nuclear localization and expression are associated with schizophrenia-relevant behavioral phenotypes (PMID:19363039).

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 1993 Medium

    Established SMARCA2 as a nuclear transcriptional co-activator, answering whether the human BRM protein had a transcriptional function and revealing it requires both a helicase-homology domain and partner DNA-binding factors.

    Evidence Transfection of hBRM into hBRM-deficient cells with GR reporter transactivation and domain-deletion mapping

    PMID:8223438

    Open questions at the time
    • Did not establish enzymatic mechanism or complex membership
    • Cooperation with GR shown on reporters, not native loci
  2. 1995 Medium

    Placed hBRM within a multi-subunit human SWI/SNF complex by demonstrating physical association with hSNF5, answering whether the human protein assembles into a complex like its yeast counterpart.

    Evidence Co-immunoprecipitation with truncation-mutant interaction mapping

    PMID:7739891

    Open questions at the time
    • Full complex composition not defined
    • No demonstration of remodeling activity
  3. 1996 Medium

    Defined cell-cycle regulation of BRM, showing it is phosphorylated, excluded from condensed chromosomes, and reduced in abundance during mitosis without disrupting the hBRM–hSNF5 interaction.

    Evidence Cell fractionation, immunofluorescence across cell-cycle stages, and co-IP

    PMID:8670841

    Open questions at the time
    • Responsible mitotic kinase not identified
    • Functional consequence of chromosomal exclusion not established
  4. 1996 Medium

    Connected BRM to growth control by showing LXCXE-mediated interaction with the pRB family is required for BRM-induced growth arrest, antagonized by E1A.

    Evidence Yeast two-hybrid plus colony-formation/flat-cell assays with pRB-binding-deficient mutants

    PMID:8657132

    Open questions at the time
    • Target genes of the arrest program not defined
    • Mechanism of pRB-BRM cooperation at promoters not resolved
  5. 1997 High

    Resolved the mechanism of BRM-mediated repression by demonstrating RB bridges BRM and E2F1 into a ternary complex requiring the RB-binding domain and ATPase site but not the bromodomain.

    Evidence Reciprocal co-IP of E2F1–hBRM–RB, transcriptional repression assays, and ATPase-dead/bromodomain mutants

    PMID:9326598

    Open questions at the time
    • Which E2F target genes are physiologically controlled not fully mapped
    • In vitro repression vs. native promoter occupancy distinction limited
  6. 1999 Medium

    Identified the AT-hook-like domain as the chromatin-tethering module required for cooperation with GR on integrated (chromatinized) reporters, distinguishing chromatin targeting from pRB-binding and bromodomain functions.

    Evidence Deletion-mutant transfection with integrated vs. episomal reporter transactivation in ras-transformed fibroblasts

    PMID:10330133

    Open questions at the time
    • Direct DNA/chromatin binding of the AT-hook not biochemically resolved here
    • Genome-wide targeting role untested
  7. 2001 High

    Provided direct biochemical proof that the hBRM complex is a bona fide ATP-dependent remodeler, establishing DNA-dependent ATPase and nucleosome-remodeling activity and lower activity than BRG1 complexes.

    Evidence Purified complex with in vitro ATPase, restriction-enzyme accessibility, nucleosome-array remodeling assays, and mSin3A binding

    PMID:11238380

    Open questions at the time
    • Structural basis of lower activity vs. BRG1 not determined
    • Physiological significance of mSin3A association not tested in cells
  8. 2001 High

    Linked BRM to oncogenesis and to apoptotic regulation through two studies: SYT-SSX1 fusion requires BRM binding for transformation, and BRM is cleaved by cathepsin G during apoptosis to release it from the nuclear matrix.

    Evidence Co-IP/domain mapping with soft-agar assays; in vitro cathepsin G cleavage with inhibitor and nuclear-matrix fractionation

    PMID:11259672 PMID:11274403

    Open questions at the time
    • Functional consequence of nuclear-matrix release for transcription not measured
    • Whether cathepsin G cleavage is a general apoptotic event unresolved
  9. 2002 Medium

    Demonstrated factor-directed recruitment of BRM to E2F promoters via prohibitin and showed BRM can functionally substitute for BRG1 in RB-mediated arrest while having a unique requirement for CD44 expression.

    Evidence Co-IP, ChIP at E2F promoters, dominant-negative rescue; transfection into double-deficient cells and BRM-null mouse tissue analysis

    PMID:11850839 PMID:12065415

    Open questions at the time
    • Why some targets require BRM specifically not mechanistically explained
    • Prohibitin–BRM interaction interface not mapped
  10. 2003 Medium

    Established the paralog-specificity principle by showing BRM, but not BRG1, uses unique protein interactions (Notch-associated ankyrin repeat proteins) to occupy distinct promoters during differentiation.

    Evidence Pulldown/co-IP of BRM-specific interactors and promoter occupancy comparison

    PMID:12620226

    Open questions at the time
    • Structural basis of BRM-specific interaction not defined
    • Breadth of BRM-exclusive interactome unknown
  11. 2004 Medium

    Extended BRM's E2F1-repressive role to a pRB-independent, TopBP1-recruited mechanism that suppresses E2F1-dependent apoptosis, broadening the recruitment routes that target BRM/BRG1 to E2F promoters.

    Evidence Co-IP of TopBP1, ChIP at E2F1 promoters, dominant-negative rescue, apoptosis assays; ChIP plus JNK1 inhibition in breast cancer cells

    PMID:15075294 PMID:15141164

    Open questions at the time
    • Selectivity for E2F1 over E2F2/3 mechanistically unexplained
    • Direct vs. indirect TopBP1–BRM contact not mapped
  12. 2007 Medium

    Consolidated BRM as a context-specific activator or repressor through distinct partners (SHP, p53/p21, osteocalcin/HDAC1, Brn3b) and identified epigenetic silencing as the primary route of BRM loss in cancer.

    Evidence Separate shRNA/inducible knockdown, ChIP, and chromatin accessibility studies; BRM sequencing showing no mutations and HDAC-inhibitor rescue

    PMID:17546055 PMID:17855369 PMID:17938176 PMID:19144648 PMID:19805516

    Open questions at the time
    • Rules governing activation vs. repression at a given locus not unified
    • RGC differentiation role rests on single low-confidence study
  13. 2008 Medium

    Linked BRM to co-transcriptional RNA processing by showing it transactivates TERT and modulates TERT splicing in association with p54(nrb)/PSF and elongating Pol II.

    Evidence shRNA knockdown, splice-variant RT-PCR, ChIP co-localization, and co-IP of splicing factors

    PMID:18042045

    Open questions at the time
    • Direct role of remodeling vs. splicing-factor scaffolding not separated
    • Generality across other genes untested
  14. 2009 Medium

    Connected SMARCA2 to neurodevelopmental phenotypes and identified regulatory and missense variants affecting expression and nuclear localization relevant to schizophrenia behaviors.

    Evidence Smarca2 knockout mouse behavioral phenotyping, cell-based localization assay for a missense variant, and postmortem brain expression analysis

    PMID:19363039

    Open questions at the time
    • Molecular link between BRM loss and behavior unresolved
    • Causality of risk SNPs in human disease not established
  15. 2010 Medium

    Expanded the factor-recruitment model into immune signaling by showing REQ/DPF2 bridges BRM to NF-κB p52 to drive noncanonical NF-κB-dependent BLC/CXCL13 transcription.

    Evidence In vitro binding, ChIP at BLC promoter, and REQ knockdown with reporter assays

    PMID:20460684

    Open questions at the time
    • Whether REQ is a dedicated or general BRM adaptor unclear
    • Broader noncanonical NF-κB target set not defined
  16. 2011 Medium

    Defined the molecular basis of cancer-associated BRM silencing as promoter polymorphisms (BRM-741/-1321) creating MEF2 sites that recruit HDAC9-containing complexes, alongside evidence for post-transcriptional suppression.

    Evidence Promoter sequencing, ChIP at polymorphic sites, MEF2D/HDAC9 knockdown; nuclear run-on and RT-PCR with HDAC-inhibitor rescue

    PMID:16007216 PMID:21478907

    Open questions at the time
    • Relative contribution of transcriptional vs. post-transcriptional silencing not reconciled
    • Reversibility in patient tumors untested
  17. 2011 Medium

    Mechanistically refined the BRM-versus-BRG1 promoter switch at STAT1/GAS elements, showing unphosphorylated STAT1 recruits BRM in an mSin3/HDAC repressive complex that is reversed by p300 acetylation and a switch to BRG1 upon activation.

    Evidence Co-IP of hBRM with STAT1, ChIP at GAS elements, chromatin accessibility and p300 acetylation experiments

    PMID:21079652

    Open questions at the time
    • In vitro STAT1–BRM interaction not validated structurally
    • Generality of the BRM-to-BRG1 switch across IFN targets unknown
  18. 2012 High

    Connected BRM remodeling to histone-modification crosstalk by showing the BRM bromodomain binds CBP and stimulates H3K27 acetylation while antagonizing H3K27me3.

    Evidence Direct domain-mapped binding, in vitro acetylation assay, mutant histone-mark analysis, and genome-wide ChIP co-localization in Drosophila

    PMID:22493065

    Open questions at the time
    • Conservation of CBP/UTX coupling in human SMARCA2 not directly demonstrated
    • Whether ATPase activity is required for the acetylation effect untested
  19. 2013 Medium

    Added hypoxia signaling and neural progenitor maintenance to BRM's roles, showing BRM/BRG1 act as HIF coactivators and that the Drosophila BRM complex partners with Earmuff and HDAC3 to suppress dedifferentiation.

    Evidence Knockdown/re-expression with ChIP and nucleosome remodeling; co-IP and genetic epistasis in Drosophila

    PMID:23897427 PMID:24618901

    Open questions at the time
    • BRM-specific vs. redundant contribution at HIF targets not fully separated
    • Direct BRM–HIF contact not mapped
  20. 2013 Medium

    Systematically dissected the enzymes controlling BRM expression and acetylation, mapping HDAC3/HDAC9 to expression, HDAC2 to acetylation, and specific KATs and MAPK signaling as regulators.

    Evidence Selective siRNA knockdown of individual HDACs, overexpression of 21 HATs, and MAPK inhibitor treatment

    PMID:23524580

    Open questions at the time
    • Direct vs. indirect enzyme effects on BRM not always distinguished
    • Integration with promoter-polymorphism silencing not resolved
  21. 2014 High

    Established the central synthetic-lethal dependency: residual SMARCA2-containing SWI/SNF is essential for proliferation of SMARCA4-mutant cancers, with depletion causing arrest, senescence, and increased H3K9me3.

    Evidence shRNA loss-of-function screens across 165 lines, co-IP of residual complex, xenografts, and H3K9me3 imaging (two concurrent papers)

    PMID:24421395 PMID:24520176

    Open questions at the time
    • Which downstream genes mediate the dependency not fully defined
    • Mechanism of H3K9me3 increase upon SMARCA2 loss unresolved
  22. 2017 High

    Defined the biochemical targeting logic and druggability of SMARCA2: the bromodomain has modest H3K14ac/DNA binding that is dispensable for global chromatin affinity, and the DNA-dependent ATPase is allosterically inhibitable by small molecules.

    Evidence ITC/SPR binding with mutagenesis and ChIP-seq in BRD-mutant ESCs; ATPase inhibition assays with xenograft validation

    PMID:28706277 PMID:30339381

    Open questions at the time
    • What does drive complex targeting if not BRD binding remains open
    • Allosteric inhibitor selectivity for BRM vs. BRG1 limited
  23. 2017 Medium

    Showed PRC2 silences SMARCA2 in SMARCA4-mutant EZH2-inhibitor-sensitive cancers, with EZH2-inhibitor-induced SMARCA2 re-expression driving apoptosis via cathepsin B; also linked BRM to JAK2/STAT3 signaling in pancreatic cancer.

    Evidence EZH2 inhibitor treatment, SMARCA2 re-expression, RNAi, and xenografts; shRNA knockdown with pSTAT3 readout

    PMID:28602977 PMID:29087303

    Open questions at the time
    • JAK2/STAT3 role rests on single low-confidence knockdown study without direct binding evidence
    • Direct vs. indirect cathepsin B derepression unresolved
  24. 2021 High

    Demonstrated a noncanonical SWI/SNF-independent SMARCA2 function and a bromodomain-dependent chromatin-binding requirement: SMARCA2 partners with NSD2 to activate PTP4A3 in myeloma, and BRD inhibition (PFI-3) destabilizes promoter binding needed for myogenic differentiation.

    Evidence SILAC-MS, co-IP, ChIP and H3K36me2 mapping with PFI-3 and xenograft; PFI-3 with ChIP and shRNA in muscle differentiation models

    PMID:33602783 PMID:34289068

    Open questions at the time
    • How SMARCA2 functions outside the canonical complex structurally unresolved
    • Generality of noncanonical NSD2 partnership beyond t(4;14) myeloma untested
  25. 2022 High

    Achieved therapeutically selective targeting by demonstrating a VHL-recruiting PROTAC (ACBI2) degrades SMARCA2 over SMARCA4 in vivo with antitumor efficacy in SMARCA4-deficient models.

    Evidence Structure-guided PROTAC design with cellular degradation, ex vivo human blood, and in vivo xenograft assays

    PMID:36216795

    Open questions at the time
    • Durability of response and resistance mechanisms not addressed
    • Off-target neomorphic effects of degradation not evaluated
  26. 2024 Medium

    Placed SMARCA2 within a lineage-specification axis, showing SETMAR-driven H3K36 methylation promotes SMARCA2 transcription and SMARCA2 in turn opens PAX8/FOXE1 enhancers to drive thyroid differentiation.

    Evidence SMARCA2 ChIP at enhancers, ATAC-seq, SETMAR knockdown/overexpression, and H3K36 methylation assays

    PMID:38900084

    Open questions at the time
    • Whether SMARCA2 acts through canonical SWI/SNF here not established
    • Direct SMARCA2–enhancer occupancy vs. indirect accessibility change not fully separated

Open questions

Synthesis pass · forward-looking unresolved questions
  • What determines genome-wide SMARCA2 targeting independent of bromodomain histone/DNA binding, and which downstream gene programs mediate the SMARCA4-mutant synthetic-lethal dependency, remain unresolved.
  • Primary determinant of complex recruitment to specific loci unknown
  • Effector genes of SMARCA2 dependency in SMARCA4-mutant cancers not defined
  • Structural basis of noncanonical (complex-independent) SMARCA2 activity unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 3 GO:0003677 DNA binding 2 GO:0042393 histone binding 2 GO:0060090 molecular adaptor activity 2 GO:0140657 ATP-dependent activity 2
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2
Pathway
R-HSA-1643685 Disease 4 R-HSA-1266738 Developmental Biology 3 R-HSA-1640170 Cell Cycle 3 R-HSA-4839726 Chromatin organization 3 R-HSA-74160 Gene expression (Transcription) 3
Partners
DPF2E2F1NSD2RB1SIN3ASMARCB1STAT1
Complex memberships
SWI/SNF (BAF) complex

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 Human SMARCA2 (hBRM) was identified as a nuclear transcriptional co-activator that cooperates with the glucocorticoid receptor (GR) to activate transcription; cooperation required the DNA-binding domain of GR and two separated regions of hBRM including a helicase-homology domain. Transfection of hBRM into cells lacking endogenous hBRM, followed by transactivation assays with GR reporters; deletion analysis of hBRM domains The EMBO journal Medium 8223438
1995 Human SMARCA2 (hBRM) co-immunoprecipitates with hSNF5 (a human SNF5 homologue), and this interaction depends on the conserved SNF5-homology domain of hSNF5, indicating that hBRM and hSNF5 are subunits of a human SWI/SNF complex. Co-immunoprecipitation from cell extracts; interaction mapping with truncation mutants Nucleic acids research Medium 7739891
1996 During mitosis, SMARCA2 (hBRM) is phosphorylated and excluded from condensed chromosomes; mitotic phosphorylation correlates with decreased affinity for the nuclear structure in early M phase but does not disrupt the hBRM–hSNF5 association. Additionally, the level of hBRM protein is strongly reduced in mitosis. Cell fractionation, Western blot, immunofluorescence across cell cycle stages; co-immunoprecipitation of hBRM with hSNF5 The EMBO journal Medium 8670841
1996 SMARCA2 (hBRM) interacts physically with the pRB family of proteins (pRB, p107, p130) via the LXCXE motif; hBRM requires an intact pRB-binding domain to induce growth arrest, and growth-arrest activity is antagonized by E1A. Yeast two-hybrid, transfection of wild-type and pRB-binding-deficient hBRM mutants into SW13 cells; colony-formation and flat-cell assays Molecular and cellular biology Medium 8657132
1997 SMARCA2 (hBRM) cooperates with RB to repress E2F1 transcriptional activity; RB bridges hBRM and E2F1 into a ternary complex in vivo; repression requires the RB-binding domain and the NTP-binding site of hBRM but not its bromodomain. The RB-binding domain of hBRM itself has transcriptional activation potential that RB can repress. Co-immunoprecipitation of E2F1–hBRM–RB complexes; transient transfection repression assays with hBRM deletion mutants; ATPase-dead and bromodomain mutants Proceedings of the National Academy of Sciences of the United States of America High 9326598
1999 A 49-amino-acid AT-hook-like domain in SMARCA2 (brm/SNF2α), rich in lysines and arginines and located downstream of the pRB interaction domain, is required for tethering of brm to chromatin and for cooperation with the glucocorticoid receptor on chromatin-integrated reporters; the LXCXE pRB-binding motif and bromodomain had only moderate effects on these activities. Transfection of deletion mutants into ras-transformed fibroblasts; transactivation assays on integrated vs. episomal reporters; domain-function correlation Molecular and cellular biology Medium 10330133
2001 Purified hBRM complex (containing hBRM as its central ATPase) can remodel nucleosomal arrays, increase restriction enzyme accessibility to nucleosomal DNA, and hydrolyze ATP in a DNA-dependent manner; the hBRM complex shows lower remodeling activity than BRG1-containing complexes and is markedly less active on mononucleosomal core particles. The hBRM complex also contains mSin3A and directly interacts with mSin3A in vitro. Epitope-tagged pull-down and fractionation of stable cell lines; in vitro ATPase assay; restriction enzyme accessibility assay on nucleosomal arrays; in vitro binding of hBRM to mSin3A Genes & development High 11238380
2001 SYT-SSX1 oncofusion protein physically associates with SMARCA2 (hBRM/hSNF2α); the binding region maps to aa 1–181 of SYT-SSX1 and aa 156–205 of hBRM; overexpression of the hBRM binding region suppressed anchorage-independent growth of SYT-SSX1-expressing cells, indicating that hBRM interaction is functionally required for transformation. Co-immunoprecipitation from expressing cells; domain mapping; soft-agar anchorage-independent growth assay with hBRM fragment overexpression Proceedings of the National Academy of Sciences of the United States of America Medium 11274403
2001 SMARCA2 (hBRM) is cleaved during apoptosis by cathepsin G (not by caspases-3, -7, or -6); cleavage removes a 20-kDa C-terminal fragment containing the bromodomain and disrupts association of hBRM with the nuclear matrix; cathepsin G redistributes from granules/Golgi to a diffuse nuclear distribution during apoptosis. In vitro cleavage assay with recombinant/purified caspases and cathepsin G; peptide inhibitor of cathepsin G in apoptosis assay; nuclear matrix fractionation of cleaved vs. full-length hBRM Proceedings of the National Academy of Sciences of the United States of America High 11259672
2002 Prohibitin recruits SMARCA2 (Brm) to E2F-responsive promoters; this recruitment is required for prohibitin-mediated repression of E2F transcription and growth suppression; prohibitin-Brm-mediated repression requires RB but the initial association of prohibitin with Brm is RB-independent. Dominant-negative Brm rescue experiment; co-immunoprecipitation of prohibitin with Brm; chromatin immunoprecipitation at E2F-responsive promoters; growth suppression assays The EMBO journal Medium 12065415
2002 SMARCA2 (BRM) can functionally substitute for BRG1 to restore RB-mediated cell cycle arrest and induce CD44 expression when transfected into BRG1/BRM double-deficient tumor cell lines; however, CD44 expression specifically requires BRM (not BRG1) under physiological conditions in vivo, as demonstrated in BRM-null mice. Transient transfection of BRM into double-deficient tumor cells; analysis of BRM-null mouse tissues for CD44 expression Oncogene Medium 11850839
2003 SMARCA2 (BRM) but not BRG1 interacts with two ankyrin repeat proteins (components of Notch signal transduction) through protein-protein interactions unique to BRM, enabling BRM-containing SWI/SNF complexes to be recruited to Notch-responsive promoters during differentiation. Pulldown and co-immunoprecipitation identifying BRM-specific interactors; promoter occupancy analysis comparing BRG1 and BRM complexes Molecular cell Medium 12620226
2004 TopBP1 recruits SMARCA2 (Brm)/BRG1 to E2F1-responsive promoters and represses E2F1 (but not E2F2 or E2F3) transcriptional activity through a pRB-independent, Brg1/Brm-dependent mechanism, thereby suppressing E2F1-dependent apoptosis during normal cell growth and DNA damage. Co-immunoprecipitation of TopBP1 with Brm/BRG1; dominant-negative Brm rescue; ChIP at E2F1 promoters; apoptosis assays with Brm knockdown Genes & development Medium 15075294
2004 SMARCA2 (Brm)/BRG1 is required for estrogen antagonist-mediated growth suppression in breast cancer cells through E2F pathway repression; prohibitin recruits Brg1/Brm to promoter-bound E2F via a JNK1 pathway, and their recruitment is induced by estrogen antagonist treatment. Dominant-negative Brm/BRG1 rescue; ChIP at native E2F-responsive promoters; pharmacological JNK1 inhibition experiments The EMBO journal Medium 15141164
2007 SMARCA2 (Brm)-containing SWI/SNF complexes, but not BRG1-containing complexes, are required for active repression of the osteocalcin promoter; BRM complexes bind the repressed osteocalcin promoter and are required for recruitment of the co-repressor HDAC1, whereas BRG1 complexes are required for activation. shRNA depletion of BRM and BRG1 separately; ChIP of BRM/BRG1 and HDAC1 at the osteocalcin promoter; osteoblast differentiation marker analysis The Journal of biological chemistry Medium 19144648
2007 Brm (SMARCA2) interacts with SHP nuclear receptor and facilitates SHP-mediated repression of CYP7A1 and auto-repression of SHP in bile acid feedback inhibition; ChIP showed Brm is recruited to both CYP7A1 and SHP promoters following FXR agonist treatment, resulting in inaccessible (repressed) chromatin. This is functionally distinct from BRG1, which interacts with FXR and promotes SHP transactivation. Co-immunoprecipitation of Brm with SHP; ChIP at CYP7A1 and SHP promoters; nucleosome remodeling assay; inducible knockdown/overexpression Molecular and cellular biology Medium 19805516
2007 SMARCA2 (Brm) promotes retinal ganglion cell differentiation by facilitating expression and function of the transcription factor Brn3b and by inhibiting Notch signaling; Brm promotes cell cycle exit during this differentiation process. Perturbation of Brm expression and function in retinal progenitors; analysis of Brn3b expression and Notch signaling markers; cell cycle analysis The Journal of biological chemistry Low 17855369
2007 SMARCA2 (Brm) is required for p21 induction by p53 specifically in BRG1-deficient cells; in cells expressing BRG1, BRG1 is the preferentially recruited ATPase for p53-dependent p21 activation. Impaired p21 induction upon BRG1 knockdown is partly due to decreased p53 binding to the p21 promoter. Inducible knockdown of Brm and BRG1 separately; p21/MDM2 mRNA quantification; ChIP of p53 at the p21 promoter The Journal of biological chemistry Medium 17938176
2007 Epigenetic silencing is the primary mechanism of BRM/SMARCA2 loss in cancer: HDAC inhibitors restore BRM expression in BRM/BRG1-deficient cancer cell lines despite the absence of inactivating mutations; HDAC inhibitors also block BRM function (via C-terminal acetylation) when present, but BRM activity is detectable after their removal. Sequencing of BRM in BRM-deficient lines (no mutations found); nuclear run-on and RT-PCR; HDAC inhibitor treatment; BRM activity assays post-inhibitor withdrawal Oncogene Medium 17546055
2008 SMARCA2 (Brm) transactivates the TERT gene and modulates splicing patterns of TERT transcripts; Brm co-localizes with p54(nrb), PSF, and phospho-Ser2 RNA Pol II at TERT exon 7 alternative splicing acceptor sites; Brm knockdown in BRG1-deficient cells reduces TERT expression and increases exon-7/8-excluded (inactive) TERT mRNA, leading to growth arrest. shRNA knockdown of Brm; RT-PCR for TERT splice variants; ChIP showing co-localization of Brm with splicing factors at TERT; co-immunoprecipitation of p54(nrb) with Brm/BRG1 The Biochemical journal Medium 18042045
2009 SMARCA2 (Brm) knockdown in Smarca2-knockout mice impairs social interaction and prepulse inhibition (schizophrenia-relevant behaviors); a missense risk SNP (rs2296212) reduces nuclear localization efficiency of BRM; intronic risk alleles (rs3763627, rs3793490) are associated with reduced SMARCA2 expression in prefrontal cortex. Smarca2 knockout mouse phenotyping (social interaction, PPI); cell-based nuclear localization assay for missense variant; postmortem brain expression analysis Human molecular genetics Medium 19363039
2009 SMARCA2 (Cdx2) and Brm-type SWI/SNF complex cooperatively regulate villin expression in gastrointestinal cells; GST pull-down demonstrated a direct interaction between Cdx2 and several SWI/SNF subunits; ChIP showed co-recruitment of Cdx2 and Brm to the villin promoter HCR-Cdx element. GST pull-down; ChIP; reporter assays; Cdx2 knockdown Experimental cell research Medium 19371634
2010 REQ/DPF2 (requiem) acts as an adaptor that bridges SMARCA2 (Brm)-containing SWI/SNF complex and the NF-κB subunit p52; REQ binds Brm and p52 simultaneously; Brm and REQ are recruited to the BLC/CXCL13 promoter upon lymphotoxin stimulation and are both required for noncanonical NF-κB-dependent BLC transcription. In vitro binding assays (co-IP); ChIP at BLC promoter; REQ knockdown experiments; reporter assays The Journal of biological chemistry Medium 20460684
2011 SMARCA2 (Brm) loss in cancer cells results from post-transcriptional suppression (cells efficiently transcribe BRM but mRNA and pre-mRNA are undetectable), and can be reversed by HDAC inhibitor treatment, demonstrating that the BRM gene is intact and functional in these tumor lines. Nuclear run-on transcription assay; RT-PCR for BRM mRNA and hnRNA; HDAC inhibitor rescue experiments Oncogene Medium 16007216
2011 BRM expression is regulated at the transcriptional level by the BRM promoter; two novel BRM promoter insertion polymorphisms (BRM-741 and BRM-1321) create MEF2-binding sites that recruit HDAC-containing complexes, leading to BRM silencing; MEF2D and HDAC9 bind these polymorphic sites (as shown by ChIP) and HDAC9 is overexpressed in BRM-negative cancer cell lines. BRM promoter sequencing; promoter swap ChIP experiments; HDAC9/MEF2D knockdown; ChIP at polymorphic sites Oncogene Medium 21478907
2011 SMARCA2 (hBRM) interacts with STAT1 in vitro; native (unphosphorylated) STAT1 selectively recruits hBRM to IFNγ-activated sequences (GAS) under basal conditions, where hBRM exists in a mSin3/HDAC co-repressor complex maintaining repressed chromatin; upon stress, hBRM is acetylated by p300 and dissociates from the repressor complex, while phospho-STAT1 recruits BRG1 instead — an hBRM-to-BRG1 switch that activates gene expression. Co-IP of hBRM with STAT1; ChIP at GAS elements; chromatin accessibility assays; p300 acetylation experiments Cell research Medium 21079652
2012 Drosophila BRM (ortholog of SMARCA2) physically associates with CBP acetyltransferase and the H3K27 demethylase UTX in vivo; BRM binds directly to conserved zinc fingers of CBP via its bromodomain-containing C-terminus; the BRM bromodomain enhances CBP PHD binding to histone H3 and stimulates in vitro acetylation of H3K27; brm mutations reduce H3K27ac and increase H3K27me3 levels. Co-immunoprecipitation and direct binding assays; in vitro acetylation assay with recombinant CBP; brm mutant analysis of histone marks; genome-wide ChIP co-localization Molecular and cellular biology High 22493065
2013 SMARCA2 (BRM) and BRG1 are required as coactivators for a subset of hypoxia-inducible factor (HIF) target genes; HIF1/HIF2 recruit BRG1 complexes to target gene promoters, which promotes nucleosome remodeling in a BRG1 ATPase-dependent manner; BRM depletion in BRG1/BRM-deficient cells reduces hypoxic induction of HIF targets. BRG1/BRM knockdown; re-expression of BRG1/BRM in deficient cells; ChIP at HIF target promoters; nucleosome remodeling assay Molecular and cellular biology Medium 23897427
2013 HDAC3 and HDAC9 regulate SMARCA2 (BRM) expression, whereas HDAC2 controls BRM acetylation; KAT6A, KAT6B, and KAT7 histone acetyltransferases induce BRM expression, and KAT2B and KAT8 induce its acetylation; the MAP kinase pathway regulates both BRM acetylation and BRM silencing. Selective siRNA knockdown of individual HDACs and overexpression of 21 HATs; MAPK pathway inhibitor treatment; BRM expression and acetylation assays Oncogene Medium 23524580
2014 SMARCA2 (BRM) is the catalytic ATPase of a residual SWI/SNF complex that is essential for proliferation of SMARCA4 (BRG1)-mutant cancer cells; loss of SMARCA4 leads to greater incorporation of SMARCA2 into SWI/SNF complexes; SMARCA2 depletion in SMARCA4-mutant cells causes cell cycle arrest, senescence, and increased global H3K9me3. shRNA-based loss-of-function screens across 165 cancer cell lines; co-immunoprecipitation demonstrating residual SMARCA2-containing complex; in vivo xenograft experiments; H3K9me3 immunofluorescence Molecular and cellular biology / Proceedings of the National Academy of Sciences High 24421395 24520176
2014 Drosophila BRM complex (SWI/SNF) associates physically with Earmuff transcription factor and HDAC3 to suppress dedifferentiation of intermediate neural progenitors (INPs) back into neuroblasts; multiple BRM complex components co-immunoprecipitate with Erm; brm and hdac3 genetically interact with erm to prevent type II neuroblast overgrowth. Co-immunoprecipitation of BRM complex subunits with Erm; genetic epistasis (double mutant analysis); brm and hdac3 knockdown phenotyping eLife Medium 24618901
2017 The bromodomain (BRD) of SMARCA2 (hBRM) has moderate specificity for H3K14ac; both BRG1 and hBRM BRDs also possess DNA-binding activity via a basic patch surface, and the BRD together with an adjacent AT-hook makes multivalent contacts with AT-rich DNA elements with robust affinity; however, histone-binding activity does not substantially contribute to nucleosome targeting in vitro, and global chromatin affinity of BRG1 in mouse ESCs does not require BRD histone or DNA binding. Binding assays (ITC/SPR) with modified histone peptides and DNA; mutagenesis of basic patch; nucleosome-binding assays; ChIP-seq in BRD-mutant mouse ESCs Nature communications High 28706277
2017 SMARCA2 expression is suppressed by PRC2 (EZH2-mediated H3K27me3) in SMARCA4-mutant cancer cells sensitive to EZH2 inhibition; induction of SMARCA2 expression by EZH2 inhibitors is required for apoptosis (but not growth arrest) through derepression of the lysosomal protease cathepsin B; re-expression of SMARCA2 can compensate for SMARCA4 loss and antagonize PRC2 targets. EZH2 inhibitor treatment; SMARCA2 re-expression experiments; RNAi depletion; gene expression analysis; in vivo xenograft models Proceedings of the National Academy of Sciences of the United States of America Medium 29087303
2017 BRM/SMARCA2 contains a DNA-dependent ATPase activity that is allosterically inhibitable by small molecules; allosteric BRM/BRG1 dual inhibitors downregulate BRM-dependent gene expression and show antiproliferative activity in BRG1-mutant xenograft models. ATPase inhibition assay; gene expression analysis after inhibitor treatment; oral xenograft tumor model Journal of medicinal chemistry Medium 30339381
2017 BRM/SMARCA2 activates JAK2/STAT3 signaling in pancreatic cancer cells; BRM knockdown reduces STAT3 phosphorylation and transcription of STAT3 target genes, reducing proliferation and increasing gemcitabine sensitivity in vitro and in vivo. shRNA knockdown; Western blot for pSTAT3; RT-PCR for STAT3 targets; xenograft tumor model Cancer letters Low 28602977
2019 SMARCA2 (BRM) directly binds to the promoter regions of Claudin genes via interaction with transcription factor Sp1, activates Claudin transcription by modulating histone modifications, and its downregulation drives TGF-β-induced breast cancer cell migration/invasion; TGF-β represses BRM transcription through targeting C/EBPβ. ChIP of BRM at Claudin promoters; co-IP of BRM with Sp1; BRM overexpression/knockdown; migration/invasion assays Biochimica et biophysica acta. Gene regulatory mechanisms Medium 30946989
2021 SMARCA2 interacts with NSD2 in a noncanonical manner independent of the full SWI/SNF complex in t(4;14) multiple myeloma; the NSD2–SMARCA2 complex occupies the PTP4A3 promoter, leading to focal H3K36me2 enrichment and transcriptional activation of PTP4A3; PFI-3 (bromodomain inhibitor of SMARCA2) displaces NSD2 from the PTP4A3 promoter and inhibits myeloma cell viability. SILAC-based mass spectrometry identifying NSD2–SMARCA2 interaction; co-IP; ChIP of NSD2 and SMARCA2 at PTP4A3 promoter; H3K36me2 ChIP; PFI-3 treatment with ChIP; xenograft in vivo Cancer research High 33602783
2021 The bromodomains of BRM and BRG1 promote stable chromatin binding at target promoters required for skeletal muscle differentiation; pharmacological inhibition with PFI-3 reduced BRM/BRG1 binding to promoters of myogenic genes, impaired cell cycle exit and muscle-specific gene expression both in vitro and in vivo. PFI-3 bromodomain inhibitor; ChIP of BRM/BRG1 after PFI-3 treatment; BRM/BRG1 shRNA depletion; differentiation marker analysis; in vivo muscle regeneration model Nucleic acids research Medium 34289068
2022 A VHL-recruiting PROTAC (ACBI2) achieves selective degradation of SMARCA2 over SMARCA4 in vivo, demonstrating that structural differences between the two paralogs can be exploited for selective targeted degradation; SMARCA2 degradation shows antitumor efficacy in SMARCA4-deficient cancer models. Structure-guided PROTAC design; cellular degradation assays; ex vivo human whole blood assay; in vivo xenograft model with selective SMARCA2 degradation Nature communications High 36216795
2024 SETMAR methylates dimethylated H3K36 in the SMARCA2 promoter region to promote SMARCA2 transcription; SMARCA2 in turn binds enhancers of thyroid differentiation transcription factors PAX8 and FOXE1 to promote their expression by enhancing chromatin accessibility; METTL3-mediated m6A methylation of SETMAR mRNA regulates this axis. ChIP of SMARCA2 at PAX8/FOXE1 enhancers; ATAC-seq for chromatin accessibility; SETMAR knockdown/overexpression; H3K36 methylation assays Advanced science Medium 38900084

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 A human homologue of Saccharomyces cerevisiae SNF2/SWI2 and Drosophila brm genes potentiates transcriptional activation by the glucocorticoid receptor. The EMBO journal 544 8223438
2014 Functional epigenetics approach identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers. Proceedings of the National Academy of Sciences of the United States of America 329 24520176
2003 Transcriptional specificity of human SWI/SNF BRG1 and BRM chromatin remodeling complexes. Molecular cell 297 12620226
1997 RB and hbrm cooperate to repress the activation functions of E2F1. Proceedings of the National Academy of Sciences of the United States of America 262 9326598
2001 Purification and characterization of mSin3A-containing Brg1 and hBrm chromatin remodeling complexes. Genes & development 241 11238380
1998 The Drosophila trithorax group proteins BRM, ASH1 and ASH2 are subunits of distinct protein complexes. Development (Cambridge, England) 239 9735357
1996 Functional interactions between the hBRM/hBRG1 transcriptional activators and the pRB family of proteins. Molecular and cellular biology 221 8657132
1996 The hbrm and BRG-1 proteins, components of the human SNF/SWI complex, are phosphorylated and excluded from the condensed chromosomes during mitosis. The EMBO journal 201 8670841
1995 The Drosophila snr1 and brm proteins are related to yeast SWI/SNF proteins and are components of a large protein complex. Molecular biology of the cell 199 7579694
2014 Residual complexes containing SMARCA2 (BRM) underlie the oncogenic drive of SMARCA4 (BRG1) mutation. Molecular and cellular biology 196 24421395
2018 Discovery of Orally Active Inhibitors of Brahma Homolog (BRM)/SMARCA2 ATPase Activity for the Treatment of Brahma Related Gene 1 (BRG1)/SMARCA4-Mutant Cancers. Journal of medicinal chemistry 194 30339381
2012 Heterozygous missense mutations in SMARCA2 cause Nicolaides-Baraitser syndrome. Nature genetics 192 22366787
2016 SWI/SNF Complex-deficient Undifferentiated/Rhabdoid Carcinomas of the Gastrointestinal Tract: A Series of 13 Cases Highlighting Mutually Exclusive Loss of SMARCA4 and SMARCA2 and Frequent Co-inactivation of SMARCB1 and SMARCA2. The American journal of surgical pathology 190 26551623
2015 Dual loss of the SWI/SNF complex ATPases SMARCA4/BRG1 and SMARCA2/BRM is highly sensitive and specific for small cell carcinoma of the ovary, hypercalcaemic type. The Journal of pathology 186 26356327
2022 A selective and orally bioavailable VHL-recruiting PROTAC achieves SMARCA2 degradation in vivo. Nature communications 170 36216795
2017 Selective Killing of SMARCA2- and SMARCA4-deficient Small Cell Carcinoma of the Ovary, Hypercalcemic Type Cells by Inhibition of EZH2: In Vitro and In Vivo Preclinical Models. Molecular cancer therapeutics 147 28292935
2016 SMARCA4 and SMARCA2 deficiency in non-small cell lung cancer: immunohistochemical survey of 316 consecutive specimens. Annals of diagnostic pathology 145 28038711
2002 Concomitant down-regulation of BRM and BRG1 in human tumor cell lines: differential effects on RB-mediated growth arrest vs CD44 expression. Oncogene 135 11850839
2001 Analysis of transforming activity of human synovial sarcoma-associated chimeric protein SYT-SSX1 bound to chromatin remodeling factor hBRM/hSNF2 alpha. Proceedings of the National Academy of Sciences of the United States of America 134 11274403
2004 TopBP1 recruits Brg1/Brm to repress E2F1-induced apoptosis, a novel pRb-independent and E2F1-specific control for cell survival. Genes & development 127 15075294
1995 A human protein with homology to Saccharomyces cerevisiae SNF5 interacts with the potential helicase hbrm. Nucleic acids research 125 7739891
1999 Functional domains of the SYT and SYT-SSX synovial sarcoma translocation proteins and co-localization with the SNF protein BRM in the nucleus. Human molecular genetics 123 10072425
2007 The reversible epigenetic silencing of BRM: implications for clinical targeted therapy. Oncogene 122 17546055
2013 Lung cancer with loss of BRG1/BRM, shows epithelial mesenchymal transition phenotype and distinct histologic and genetic features. Cancer science 117 23163725
2002 Prohibitin requires Brg-1 and Brm for the repression of E2F and cell growth. The EMBO journal 115 12065415
2007 Aberrant expression of SWI/SNF catalytic subunits BRG1/BRM is associated with tumor development and increased invasiveness in prostate cancers. The Prostate 108 17075831
2012 Histone demethylase UTX and chromatin remodeler BRM bind directly to CBP and modulate acetylation of histone H3 lysine 27. Molecular and cellular biology 106 22493065
1998 Sth1p, a Saccharomyces cerevisiae Snf2p/Swi2p homolog, is an essential ATPase in RSC and differs from Snf/Swi in its interactions with histones and chromatin-associated proteins. Genetics 96 9799253
2009 Involvement of SMARCA2/BRM in the SWI/SNF chromatin-remodeling complex in schizophrenia. Human molecular genetics 94 19363039
2005 The Brm gene suppressed at the post-transcriptional level in various human cell lines is inducible by transient HDAC inhibitor treatment, which exhibits antioncogenic potential. Oncogene 94 16007216
2019 Low mutation burden and frequent loss of CDKN2A/B and SMARCA2, but not PRC2, define premalignant neurofibromatosis type 1-associated atypical neurofibromas. Neuro-oncology 91 30722027
2016 Loss of expression of SMARCA4 (BRG1), SMARCA2 (BRM) and SMARCB1 (INI1) in undifferentiated carcinoma of the endometrium is not uncommon and is not always associated with rhabdoid morphology. Histopathology 90 27656868
2009 Antagonistic roles for BRM and BRG1 SWI/SNF complexes in differentiation. The Journal of biological chemistry 87 19144648
2007 Frequent loss of Brm expression in gastric cancer correlates with histologic features and differentiation state. Cancer research 85 18006815
2016 MicroRNA-276 promotes egg-hatching synchrony by up-regulating brm in locusts. Proceedings of the National Academy of Sciences of the United States of America 84 26729868
2010 SMARCA2 and other genome-wide supported schizophrenia-associated genes: regulation by REST/NRSF, network organization and primate-specific evolution. Human molecular genetics 76 20457675
2017 PRC2-mediated repression of SMARCA2 predicts EZH2 inhibitor activity in SWI/SNF mutant tumors. Proceedings of the National Academy of Sciences of the United States of America 73 29087303
1999 The activity of mammalian brm/SNF2alpha is dependent on a high-mobility-group protein I/Y-like DNA binding domain. Molecular and cellular biology 68 10330133
2005 The expression of the SWI/SNF ATPase subunits BRG1 and BRM in normal human tissues. Applied immunohistochemistry & molecular morphology : AIMM 67 15722796
2005 The BRG1- and hBRM-associated factor BAF57 induces apoptosis by stimulating expression of the cylindromatosis tumor suppressor gene. Molecular and cellular biology 65 16135788
2017 BRM/SMARCA2 promotes the proliferation and chemoresistance of pancreatic cancer cells by targeting JAK2/STAT3 signaling. Cancer letters 62 28602977
2017 DNA binding drives the association of BRG1/hBRM bromodomains with nucleosomes. Nature communications 60 28706277
2004 BRG1/BRM and prohibitin are required for growth suppression by estrogen antagonists. The EMBO journal 60 15141164
2015 Concomitant loss of SMARCA2 and SMARCA4 expression in small cell carcinoma of the ovary, hypercalcemic type. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 59 26564006
2007 The activity of p53 is differentially regulated by Brm- and Brg1-containing SWI/SNF chromatin remodeling complexes. The Journal of biological chemistry 59 17938176
2014 The Brm-HDAC3-Erm repressor complex suppresses dedifferentiation in Drosophila type II neuroblast lineages. eLife 56 24618901
2019 BRM: the core ATPase subunit of SWI/SNF chromatin-remodelling complex-a tumour suppressor or tumour-promoting factor? Epigenetics & chromatin 49 31722744
2017 Co-regulation of transcription by BRG1 and BRM, two mutually exclusive SWI/SNF ATPase subunits. Epigenetics & chromatin 47 29273066
2013 Identifying targets for the restoration and reactivation of BRM. Oncogene 47 23524580
2010 Requiem protein links RelB/p52 and the Brm-type SWI/SNF complex in a noncanonical NF-kappaB pathway. The Journal of biological chemistry 47 20460684
2020 Loss of the SWI/SNF-ATPase subunit members SMARCF1 (ARID1A), SMARCA2 (BRM), SMARCA4 (BRG1) and SMARCB1 (INI1) in oesophageal adenocarcinoma. BMC cancer 46 31906887
2011 Two novel BRM insertion promoter sequence variants are associated with loss of BRM expression and lung cancer risk. Oncogene 45 21478907
2020 De novo SMARCA2 variants clustered outside the helicase domain cause a new recognizable syndrome with intellectual disability and blepharophimosis distinct from Nicolaides-Baraitser syndrome. Genetics in medicine : official journal of the American College of Medical Genetics 44 32694869
2013 BRG1 and BRM chromatin-remodeling complexes regulate the hypoxia response by acting as coactivators for a subset of hypoxia-inducible transcription factor target genes. Molecular and cellular biology 44 23897427
2001 The human brm protein is cleaved during apoptosis: the role of cathepsin G. Proceedings of the National Academy of Sciences of the United States of America 44 11259672
2019 The chromatin remodeling protein BRM regulates the transcription of tight junction proteins: Implication in breast cancer metastasis. Biochimica et biophysica acta. Gene regulatory mechanisms 43 30946989
2009 Functional specificities of Brm and Brg-1 Swi/Snf ATPases in the feedback regulation of hepatic bile acid biosynthesis. Molecular and cellular biology 41 19805516
2024 BRG1/BRM inhibitor targets AML stem cells and exerts superior preclinical efficacy combined with BET or menin inhibitor. Blood 40 38437498
2023 Discovery of SMD-3040 as a Potent and Selective SMARCA2 PROTAC Degrader with Strong in vivo Antitumor Activity. Journal of medicinal chemistry 39 37523716
2019 SMARCA2-deficiency confers sensitivity to targeted inhibition of SMARCA4 in esophageal squamous cell carcinoma cell lines. Scientific reports 39 31406271
2014 The silencing of the SWI/SNF subunit and anticancer gene BRM in Rhabdoid tumors. Oncotarget 39 24913006
2012 Alterations of the SWI/SNF chromatin remodelling subunit-BRG1 and BRM in hepatocellular carcinoma. Liver international : official journal of the International Association for the Study of the Liver 39 23088494
2008 Brm transactivates the telomerase reverse transcriptase (TERT) gene and modulates the splicing patterns of its transcripts in concert with p54(nrb). The Biochemical journal 39 18042045
2022 Exquisite Sensitivity to Dual BRG1/BRM ATPase Inhibitors Reveals Broad SWI/SNF Dependencies in Acute Myeloid Leukemia. Molecular cancer research : MCR 38 34799403
2021 SMARCA4/SMARCA2-deficient Carcinoma of the Esophagus and Gastroesophageal Junction. The American journal of surgical pathology 38 33027072
2018 Inactivation of SMARCA2 by promoter hypermethylation drives lung cancer development. Gene 37 30447346
2007 SWI/SNF chromatin remodeling ATPase Brm regulates the differentiation of early retinal stem cells/progenitors by influencing Brn3b expression and Notch signaling. The Journal of biological chemistry 37 17855369
2009 Cdx2 and the Brm-type SWI/SNF complex cooperatively regulate villin expression in gastrointestinal cells. Experimental cell research 33 19371634
2016 Loss of the SWI/SNF ATPase subunits BRM and BRG1 drives lung cancer development. Oncoscience 32 28105457
2016 BRG1 and BRM SWI/SNF ATPases redundantly maintain cardiomyocyte homeostasis by regulating cardiomyocyte mitophagy and mitochondrial dynamics in vivo. Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology 31 27039070
2002 A putative nuclear receptor coactivator (TMF/ARA160) associates with hbrm/hSNF2 alpha and BRG-1/hSNF2 beta and localizes in the Golgi apparatus. FEBS letters 31 12044884
2019 BRM transcriptionally regulates miR-302a-3p to target SOCS5/STAT3 signaling axis to potentiate pancreatic cancer metastasis. Cancer letters 30 30790683
2015 SWI/SNF chromatin-remodeling enzymes Brahma-related gene 1 (BRG1) and Brahma (BRM) are dispensable in multiple models of postnatal angiogenesis but are required for vascular integrity in infant mice. Journal of the American Heart Association 30 25904594
2014 Concurrent loss of INI1, PBRM1, and BRM expression in epithelioid sarcoma: implications for the cocontributions of multiple SWI/SNF complex members to pathogenesis. Human pathology 30 25200863
2010 A switch from hBrm to Brg1 at IFNγ-activated sequences mediates the activation of human genes. Cell research 30 21079652
2021 The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation. Nucleic acids research 29 34289068
2019 New insights into DNA methylation signatures: SMARCA2 variants in Nicolaides-Baraitser syndrome. BMC medical genomics 29 31288860
2013 Association of two BRM promoter polymorphisms with head and neck squamous cell carcinoma risk. Carcinogenesis 29 23322154
2018 Degron mediated BRM/SMARCA2 depletion uncovers novel combination partners for treatment of BRG1/SMARCA4-mutant cancers. Biochemical and biophysical research communications 27 30527810
2011 BRM and BRG1 subunits of the SWI/SNF chromatin remodelling complex are downregulated upon progression of benign skin lesions into invasive tumours. The British journal of dermatology 26 21564052
2011 The glucocorticoid receptor and the coregulator Brm selectively modulate each other's occupancy and activity in a gene-specific manner. Molecular and cellular biology 26 21646426
2022 Switch/sucrose-non-fermentable (SWI/SNF) complex (SMARCA4, SMARCA2, INI1/SMARCB1)-deficient colorectal carcinomas are strongly associated with microsatellite instability: an incidence study in 4508 colorectal carcinomas. Histopathology 25 34951482
2008 Polycythemia vera transforming to acute myeloid leukemia and complex abnormalities including 9p homogeneously staining region with amplification of MLLT3, JMJD2C, JAK2, and SMARCA2. Cancer genetics and cytogenetics 25 18068534
2008 Manipulation of SMARCA2 and SMARCA4 transcript levels in porcine embryos differentially alters development and expression of SMARCA1, SOX2, NANOG, and EIF1. Reproduction (Cambridge, England) 24 18845624
1999 Nps1/Sth1p, a component of an essential chromatin-remodeling complex of Saccharomyces cerevisiae, is required for the maximal expression of early meiotic genes. Genes to cells : devoted to molecular & cellular mechanisms 24 10320476
2024 PROTACs Targeting BRM (SMARCA2) Afford Selective In Vivo Degradation over BRG1 (SMARCA4) and Are Active in BRG1 Mutant Xenograft Tumor Models. Journal of medicinal chemistry 23 38180485
2021 SMARCA2-NR4A3 is a novel fusion gene of extraskeletal myxoid chondrosarcoma identified by RNA next-generation sequencing. Genes, chromosomes & cancer 23 34124809
2018 Targeting of BRM Sensitizes BRG1-Mutant Lung Cancer Cell Lines to Radiotherapy. Molecular cancer therapeutics 23 30478150
2018 Identification of small molecule inhibitors targeting the SMARCA2 bromodomain from a high-throughput screening assay. Acta pharmacologica Sinica 22 29795359
2015 Frequent co-inactivation of the SWI/SNF subunits SMARCB1, SMARCA2 and PBRM1 in malignant rhabdoid tumours. Histopathology 22 25496315
2014 Loss of BRM expression is a frequently observed event in poorly differentiated clear cell renal cell carcinoma. Histopathology 22 24471421
2011 Complex alternative splicing of the smarca2 gene suggests the importance of smarca2-B variants. Journal of Cancer 21 21811517
2006 Role for Brm in cell growth control. Cancer research 21 16707429
2021 SMARCA2 Is a Novel Interactor of NSD2 and Regulates Prometastatic PTP4A3 through Chromatin Remodeling in t(4;14) Multiple Myeloma. Cancer research 20 33602783
2020 SMARCA2 is regulated by NORFA-miR-29c, a novel pathway that controls granulosa cell apoptosis and is related to female fertility. Journal of cell science 20 33148612
2018 SMARCA2-regulated host cell factors are required for MxA restriction of influenza A viruses. Scientific reports 20 29391557
2025 Discovery of FHD-286, a First-in-Class, Orally Bioavailable, Allosteric Dual Inhibitor of the Brahma Homologue (BRM) and Brahma-Related Gene 1 (BRG1) ATPase Activity for the Treatment of SWItch/Sucrose Non-Fermentable (SWI/SNF) Dependent Cancers. Journal of medicinal chemistry 19 39801091
2024 SETMAR Facilitates the Differentiation of Thyroid Cancer by Regulating SMARCA2-Mediated Chromatin Remodeling. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 19 38900084
2024 SMARCA4 and SMARCA2 co-deficiency: An uncommon molecular signature defining a subset of rare, aggressive and undifferentiated malignancies associated with defective chromatin remodeling. Cancer letters 19 39369768
2017 BRG1 and BRM function antagonistically with c-MYC in adult cardiomyocytes to regulate conduction and contractility. Journal of molecular and cellular cardiology 18 28232072

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