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
2026-06-10
36 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

SMARCAD1 is an ATP-dependent SWI/SNF-family chromatin remodeler that uses nucleosome mobilization to coordinate DNA double-strand break repair, replication fork integrity, mismatch repair, and heterochromatin maintenance (PMID:22960744, PMID:21549307, PMID:34652950). Biochemically it can transfer entire histone octamers between DNA segments, assemble nucleosomes de novo by simultaneously engaging all four histones, and stimulate CBP-mediated H2A acetylation in an ATP-dependent manner, with a strong substrate preference for subnucleosomal hexasomes over canonical nucleosomes that is structurally explained by family-specific elements engaging the hexasome and an inactive binding mode on the full nucleosome (PMID:34652950, PMID:26888216, PMID:40468067). At DNA breaks SMARCAD1 promotes Exo1- and Sgs1-dependent 5'-to-3' end resection through its ATPase activity, channeling repair toward homologous recombination (PMID:22960744); recruitment to breaks depends on ATM phosphorylation at T906, which licenses RING1-mediated ubiquitination at K905 (PMID:29888761), and is reinforced by direct interaction with the MSH2-MSH3 complex that enhances EXO1 activity while blocking POLθ-dependent end joining (PMID:37140056). At replication forks SMARCAD1 prevents accumulation of 53BP1-associated nucleosomes, thereby blocking 53BP1/ATAD5-mediated premature PCNA unloading and stabilizing active forks (PMID:33952518). In heterochromatin, its ATPase activity drives histone H3/H4 deacetylation and H3K9 methylation in concert with KAP1/TRIM28, HDAC1/2, and G9a/GLP, with the CUE1 domain binding the KAP1 RBCC domain to mediate nuclear retention and genomic targeting (PMID:21549307, PMID:29284678). SMARCAD1 also facilitates mismatch repair in a chromatin context by enabling nucleosome exclusion at mismatches and recruitment of MutLα to chromatin-bound MutSα (PMID:29899141, PMID:31843968). A splice-site mutation in a skin-specific short isoform of SMARCAD1 causes autosomal-dominant adermatoglyphia (PMID:21820097).

Mechanistic history

Synthesis pass · year-by-year structured walk · 21 steps
  1. 2008 Medium

    Established the first physical and chromatin-binding context for SMARCAD1, linking it to the corepressor KAP1/TRIM28 and to promoter-proximal genomic sites.

    Evidence Endogenous Co-IP and ChIP with tiling microarrays in human cells

    PMID:18675275

    Open questions at the time
    • No remodeling activity demonstrated
    • Functional consequence of TRIM28 binding undefined
  2. 2011 High

    Defined SMARCAD1 as an ATPase-dependent driver of histone deacetylation and H3K9 methylation that couples heterochromatin maintenance to replication via PCNA.

    Evidence ATPase mutant complementation, Co-IP with KAP1/HDAC1-2/G9a-GLP, histone-mark ChIP, replication-foci imaging

    PMID:21549307

    Open questions at the time
    • Direct enzymatic remodeling step not reconstituted in vitro
    • Order of deacetylation vs methylation events unresolved
  3. 2011 Medium

    Connected SMARCAD1 to a human Mendelian phenotype, showing a skin-specific isoform splice defect underlies adermatoglyphia.

    Evidence Linkage, Sanger sequencing, minigene splicing assay, RT-PCR stability

    PMID:21820097

    Open questions at the time
    • Mechanism linking isoform loss to dermatoglyph development unknown
    • Single-family/locus depth
  4. 2012 High

    Placed SMARCAD1/Fun30 directly in DSB end resection, identifying it as an ATPase-dependent promoter of Exo1/Sgs1 pathways feeding homologous recombination.

    Evidence ChIP at DSBs, ATPase-dead mutants, epistasis with Exo1/Sgs1, drug-sensitivity assays in yeast and human cells

    PMID:22960744

    Open questions at the time
    • Nucleosome substrate at the break not structurally defined
    • Recruitment signal to DSBs not identified
  5. 2016 High

    Showed SMARCAD1 acts as a positive cofactor for histone acetylation/transcription, broadening its activity beyond repression.

    Evidence Activity purification from Drosophila extracts, in vitro H2A acetylation and transcription assays, ChIP-seq, fly genetics

    PMID:26888216

    Open questions at the time
    • Mechanism by which ATPase stimulates CBP unclear
    • Mammalian generality of transcriptional activation not established
  6. 2017 High

    Mapped the CUE1 domain to KAP1 RBCC binding, explaining how SMARCAD1 achieves nuclear retention and targeting to imprinted/ZFP loci.

    Evidence Endogenous Co-IP, purified-protein binding, domain mutants, ChIP, nuclear fractionation

    PMID:29284678

    Open questions at the time
    • Whether KAP1 binding regulates remodeling activity untested
    • Targeting at non-KAP1 loci unexplained
  7. 2017 Medium

    Linked SMARCAD1 to a histone-mark reader function (H3R26 citrullination) that restrains H3K9me3 and supports naive pluripotency.

    Evidence Histone peptide array, ChIP-seq, knockdown, embryoid body/chimera assays

    PMID:28355564

    Open questions at the time
    • Direct binding domain for H3R26Cit not mapped
    • Relationship to its heterochromatin-promoting role unresolved
  8. 2018 Medium

    Identified the ATM-T906 phosphorylation/RING1-K905 ubiquitination switch governing SMARCAD1 recruitment to breaks for resection and HR.

    Evidence T906/K905 mutagenesis, phospho-specific antibodies, IR-foci and HR reporter assays

    PMID:29888761

    Open questions at the time
    • RING1 E3 specificity not validated reciprocally
    • Single-lab data
  9. 2018 High

    Extended SMARCAD1 function to mismatch repair, showing Msh2-dependent recruitment and nucleosome exclusion around mismatches.

    Evidence Xenopus extract chromatin assembly/disassembly, immunodepletion, yeast genetic epistasis with MSH6/MSH3

    PMID:29899141

    Open questions at the time
    • Whether remodeling precedes or follows MutSα binding unclear
    • Direct MSH2 contact not mapped
  10. 2019 Medium

    Showed SMARCAD1 ATPase activity is needed for MutLα recruitment to chromatin-bound MutSα, coupling remodeling to MMR signaling and apoptosis.

    Evidence KO and ATPase-mutant rescue, chromatin-fraction Co-IP after MNU, sub-G1/caspase readouts

    PMID:31843968

    Open questions at the time
    • Direct vs indirect effect on MutLα loading unresolved
    • Single-lab
  11. 2021 High

    Defined a replication-fork protection role: SMARCAD1 evicts 53BP1-associated nucleosomes to prevent ATAD5-driven premature PCNA unloading.

    Evidence KO/KD, 53BP1/BRCA1/ATAD5 epistasis, DNA fiber, iPOND, rescue experiments

    PMID:33952518

    Open questions at the time
    • Structural basis of 53BP1-nucleosome eviction not defined
    • How SMARCAD1 distinguishes fork nucleosomes unknown
  12. 2021 High

    Provided the biochemical/structural foundation: SMARCAD1 performs ATP-dependent octamer exchange and de novo assembly, binding all four histones, with an atypical ATPase-nucleosome engagement.

    Evidence In vitro histone exchange/assembly assays and cryo-EM of purified components

    PMID:34652950

    Open questions at the time
    • In vivo substrate that requires octamer transfer not pinpointed
    • Regulation of assembly vs eviction modes unclear
  13. 2023 Medium

    Identified MSH2-MSH3 as a direct DSB partner that, with SMARCAD1, enhances EXO1 resection and suppresses POLθ/TMEJ.

    Evidence Co-IP, in vitro EXO1 activity assays, recruitment and HR/TMEJ reporters, knockdown epistasis

    PMID:37140056

    Open questions at the time
    • Stoichiometry/order of SMARCAD1-MSH2/3-EXO1 assembly unresolved
    • Single-lab
  14. 2023 Medium

    Expanded the SMARCAD1 interactome to TFIIIC, cohesin, laminB and DDX5, implicating it in higher-order chromatin organization and Pol III contexts.

    Evidence Endogenous Co-IP across cell types plus purified-protein direct binding

    PMID:37761933

    Open questions at the time
    • Functional consequence of TFIIIC interaction untested
    • Whether interactions are simultaneous or distinct complexes unknown
  15. 2024 Medium

    Showed phosphorylation tunes SMARCAD1 activity by weakening nucleosome/DNA/H2A-H2B binding and ATP hydrolysis, and identified the N-terminus as critical for assembly/exchange.

    Evidence In vitro ATPase/exchange/assembly assays with phospho-site mutants and mass spectrometry

    PMID:39424143

    Open questions at the time
    • Responsible kinase(s) in this context not defined
    • In vivo relevance of these phospho-sites untested
  16. 2024 Medium

    Implicated SMARCAD1 in proviral silencing, showing it stabilizes Trim28 binding and H3.3 deposition to repress MLV in ESCs.

    Evidence MLV-GFP reporter, ChIP for Trim28/H3.3, single and double knockdown

    PMID:38468276

    Open questions at the time
    • Mechanism of H3.3 deposition support unclear
    • Trim28-independent component undefined
  17. 2024 Medium

    Proposed SMARCAD1 as an R-loop-resolving factor at replication forks, binding R-loops via its ATPase domain and the replisome via its N-terminus (preprint).

    Evidence In vitro R-loop binding, replisome Co-IP, domain mutants, DRIP-seq (preprint)

    PMID:bio_10.1101_2024.09.13.612941

    Open questions at the time
    • Preprint, not peer-reviewed
    • Direct enzymatic R-loop resolution vs displacement not distinguished
  18. 2025 High

    Resolved the structural basis of substrate selectivity, showing SMARCAD1 prefers hexasomes over canonical nucleosomes and is co-activated by FACT plus H2A-H2B.

    Evidence Cryo-EM of SMARCAD1-hexasome and -nucleosome complexes, remodeling assays, mutagenesis of family-specific elements, FACT co-activity

    PMID:40468067

    Open questions at the time
    • When hexasome substrates arise in vivo not defined
    • Link between hexasome preference and specific repair pathways unclear
  19. 2025 Medium

    Tied SMARCAD1 to embryonic heterochromatin via TOPBP1 partnership, with depletion causing H3K9me3 loss and developmental arrest.

    Evidence Chromatome profiling, live-cell imaging in ESC vs 2C-like cells, embryo depletion, H3K9me3 ChIP/immunostaining

    PMID:39969508

    Open questions at the time
    • Direct vs indirect TOPBP1 contact not mapped
    • Mechanism of nuclear export in 2C-like state unknown
  20. 2025 Medium

    Reconstituted SMARCAD1's role in chromatin-context MMR across O6-methylguanine lesions, showing it sustains single-strand break retention during futile MMR cycling.

    Evidence Xenopus egg extract MMR reconstitution with Smarcad1 immunodepletion

    PMID:39882945

    Open questions at the time
    • Molecular step of SSB retention unclear
    • Mammalian cell confirmation lacking
  21. 2025 Medium

    Showed the yeast ortholog Fun30 dampens checkpoint signaling by displacing Rad9 with Slx4, enabling Exo1 resection and fork stabilization.

    Evidence Locus-specific ChIP at CPT-stalled forks, Fun30/Slx4/Exo1 epistasis, checkpoint and fiber assays

    PMID:41978269

    Open questions at the time
    • Conservation of Rad9/53BP1 displacement mechanism to human SMARCAD1 untested at this locus
    • Yeast ortholog data

Open questions

Synthesis pass · forward-looking unresolved questions
  • How SMARCAD1's distinct activities (resection, fork protection, MMR, heterochromatin assembly, transcriptional activation) are selectively deployed at the right substrate and locus remains unresolved.
  • No unified model linking hexasome preference and phospho-regulation to pathway choice
  • In vivo upstream signals that partition functions undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140657 ATP-dependent activity 4 GO:0140096 catalytic activity, acting on a protein 3 GO:0008092 cytoskeletal protein binding 2 GO:0042393 histone binding 2 GO:0003677 DNA binding 1
Localization
GO:0005694 chromosome 3 GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 2
Pathway
R-HSA-4839726 Chromatin organization 3 R-HSA-73894 DNA Repair 3 R-HSA-69306 DNA Replication 2
Partners
HDAC1MLH1MSH2MSH6PCNATFIIICTOPBP1TRIM28

Evidence

Reading pass · 24 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 directly promotes both Exo1- and Sgs1-dependent 5'-to-3' end resection through a mechanism requiring its ATPase activity, facilitating homologous recombination repair. Chromatin immunoprecipitation at DSBs, ATPase-dead mutant analysis, epistasis with Exo1/Sgs1, camptothecin/PARP inhibitor sensitivity assays Nature High 22960744
2011 SMARCAD1's ATPase activity is required for global deacetylation of histones H3/H4, which promotes H3K9 methylation and heterochromatin establishment; SMARCAD1 associates with KAP1, HDAC1/2, and G9a/GLP, modulates HDAC1-KAP1 interaction at heterochromatin, and directly interacts with PCNA to be recruited to replication sites. ATPase mutant complementation, Co-immunoprecipitation, histone modification ChIP, live-cell imaging at replication foci, chromosome segregation assay Molecular cell High 21549307
2018 ATM kinase phosphorylates SMARCAD1 at T906 in response to ionizing radiation; this phosphorylation is required for SMARCAD1 recruitment to DSBs, and T906 phosphorylation also enables subsequent ubiquitination of SMARCAD1 at K905 by RING1. Both PTMs are required for SMARCAD1's role in DNA end resection and HR-mediated repair. Site-directed mutagenesis of T906 and K905, phospho-specific antibodies, Co-immunoprecipitation, IR-induced foci assays, HR reporter assay iScience Medium 29888761
2017 SMARCAD1 preferentially binds H3R26-citrullinated histone peptides and co-localizes genome-wide with H3R26Cit; SMARCAD1 occupancy at H3R26Cit sites suppresses H3K9me3 accumulation, and its knockdown increases H3K9me3 at those loci, linking it to maintenance of naive pluripotency. Histone peptide array binding (384 modifications), ChIP-seq, Smarcad1 knockdown, gene expression analysis, embryoid body and chimera assays Cell reports Medium 28355564
2017 The CUE1 domain of SMARCAD1 directly mediates binding to the RBCC domain of KAP1 (TRIM28); this interaction occurs on chromatin and is required for SMARCAD1 nuclear retention and its association with KAP1 target genes including ZFP and imprinted genes. Co-immunoprecipitation of endogenous proteins, CUE1 domain mutations in vitro and in vivo, ChIP, nuclear fractionation The Journal of biological chemistry High 29284678
2018 In Xenopus egg extracts, Smarcad1 is recruited to mismatch-containing DNA in an Msh2-dependent but Mlh1-independent manner, and facilitates nucleosome exclusion around mismatches; it assists mismatch repair when nucleosomes are preassembled on DNA. In yeast, Fun30 deletion combined with MSH6 or MSH3 deletion synergistically increases spontaneous mutations. Xenopus egg extract chromatin assembly/disassembly assay, immunodepletion, genetic epistasis in yeast (double mutants), nucleosome occupancy assays Genes & development High 29899141
2019 SMARCAD1 ATPase activity is required for recruitment of MutLα (MLH1-PMS2) to chromatin-bound MutSα (MSH2-MSH6) after alkylating-agent-induced DNA damage; loss of SMARCAD1 impairs this recruitment, suppresses apoptosis, and increases mutation frequency. SMARCAD1 knockout cells, MNU treatment, co-immunoprecipitation of MutSα and MutLα from chromatin fractions, ATPase-dead mutant complementation, sub-G1/caspase assays The Journal of biological chemistry Medium 31843968
2021 SMARCAD1 stabilizes active replication forks by preventing accumulation of 53BP1-associated nucleosomes at forks; in SMARCAD1-deficient cells, 53BP1 mediates premature PCNA removal via the PCNA-unloader ATAD5, causing fork stalling and ssDNA accumulation. Loss of 53BP1 rescues these defects but requires BRCA1-mediated fork protection. SMARCAD1 KO/knockdown, 53BP1 co-depletion epistasis, DNA fiber assays, PCNA/ATAD5 interaction studies, iPOND, genetic rescue experiments Science advances High 33952518
2021 SMARCAD1 can transfer an entire histone octamer from one DNA segment to another in an ATP-dependent manner (histone octamer exchange), and can also perform de novo nucleosome assembly from histone octamer due to its ability to simultaneously bind all four histones. Cryo-EM reveals that the ATPase domains engage the nucleosome differently from other chromatin remodelers. In vitro histone exchange assay, de novo nucleosome assembly assay, cryo-EM structure determination, biochemical binding assays Science advances High 34652950
2016 SMARCAD1 acts as an ATP-dependent stimulator of CBP-mediated H2A acetylation (K5 and K8) on nucleosomes; SMARCAD1 enhances CBP acetyltransferase activity in an ATP-dependent manner and activates transcription of target genes using native chromatin templates. Drosophila genetic experiments show functional interaction between SMARCAD1/Etl1 and CBP/nej during development. Column purification of activity from Drosophila nuclear extracts, in vitro H2A acetylation assay, knockdown expression arrays, ChIP-seq, in vitro transcription on native chromatin, Drosophila genetics Scientific reports High 26888216
2008 Endogenous SMARCAD1 binds TRIM28 (KAP1) as detected by protein co-immunoprecipitation, and chromatin immunoprecipitation with tiling microarrays shows SMARCAD1 binding near transcriptional start sites of 69 candidate target genes. Co-immunoprecipitation with specific antibody, ChIP with genome tiling microarray Journal of molecular biology Medium 18675275
2011 A heterozygous splice-site mutation in a skin-specific short isoform of SMARCAD1 (disrupting exon donor site) causes autosomal-dominant adermatoglyphia by decreasing stability of the short skin-specific RNA isoform, as demonstrated by minigene splicing assay. Linkage analysis, Sanger sequencing, minigene splicing assay, RT-PCR stability analysis American journal of human genetics Medium 21820097
2023 MSH2-MSH3 mismatch repair complex is recruited to DSB sites through direct interaction with SMARCAD1; this complex then facilitates EXO1 recruitment and enhances EXO1 enzymatic activity for long-range end resection, while also blocking POLθ access to DSBs to prevent TMEJ. Co-immunoprecipitation, in vitro EXO1 activity assay, DSB recruitment assays, HR vs TMEJ reporter assays, knockdown epistasis Nucleic acids research Medium 37140056
2024 Phosphorylation of SMARCAD1 reduces its binding to nucleosomes, DNA, and histones H2A-H2B, and impairs ATP hydrolysis and histone exchange activity, but has only marginal effect on histone H3-H4 binding and nucleosome assembly. The flexible N-terminal region of SMARCAD1 is critical for nucleosome assembly and histone exchange. Mutational analysis of phosphorylation sites, in vitro activity assays (ATPase, histone exchange, nucleosome assembly), mass spectrometry, nucleosome binding assays The Journal of biological chemistry Medium 39424143
2023 SMARCAD1 interacts directly with TFIIIC (RNA polymerase III general transcription factor) in mouse and human cells; this interaction is conserved across somatic and pluripotent cell types. SMARCAD1 also associates with cohesin, laminB, and DDX5 in mammalian cells. Endogenous co-immunoprecipitation in multiple cell types, purified-protein direct interaction assay, gene expression analysis Genes Medium 37761933
2025 SMARCAD1 exhibits substrate preference for subnucleosomal hexasomes over canonical nucleosomes; cryo-EM structures show SMARCAD1 binds hexasome through family-specific elements required for function in vitro and in cells, and binds the canonical nucleosome in an inactive conformation. The FACT complex acts synergistically with H2A-H2B to promote SMARCAD1 remodeling activity on nucleosomes. Cryo-EM structure determination of SMARCAD1-hexasome and SMARCAD1-nucleosome complexes, in vitro remodeling assays, mutagenesis of family-specific elements, FACT complex co-activity assays, cell-based functional assays Nature High 40468067
2025 SMARCAD1 associates with TOPBP1 and both localize to H3K9me3 heterochromatin in mouse ESCs; SMARCAD1 nuclear localization is lost in 2C-like cells, and depletion of SMARCAD1 or TOPBP1 in mouse embryos leads to developmental arrest, reduction of H3K9me3, and remodeling of heterochromatin foci. Chromatome profiling (chromatin-bound proteome), live-cell imaging of nuclear localization in ESCs vs 2C-like cells, SMARCAD1/TOPBP1 depletion in mouse embryos, H3K9me3 ChIP/immunostaining eLife Medium 39969508
2020 Fun30 (yeast SMARCAD1 ortholog) is enriched in gene bodies of intron-containing genes, and its depletion impairs pre-mRNA splicing efficiency and spliceosome recruitment in a manner dependent on Fun30's chromatin remodeling activity. The mammalian homolog SMARCAD1 was shown to regulate alternative splicing. RNA-seq splicing analysis in Fun30-depleted yeast, ChIP of Fun30 at intron-containing genes, spliceosome recruitment assay, ATPase mutant analysis, mammalian alternative splicing analysis Biochemical and biophysical research communications Low 32234239
2024 On broken replication forks (single-ended DSBs), SMARCAD1 displaces 53BP1 to facilitate localization of ubiquitinated PCNA and PIF1 to DSBs for break-induced replication (BIR) activation. Genetic epistasis, foci analysis, BIR reporter assay, KO cell lines 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-terminus; both interactions are required for resolving R-loops at active replication forks. SMARCAD1 mutant cells accumulate excess R-loops genome-wide, particularly at regions that overlap with cancer mutation hotspots in germline tumors. In vitro R-loop binding assay, replisome co-immunoprecipitation, ATPase-domain and N-terminus mutant analysis, genome-wide R-loop mapping (DRIP-seq), mutagenesis analysis in cancer data bioRxivpreprint Medium bio_10.1101_2024.09.13.612941
2025 In yeast, Fun30 (SMARCAD1 ortholog) displaces the checkpoint mediator Rad9 at replication stress sites together with Slx4, locally dampening S-phase checkpoint signaling; this allows Exo1-dependent resection of stalled forks and homologous recombination factor access for fork stabilization. Locus-specific ChIP at CPT-stalled forks, genetic epistasis (Fun30/Slx4/Exo1 mutants), checkpoint signaling assays, DNA fiber analysis Nucleic acids research Medium 41978269
2025 SMARCAD1 depletion in Xenopus egg extract impairs retention of single-strand breaks generated during futile MMR cycling on O6-methylguanine-containing chromatin, establishing Smarcad1 as a chromatin remodeler that facilitates MMR activity in the chromatin context during replication across meG lesions. Xenopus egg extract reconstitution of MMR on replication-competent chromatin, Smarcad1 immunodepletion, single-strand break retention assay Journal of biochemistry Medium 39882945
2025 SMARCA4 binds the transcriptional regulatory region of SMARCAD1 and acts as a transcriptional suppressor of SMARCAD1; under replication stress, SMARCA4 binding to the SMARCAD1 locus decreases, leading to upregulation of SMARCAD1, which then accumulates at stalled replication forks. ChIP assay at SMARCAD1 regulatory region, quantitative RT-PCR, immunofluorescence at stalled forks, clonogenic assays in NSCLC cell lines Fujita medical journal Low 41641123
2024 SMARCAD1 is recruited to MLV provirus immediately after integration in mouse ESCs; Smarcad1 is critical for establishment and maintenance of MLV repression, stabilizes Trim28 binding to the provirus over time, and its presence is required for proper deposition of histone variant H3.3 on the provirus. Combined depletion of Smarcad1 and Trim28 causes enhanced derepression, suggesting partially independent mechanisms. MLV-GFP reporter repression assay, ChIP at provirus for Trim28 and H3.3, Smarcad1/Trim28 single and double knockdown Mobile DNA Medium 38468276

Source papers

Stage 0 corpus · 36 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 219 22960744
2011 Maintenance of silent chromatin through replication requires SWI/SNF-like chromatin remodeler SMARCAD1. Molecular cell 148 21549307
2018 SMARCAD1 Phosphorylation and Ubiquitination Are Required for Resection during DNA Double-Strand Break Repair. iScience 46 29888761
2017 SMARCAD1 Contributes to the Regulation of Naive Pluripotency by Interacting with Histone Citrullination. Cell reports 41 28355564
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
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
2021 SMARCAD1-mediated active replication fork stability maintains genome integrity. Science advances 30 33952518
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 is an ATP-dependent histone octamer exchange factor with de novo nucleosome assembly activity. Science advances 27 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 25 29284678
2016 SMARCAD1 is an ATP-dependent stimulator of nucleosomal H2A acetylation via CBP, resulting in transcriptional regulation. Scientific reports 23 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 21 37140056
2016 SMARCAD1 knockdown uncovers its role in breast cancer cell migration, invasion, and metastasis. Expert opinion on therapeutic targets 17 27232533
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 4 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
2024 Phosphorylation regulates the chromatin remodeler SMARCAD1 in nucleosome binding, ATP hydrolysis, and histone exchange. The Journal of biological chemistry 2 39424143
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
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
2026 Loss of SMARCAD1 Mitigates Tauopathy. Aging cell 0 42204442
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

Missed literature

Know a paper Affinage missed for SMARCAD1? Flag it for the maintainers and the community.

No submissions yet.