Affinage

SMARCAD1

SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A containing DEAD/H box 1 · UniProt Q9H4L7

Length
1026 aa
Mass
117.4 kDa
Annotated
2026-04-28
38 papers in source corpus 23 papers cited in narrative 23 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCAD1 is an ATP-dependent chromatin remodeler of the SNF2 family that maintains heterochromatin, facilitates DNA repair, and supports genome integrity during replication. It catalyzes histone octamer exchange and de novo nucleosome assembly, preferentially remodeling subnucleosomal hexasomes over canonical nucleosomes, with its activity modulated by phosphorylation and synergy with the FACT chaperone complex (PMID:34652950, PMID:40468067, PMID:39424143). At DNA double-strand breaks, ATM-dependent phosphorylation at T906 and RING1-mediated ubiquitination at K905 recruit SMARCAD1 to promote EXO1/Sgs1-dependent end resection and homologous recombination, while its interaction with MSH2-MSH3 coordinates repair pathway choice by inhibiting polymerase theta-mediated end joining; SMARCAD1 also facilitates MutLα recruitment to MutSα for mismatch repair-dependent apoptosis (PMID:22960744, PMID:29888761, PMID:37140056, PMID:31843968). During replication, SMARCAD1 binds PCNA directly and associates with KAP1, HDAC1/2, and G9a/GLP to re-establish repressive H3K9me3 heterochromatin on nascent chromatin, stabilizes active forks by displacing 53BP1 to prevent ATAD5-mediated PCNA unloading, and is essential for heterochromatin maintenance during early embryonic development; mutations in its skin-specific isoform cause autosomal-dominant adermatoglyphia (PMID:21549307, PMID:33952518, PMID:39969508, PMID:21820097).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 2008 Medium

    Establishing that SMARCAD1 physically associates with KAP1/TRIM28 and occupies transcriptional start sites opened the question of whether it functions in gene regulation through heterochromatin.

    Evidence Co-immunoprecipitation and ChIP-chip in human cells

    PMID:18675275

    Open questions at the time
    • Single Co-IP without independent biochemical validation of directness
    • No functional consequence of the interaction demonstrated
    • Target gene regulation not tested
  2. 2011 High

    Two contemporaneous studies established SMARCAD1's dual roles: maintaining repressive heterochromatin through PCNA-coupled recruitment to replication forks (with KAP1, HDAC1/2, G9a/GLP), and causing adermatoglyphia through haploinsufficiency of a skin-specific isoform — linking chromatin remodeling to both epigenetic inheritance and human disease.

    Evidence Co-IP, PCNA interaction assays, histone modification analysis, ATPase mutant rescue in human cells; linkage analysis, minigene splicing assay, and RT-PCR in adermatoglyphia families

    PMID:21549307 PMID:21820097

    Open questions at the time
    • Mechanism by which SMARCAD1 ATPase activity promotes HDAC1/2 and G9a deacetylation/methylation not resolved
    • Skin-specific isoform function at the protein level unknown
    • Whether PCNA binding is direct or bridged was not structurally defined
  3. 2012 High

    Demonstrating that SMARCAD1/Fun30 promotes 5ʹ-to-3ʹ DNA end resection via both EXO1- and Sgs1-dependent pathways established it as a key chromatin remodeler enabling homologous recombination at DSBs.

    Evidence ChIP at DSBs, resection assays, ATPase mutant analysis, genetic epistasis in yeast and human cells

    PMID:22960744

    Open questions at the time
    • How SMARCAD1 remodeling at break ends mechanistically facilitates nuclease access was not defined
    • Whether SMARCAD1 acts on nucleosomes directly at DSBs or indirectly was unclear
  4. 2016 High

    Showing that SMARCAD1 cooperates with CBP to stimulate ATP-dependent H2A acetylation at K5/K8 on chromatin templates revealed a transcription-activating function distinct from its heterochromatin maintenance role.

    Evidence Biochemical reconstitution from Drosophila nuclear extracts, in vitro histone acetylation assays, ChIP-seq, genetic interaction in Drosophila

    PMID:26888216

    Open questions at the time
    • Whether this activating function operates at specific gene classes in mammalian cells not shown
    • Relationship between H2A acetylation and octamer exchange activity unclear
  5. 2017 High

    Mapping the CUE1 domain as the direct interface for KAP1 binding and showing its requirement for nuclear retention and target gene occupancy defined the structural basis of SMARCAD1's heterochromatin partnership, while recognition of H3R26Cit revealed a chromatin mark that directs SMARCAD1 to suppress H3K9me3 in naive pluripotent cells.

    Evidence Reciprocal Co-IP, in vitro pulldown with purified proteins, CUE1 mutants, ChIP at KAP1 targets; histone peptide array, ChIP-seq in ESCs, knockdown phenotype

    PMID:28355564 PMID:29284678

    Open questions at the time
    • Whether H3R26Cit is a direct binding determinant in the context of full nucleosomes not reconstituted
    • How CUE1-KAP1 binding is coordinated with PCNA interaction at replication forks unknown
  6. 2018 High

    Identification of ATM-dependent T906 phosphorylation and RING1-mediated K905 ubiquitination as sequential, essential modifications for DSB recruitment resolved how SMARCAD1 is targeted to damage sites, while its Msh2-dependent recruitment to mismatches — counteracting CAF-1 chromatin assembly — extended its repair roles to mismatch repair.

    Evidence Phosphorylation mapping, ATM inhibitor experiments, site-directed mutagenesis and HR assays; Xenopus egg extract reconstitution and yeast genetic epistasis

    PMID:29888761 PMID:29899141

    Open questions at the time
    • Whether T906 phosphorylation creates a specific reader-binding motif is unknown
    • How SMARCAD1 counteracts CAF-1 nucleosome deposition mechanistically not defined
  7. 2019 High

    Demonstrating that SMARCAD1 ATPase activity facilitates MutLα recruitment to chromatin-bound MutSα after alkylation damage established SMARCAD1 as a chromatin remodeling link between mismatch recognition and apoptotic signaling.

    Evidence SMARCAD1 KO cells, MNU treatment, Co-IP of MutLα with chromatin-bound MutSα, caspase-9 activation, ATPase mutant analysis

    PMID:31843968

    Open questions at the time
    • Whether SMARCAD1 directly remodels nucleosomes at mismatch sites or acts indirectly not distinguished
    • Relationship between MMR apoptotic function and mismatch correction function not resolved
  8. 2021 High

    Biochemical and structural characterization revealed SMARCAD1 as a histone octamer exchange factor capable of de novo nucleosome assembly, with a unique cryo-EM-defined nucleosome engagement mode, while parallel work showed it stabilizes replication forks by displacing 53BP1 to prevent ATAD5-mediated PCNA unloading.

    Evidence In vitro octamer transfer/assembly assays, cryo-EM structure; DNA fiber assays in SMARCAD1 KO with 53BP1/BRCA1/ATAD5 epistasis

    PMID:33952518 PMID:34652950

    Open questions at the time
    • How octamer exchange relates to 53BP1 displacement at forks mechanistically unclear
    • Whether fork stabilization requires ATPase-driven remodeling or protein-protein displacement not resolved
  9. 2022 Medium

    Linking SMARCAD1 to SIRT1 chromatin dynamics during heat stress showed that SMARCAD1 depletion phenocopies hyperthermia in impairing resection, expanding its role to stress-responsive chromatin modulation at DSBs.

    Evidence Histone modification analysis, SIRT1 ChIP, SMARCAD1 depletion, resection assays after heat shock

    PMID:35434547

    Open questions at the time
    • Whether SMARCAD1 directly opposes SIRT1 or acts indirectly through chromatin state not resolved
    • Single study without independent replication
  10. 2023 Medium

    Demonstrating that the MSH2-MSH3–SMARCAD1 complex recruits and activates EXO1 while blocking POLθ access at DSBs established a molecular mechanism for SMARCAD1-mediated repair pathway choice favoring HR over TMEJ, and identification of a direct TFIIIC interaction expanded SMARCAD1's interactome beyond repair and heterochromatin.

    Evidence Co-IP, EXO1 activity assays, HR vs TMEJ pathway assays; endogenous reciprocal Co-IP and purified protein binding for TFIIIC

    PMID:37140056 PMID:37761933

    Open questions at the time
    • Functional consequence of TFIIIC interaction for Pol III transcription not established
    • Whether MSH2-MSH3 binding to SMARCAD1 is direct or mediated through DNA/chromatin substrates not fully resolved
  11. 2024 High

    Phosphorylation was shown to inhibit SMARCAD1's nucleosome binding, ATPase, and histone exchange activities while sparing H3-H4 binding and nucleosome assembly, revealing a regulatory switch that may tune its remodeling output; separately, SMARCAD1 was found essential for retroviral silencing through stabilizing KAP1 at proviral DNA and promoting H3.3 deposition.

    Evidence In vitro activity assays with phosphomimetic mutants, mass spectrometry; ChIP kinetics of SMARCAD1/KAP1/H3.3 at MLV provirus, GFP-reporter repression assay

    PMID:38468276 PMID:39424143

    Open questions at the time
    • Which kinase(s) phosphorylate SMARCAD1 at the inhibitory sites in vivo not identified
    • Whether H3.3 deposition at provirus requires SMARCAD1's octamer exchange activity directly is untested
  12. 2025 High

    Cryo-EM structures of SMARCAD1 bound to hexasomes and nucleosomes revealed that it preferentially remodels hexasomes through family-specific structural elements, with FACT synergistically promoting its activity, providing a mechanistic basis for its substrate selectivity; concurrent work showed SMARCAD1 and TOPBP1 are required for heterochromatin maintenance and chromocenter integrity during early embryonic development.

    Evidence Cryo-EM structures, in vitro hexasome/nucleosome remodeling with mutagenesis, FACT co-activity assays; chromatome proteomics, SMARCAD1 depletion in mouse embryos with H3K9me3 and chromocenter phenotyping

    PMID:39969508 PMID:40468067

    Open questions at the time
    • Whether hexasome preference operates genome-wide in vivo or at specific loci is unknown
    • Mechanistic link between SMARCAD1 and TOPBP1 at heterochromatin not reconstituted
    • How FACT–SMARCAD1 cooperation is regulated in cells not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unknown how SMARCAD1's distinct activities — octamer exchange, 53BP1 displacement, end resection promotion, heterochromatin maintenance, and mismatch repair facilitation — are coordinately regulated at specific genomic loci and cell cycle stages, and whether its hexasome preference underlies its replication fork functions.
  • No integrated model connecting phosphorylation-dependent activity modulation to specific in vivo functions
  • Structural basis of PCNA interaction and its relationship to hexasome remodeling unknown
  • Cell-cycle-dependent regulation of SMARCAD1's repair versus heterochromatin functions not resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 7 GO:0042393 histone binding 4 GO:0140096 catalytic activity, acting on a protein 3 GO:0003677 DNA binding 2
Localization
GO:0005634 nucleus 4 GO:0005694 chromosome 4
Pathway
R-HSA-4839726 Chromatin organization 6 R-HSA-73894 DNA Repair 6 R-HSA-69306 DNA Replication 2 R-HSA-74160 Gene expression (Transcription) 2
Partners
EHMT2HDAC1HDAC2KAP1MSH2MSH3PCNARING1
Complex memberships
SMARCAD1-KAP1-HDAC1/2-G9a/GLPSMARCAD1-MSH2-MSH3

Evidence

Reading pass · 23 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 SMARCAD1 (and its yeast ortholog Fun30) is recruited to DNA double-strand break ends and promotes both Exo1- and Sgs1-dependent 5'-to-3' DNA end resection through a mechanism requiring its ATPase activity, facilitating homologous recombination repair. ChIP at DSBs, resection assays, ATPase mutant analysis, genetic epistasis with Exo1/Sgs1, camptothecin/PARP inhibitor sensitivity assays Nature High 22960744
2011 SMARCAD1 ATPase activity is required for global deacetylation of histones H3/H4 and subsequent H3K9 methylation; SMARCAD1 associates with KAP1, HDAC1/2, and the histone methyltransferase G9a/GLP, and directly interacts with PCNA to be recruited to replication forks, thereby maintaining repressive heterochromatin after replication. Co-immunoprecipitation, PCNA interaction assays, histone modification analysis, ATPase mutant rescue, RNAi knockdown with heterochromatin/chromosome segregation phenotype readout Molecular cell High 21549307
2018 ATM kinase phosphorylates SMARCAD1 at T906 in response to ionizing radiation, which is required for SMARCAD1 recruitment to DSBs; T906 phosphorylation is also required for subsequent ubiquitination of SMARCAD1 at K905 by RING1, and both modifications are essential for DNA end resection and HR-mediated repair. In vivo phosphorylation mapping, ATM inhibitor experiments, site-directed mutagenesis (T906A, K905R), Co-IP, HR repair assays, cell survival assays iScience High 29888761
2018 Nucleosomes are excluded from a >1-kb region surrounding a mismatched base pair in a process dependent on Msh2-Msh6; Smarcad1/Fun30 is recruited to mismatch-carrying DNA in an Msh2-dependent but Mlh1-independent manner and facilitates mismatch repair by counteracting CAF-1-mediated chromatin assembly. Xenopus egg extract chromatin assembly/MMR assays, depletion experiments, genetic epistasis in budding yeast (double mutants with MSH2/3/6 and CAF-1) Genes & development High 29899141
2017 The CUE1 domain of SMARCAD1 directly mediates interaction with the RBCC domain of KAP1 (TRIM28), and this interaction is required for nuclear retention of SMARCAD1 and its binding to KAP1 target genes including zinc finger protein and imprinted genes. Reciprocal Co-IP, in vitro pulldown with purified proteins, CUE1 domain mutants, ChIP at KAP1 target genes, nuclear fractionation The Journal of biological chemistry High 29284678
2021 SMARCAD1 is an ATP-dependent histone octamer exchange factor capable of transferring the entire histone octamer from one DNA segment to another, and can perform de novo nucleosome assembly from histone octamer due to simultaneous binding of all histones; cryo-EM structure shows its ATPase domains engage the nucleosome differently from other remodelers. In vitro biochemical assays (octamer transfer, nucleosome assembly), cryo-EM structure determination, ATPase assays Science advances High 34652950
2021 SMARCAD1 stabilizes active replication forks by preventing accumulation of 53BP1-associated nucleosomes; loss of SMARCAD1 allows 53BP1-mediated untimely PCNA removal via ATAD5, causing fork stalling, impaired fork restart, and ssDNA accumulation, which is rescued by 53BP1 loss in a BRCA1-dependent manner. Replication fork assays (DNA fiber), SMARCAD1 KO, epistasis with 53BP1/BRCA1/ATAD5, PCNA unloading assays, ssDNA detection Science advances High 33952518
2019 SMARCAD1 promotes MMR-dependent apoptosis by facilitating recruitment of MutLα (MLH1-PMS2) to chromatin-bound MutSα (MSH2-MSH6) in response to O6-methylguanine; this function depends on SMARCAD1's ATPase activity. SMARCAD1 knockout cells, MNU treatment, co-immunoprecipitation of MutLα with chromatin-bound MutSα, caspase-9 activation assay, ATPase mutant analysis The Journal of biological chemistry High 31843968
2016 SMARCAD1 acts with CBP to stimulate H2A acetylation at K5 and K8 within nucleosomes in an ATP-dependent manner, thereby activating transcription from chromatin templates; CBP is recruited to promoters prior to SMARCAD1, and genetic interaction between SMARCAD1/Etl1 and CBP/nej was confirmed in Drosophila. Biochemical column purification of activity from Drosophila nuclear extracts, in vitro histone acetylation assays, ChIP-seq, expression arrays, RNAi knockdown, Drosophila genetics Scientific reports High 26888216
2017 SMARCAD1 preferentially associates with H3 arginine 26 citrullination (H3R26Cit); genome-wide co-localization of H3R26Cit and SMARCAD1 binding is extensive, and SMARCAD1 suppresses H3K9me3 heterochromatin formation at H3R26Cit-marked regions to maintain naive pluripotency. Histone peptide array binding (384 modifications), ChIP-seq, Smarcad1 knockdown in ESCs, H3Cit inhibition experiments Cell reports Medium 28355564
2011 A skin-specific short isoform of SMARCAD1 is exclusively expressed in skin; splice-site mutations in the noncoding exon of this isoform cause autosomal-dominant adermatoglyphia by reducing stability of this short RNA isoform, implicating this isoform in dermatoglyph (fingerprint) development. Linkage/haplotype analysis, sequencing, minigene splicing assay, RT-PCR stability analysis American journal of human genetics Medium 21820097
2008 Endogenous SMARCAD1 forms a protein complex with TRIM28 (KAP1) and binds in the vicinity of transcriptional start sites of candidate target genes. Protein co-immunoprecipitation, ChIP with genome tiling microarrays Journal of molecular biology Medium 18675275
2023 MSH2-MSH3 is recruited to DNA DSB sites through interaction with SMARCAD1, and the MSH2-MSH3-SMARCAD1 complex facilitates recruitment of EXO1 for long-range resection, enhances EXO1 enzymatic activity, and inhibits POLθ access to DSBs, thereby promoting HR over polymerase theta-mediated end-joining. Co-immunoprecipitation, DSB recruitment assays, EXO1 activity assays, HR vs TMEJ repair pathway assays, knockdown/knockout experiments Nucleic acids research Medium 37140056
2023 SMARCAD1 directly interacts with the RNA Pol III transcription factor TFIIIC in mouse and human cells; this interaction is conserved across somatic and pluripotent cell types. SMARCAD1 also associates with architectural proteins cohesin, laminB, and DDX5 in mammalian cells. Endogenous co-immunoprecipitation, purified protein direct interaction assay, ChIP-seq, gene expression analysis Genes Medium 37761933
2024 Phosphorylation of SMARCAD1 reduces its binding to nucleosomes, DNA, and histones H2A-H2B, and inhibits its ATP hydrolysis and histone exchange activities; the N-terminal region of SMARCAD1 is critical for nucleosome assembly and histone exchange. Phosphorylation has only marginal effect on H3-H4 binding and nucleosome assembly. Mutational analysis, in vitro activity assays (ATPase, histone exchange, nucleosome assembly), mass spectrometry phosphorylation mapping The Journal of biological chemistry High 39424143
2025 SMARCAD1 preferentially remodels subnucleosomal hexasomes over canonical nucleosomes; cryo-EM structures of SMARCAD1 bound to nucleosome and hexasome reveal family-specific elements mediating hexasome binding; SMARCAD1 binds the canonical nucleosome in an inactive conformation. The FACT histone chaperone complex acts synergistically with H2A-H2B to promote SMARCAD1 activity in nucleosome remodeling. Cryo-EM structure determination, in vitro remodeling assays with hexasomes and nucleosomes, mutagenesis of family-specific elements, FACT co-activity assays Nature High 40468067
2025 SMARCAD1 and TOPBP1 associate with H3K9me3-heterochromatin in ESCs and are required for maintenance of chromocenters at the transition from the 2C-like to the pluripotent state; SMARCAD1 nuclear localization is lost in 2C-like cells, and depletion of SMARCAD1 in mouse embryos causes developmental arrest, reduction of H3K9me3, and remodeling of heterochromatin foci. Chromatome profiling (genome capture proteomics), SMARCAD1/TOPBP1 depletion in mouse embryos, H3K9me3 ChIP/immunofluorescence, inducible 2C-like conversion system eLife Medium 39969508
2024 At broken replication forks (single-ended DSBs), SMARCAD1 displaces 53BP1 to facilitate localization of ubiquitinated PCNA and PIF1 to DSBs, thereby activating break-induced replication (BIR). Epistasis analysis in cells, foci/localization assays for ubiquitinated PCNA and PIF1, SMARCAD1 knockdown, 53BP1 knockout bioRxivpreprint Low bio_10.1101_2024.09.11.612483
2024 SMARCAD1 directly binds R-loops via its ATPase domain and associates with the replisome through its N-terminal region; loss of these interactions leads to R-loop accumulation at active replication forks and increased mutagenesis at cancer mutation hotspots. In vitro R-loop binding assays, domain mutant analysis, genome-wide R-loop mapping (DRIP-seq), mutagenesis assays, SMARCAD1 mutant cell lines bioRxivpreprint Medium bio_10.1101_2024.09.13.612941
2024 PARP1-mediated recruitment of the SMARCAD1-MSH2/MSH3 complex to DSBs inhibits loading of DNA polymerase theta (POLθ), thereby suppressing TMEJ; this repressive complex is diminished in DNMT3A-mutant leukemia cells. Co-immunoprecipitation of SMARCAD1-MSH2/MSH3 complex, PARP1 inhibition experiments, POLθ loading assays at DSBs bioRxivpreprint Low bio_10.1101_2024.09.15.613155
2020 The yeast Fun30 chromatin remodeling enzyme (SMARCAD1 ortholog) is required for efficient pre-mRNA splicing; Fun30 is enriched in the gene body of intron-containing genes, and its chromatin remodeling activity is required for spliceosome recruitment. In mammalian cells, SMARCAD1 regulates alternative splicing. RNA-seq splicing analysis in fun30Δ yeast, ChIP of Fun30 at intron-containing genes, spliceosome recruitment ChIP, SMARCAD1 knockdown alternative splicing assay Biochemical and biophysical research communications Low 32234239
2024 Smarcad1 is recruited to MLV provirus immediately upon integration and is required for establishment and maintenance of Trim28-dependent retroviral silencing; Smarcad1 stabilizes Trim28 binding to the provirus and is needed for proper deposition of histone H3.3 on the provirus. ChIP of Smarcad1/Trim28 at provirus, GFP-reporter MLV repression kinetics, Smarcad1 KD, H3.3 ChIP Mobile DNA Medium 38468276
2022 Heat-induced SIRT1 recruitment to chromatin and H4K16 deacetylation impairs DNA end resection and HR repair; depletion of SMARCAD1 antagonizes SIRT1 recruitment to chromatin, and loss of SMARCAD1 phenocopies hyperthermia in impairing resection. Histone modification analysis after heat shock, SIRT1 ChIP, SMARCAD1 depletion, resection assays, γ-H2AX analysis iScience Medium 35434547

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 The yeast Fun30 and human SMARCAD1 chromatin remodellers promote DNA end resection. Nature 218 22960744
2011 Maintenance of silent chromatin through replication requires SWI/SNF-like chromatin remodeler SMARCAD1. Molecular cell 147 21549307
2018 SMARCAD1 Phosphorylation and Ubiquitination Are Required for Resection during DNA Double-Strand Break Repair. iScience 46 29888761
1992 The mouse Enhancer trap locus 1 (Etl-1): a novel mammalian gene related to Drosophila and yeast transcriptional regulator genes. Mechanisms of development 41 1489724
2000 SMARCAD1, a novel human helicase family-defining member associated with genetic instability: cloning, expression, and mapping to 4q22-q23, a band rich in breakpoints and deletion mutants involved in several human diseases. Genomics 40 11031099
2017 SMARCAD1 Contributes to the Regulation of Naive Pluripotency by Interacting with Histone Citrullination. Cell reports 39 28355564
1999 Skeletal dysplasias, growth retardation, reduced postnatal survival, and impaired fertility in mice lacking the SNF2/SWI2 family member ETL1. Mechanisms of development 36 10415348
2019 SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT. International journal of biological sciences 34 30745850
2011 A mutation in a skin-specific isoform of SMARCAD1 causes autosomal-dominant adermatoglyphia. American journal of human genetics 34 21820097
2018 Nucleosomes around a mismatched base pair are excluded via an Msh2-dependent reaction with the aid of SNF2 family ATPase Smarcad1. Genes & development 29 29899141
2021 SMARCAD1-mediated active replication fork stability maintains genome integrity. Science advances 28 33952518
2021 SMARCAD1 is an ATP-dependent histone octamer exchange factor with de novo nucleosome assembly activity. Science advances 26 34652950
2008 The novel protein complex with SMARCAD1/KIAA1122 binds to the vicinity of TSS. Journal of molecular biology 26 18675275
2017 The CUE1 domain of the SNF2-like chromatin remodeler SMARCAD1 mediates its association with KRAB-associated protein 1 (KAP1) and KAP1 target genes. The Journal of biological chemistry 24 29284678
2016 SMARCAD1 is an ATP-dependent stimulator of nucleosomal H2A acetylation via CBP, resulting in transcriptional regulation. Scientific reports 22 26888216
2023 MSH2-MSH3 promotes DNA end resection during homologous recombination and blocks polymerase theta-mediated end-joining through interaction with SMARCAD1 and EXO1. Nucleic acids research 18 37140056
2016 SMARCAD1 knockdown uncovers its role in breast cancer cell migration, invasion, and metastasis. Expert opinion on therapeutic targets 17 27232533
1993 The Etl-1 gene encodes a nuclear protein differentially expressed during early mouse development. Developmental dynamics : an official publication of the American Association of Anatomists 17 8219362
2019 Nucleosome Remodeling by Fun30SMARCAD1 in the DNA Damage Response. Frontiers in molecular biosciences 16 31555662
2018 SMARCAD1 in Breast Cancer Progression. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 14 30308496
2019 SMARCAD1-mediated recruitment of the DNA mismatch repair protein MutLα to MutSα on damaged chromatin induces apoptosis in human cells. The Journal of biological chemistry 13 31843968
2016 Genome-wide linkage analysis and whole-genome sequencing identify a recurrent SMARCAD1 variant in a unique Chinese family with Basan syndrome. European journal of human genetics : EJHG 13 26932190
2022 Heat-induced SIRT1-mediated H4K16ac deacetylation impairs resection and SMARCAD1 recruitment to double strand breaks. iScience 11 35434547
2014 Mutations in SMARCAD1 cause autosomal dominant adermatoglyphia and perturb the expression of epidermal differentiation-associated genes. The British journal of dermatology 11 24909267
2020 The Mechanism of Chromatin Remodeler SMARCAD1/Fun30 in Response to DNA Damage. Frontiers in cell and developmental biology 10 33102471
2018 Basan gets a new fingerprint: Mutations in the skin-specific isoform of SMARCAD1 cause ectodermal dysplasia syndromes with adermatoglyphia. American journal of medical genetics. Part A 9 30289605
2024 The role of Smarcad1 in retroviral repression in mouse embryonic stem cells. Mobile DNA 3 38468276
2023 Antler-derived microRNA PC-5p-1090 inhibits HCC cell proliferation, migration, and invasion by targeting MARCKS, SMARCAD1, and SOX9. Functional & integrative genomics 3 37165199
2023 The Conserved Chromatin Remodeler SMARCAD1 Interacts with TFIIIC and Architectural Proteins in Human and Mouse. Genes 3 37761933
2025 SMARCAD1 and TOPBP1 contribute to heterochromatin maintenance at the transition from the 2C-like to the pluripotent state. eLife 2 39969508
2020 Role of the ATP-dependent chromatin remodeling enzyme Fun30/Smarcad1 in the regulation of mRNA splicing. Biochemical and biophysical research communications 2 32234239
2025 Replication across O6-methylguanine activates futile cycling of DNA mismatch repair attempts assisted by the chromatin-remodelling enzyme Smarcad1. Journal of biochemistry 1 39882945
2024 Phosphorylation regulates the chromatin remodeler SMARCAD1 in nucleosome binding, ATP hydrolysis, and histone exchange. The Journal of biological chemistry 1 39424143
2022 Association between Mutation in SMARCAD1 and Basan Syndrome with Cutaneous Squamous Cell Carcinoma. Disease markers 1 35592705
2026 Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks. Nucleic acids research 0 41978269
2025 Subnucleosome preference of human chromatin remodeller SMARCAD1. Nature 0 40468067
2025 SMARCA4 regulates SMARCAD1 expression for toleration of replication stress in non-small cell lung cancer. Fujita medical journal 0 41641123
2023 Retracted: Association between Mutation in SMARCAD1 and Basan Syndrome with Cutaneous Squamous Cell Carcinoma. Disease markers 0 37387737