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Showing MAU2 — SCC4 is a alias.

MAU2

MAU2 chromatid cohesion factor homolog · UniProt Q9Y6X3

Length
613 aa
Mass
69.1 kDa
Annotated
2026-06-10
61 papers in source corpus 18 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAU2 (SCC4) is an essential cohesin-loading factor that, together with NIPBL (SCC2), directs the ATP-dependent topological loading of the cohesin ring onto chromatin to enable sister chromatid cohesion and chromosome organization (PMID:10882066, PMID:16682347, PMID:22628566). MAU2 forms an obligate heterodimer with NIPBL through an N-terminal interface: MAU2 is a TPR-repeat superhelix that envelops an extended NIPBL N-terminal peptide, and MAU2 cannot engage cohesin in the absence of NIPBL (PMID:26038942, PMID:26212329, PMID:27280786). The heterodimer interacts with the Smc1–Smc3 heterodimer and loads cohesin onto double-stranded DNA, a reaction that in vitro requires pre-replication complex formation (PMID:22628566). MAU2 determines where loading occurs: a conserved MAU2 surface patch recruits the loader to centromeres to build pericentromeric cohesion, and MAU2 acts as a chromatin adaptor enabling loading onto chromatinized—not merely naked—DNA (PMID:26038942, PMID:26212329). Genomic targeting is further shaped by the RSC chromatin remodeling complex, which recruits the loader to nucleosome-free regions (PMID:25173104), and by transcription factors including the glucocorticoid receptor, which form ternary complexes with NIPBL–MAU2 to position cohesin at enhancers (PMID:40377219). Loss of MAU2 abolishes cohesin association with chromatin and causes precocious sister chromatid separation and prometaphase arrest (PMID:16682347, PMID:16802858). Beyond mitotic chromosomes, the heterodimer localizes to meiotic chromosomal axes (PMID:24287868), and MAU2 supports craniofacial and neural crest development in mice (PMID:24700590). Heterozygous MAU2 variants that impair the NIPBL interaction or cause MAU2 haploinsufficiency cause Cornelia de Lange syndrome, recapitulated in a heterozygous Mau2 knockout mouse (PMID:32433956, PMID:41912533).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 2000 High

    Established that cohesin loading onto chromosomes is a distinct step from cohesin assembly, mediated by a dedicated Scc2/Scc4 complex.

    Evidence Genetic epistasis, co-immunoprecipitation and chromatin binding assays in budding yeast

    PMID:10882066

    Open questions at the time
    • Did not resolve the molecular mechanism of loading
    • Mammalian relevance not yet shown
  2. 2006 High

    Demonstrated that the loader is conserved across metazoans and fungi, with MAU2/Scc4 binding NIPBL/Scc2 via N-terminal regions and being required for cohesin chromatin association and faithful chromosome segregation.

    Evidence siRNA knockdown, Co-IP, chromatin fractionation in HeLa cells; interaction domain mapping and RNAi across Drosophila, C. elegans, Xenopus; Co-IP/ChIP with cell-cycle resolution in S. pombe

    PMID:16682347 PMID:16682348 PMID:16802858

    Open questions at the time
    • Direct enzymatic loading not yet reconstituted
    • Determinants of genomic targeting unknown
  3. 2009 High

    Showed that the loader, not cohesin itself, dictates the nonrandom genomic distribution of cohesin, with kinetochore-dependent enrichment at pericentromeres.

    Evidence Genome-wide ChIP mapping of Scc2 and Scc4 in budding yeast

    PMID:19797771

    Open questions at the time
    • Recruitment cues to specific loci not defined
    • Yeast-only mapping
  4. 2012 High

    Reconstituted human NIPBL/MAU2 loading of cohesin in vitro and linked it to DNA replication licensing.

    Evidence In vitro loading assay with purified human proteins, Co-IP, Xenopus extract depletion/complementation; loading required pre-RC and was blocked by geminin

    PMID:22628566

    Open questions at the time
    • Role of MAU2 versus NIPBL in catalysis not separated
    • Chromatin-template requirements not addressed
  5. 2014 Medium

    Placed the loader downstream of chromatin remodeling, showing RSC recruits the complex to nucleosome-free regions, and connected MAU2 to developmental gene regulation in mammals.

    Evidence MNase-seq, ChIP and genetic epistasis in yeast; conditional neural-crest Mau2 knockout in mice

    PMID:24700590 PMID:25173104

    Open questions at the time
    • Direct RSC–MAU2 contact not structurally defined
    • How loader maintains nucleosome-free regions unresolved
  6. 2015 High

    Defined the molecular basis of the heterodimer: MAU2 is a TPR superhelix wrapping the NIPBL N-terminus, with a conserved surface patch driving centromere recruitment and a chromatin-adaptor role for loading onto nucleosomal DNA.

    Evidence X-ray crystallography, electron microscopy, in vitro loading on circular and chromatinized DNA, and in vivo cohesion/recruitment assays in yeast

    PMID:26038942 PMID:26212329

    Open questions at the time
    • Structure of the full loader engaging cohesin not resolved
    • Human structural confirmation absent
  7. 2016 Medium

    Genetically dissected MAU2/Scc4 functional domains, confirming its N-terminal region is essential and that it requires NIPBL to engage cohesin.

    Evidence Dominant-negative insertion screen, viability/cohesion assays, Co-IP in budding yeast

    PMID:27280786

    Open questions at the time
    • No structural confirmation of mutant defects
    • Yeast-only analysis
  8. 2020 High

    Revealed that the NIPBL–MAU2 interaction, though required normally, can be bypassed: an N-terminally truncated NIPBL lacking the MAU2-binding region still binds DNA and loads cohesin.

    Evidence Patient variant characterization, Co-IP, engineered NIPBL-truncation cell lines, cohesin ChIP

    PMID:32433956

    Open questions at the time
    • Physiological contribution of MAU2-independent loading unclear
    • Efficiency relative to intact heterodimer not quantified
  9. 2025 Medium

    Connected loader targeting to transcription factor signaling, showing NIPBL LxxLL motifs bridge MAU2 and steroid receptors to form ternary complexes positioning cohesin at enhancers.

    Evidence LxxLL mutagenesis, Co-IP, AlphaFold2 modeling with docking, reporter assays

    PMID:40377219

    Open questions at the time
    • Ternary complex structure is computational, not experimentally determined
    • Direct MAU2 contacts with receptors not mapped
  10. 2025 High

    Confirmed MAU2 as a causal CdLS gene, distinguishing two pathogenic mechanisms—impaired NIPBL interaction versus MAU2 haploinsufficiency with secondary NIPBL reduction—and recapitulating the phenotype in mice.

    Evidence Functional analysis of 15 variants across 18 patients, Co-IP, Western blot, methylation episignature, heterozygous Mau2 knockout mouse

    PMID:41912533

    Open questions at the time
    • Mechanism linking cohesin loading defect to specific craniofacial/growth phenotypes unresolved
    • Genotype-phenotype correlations incomplete

Open questions

Synthesis pass · forward-looking unresolved questions
  • How MAU2-dependent loader targeting integrates chromatin remodeling, replication licensing, and transcription-factor cues to specify cohesin loading sites genome-wide remains unresolved.
  • No unified human structure of the loader engaging chromatin and cohesin
  • Quantitative contribution of each targeting pathway unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005694 chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-1640170 Cell Cycle 3 R-HSA-1266738 Developmental Biology 2 R-HSA-4839726 Chromatin organization 2
Partners
NIPBLNR3C1SMC1SMC3
Complex memberships
NIPBL/MAU2 cohesin loader complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Scc4 (yeast ortholog of MAU2) forms a complex with Scc2 and this heterodimeric complex is required for loading cohesin onto chromosomes. In scc4 mutants, cohesin complexes form normally but fail to bind centromeres and chromosome arms, establishing that Scc2/Scc4 facilitates cohesin loading rather than cohesin assembly. Genetic epistasis, co-immunoprecipitation, chromatin binding assays in budding yeast Molecular cell High 10882066
2006 Human MAU2 (SCC4) is the ortholog of yeast Scc4. It associates with NIPBL (Scc2 ortholog), is bound to chromatin from telophase until prophase, and is required for cohesin association with chromatin during interphase. Depletion of MAU2 causes precocious sister-chromatid separation and prometaphase arrest; mitotic chromosomes lack cohesin even though Sgo1/Bub1 are normally enriched at centromeres. siRNA knockdown, co-immunoprecipitation, chromatin fractionation, immunofluorescence in HeLa cells Current biology : CB High 16682347
2006 Metazoan MAU2 orthologs (human MAU2, Drosophila MAU-2) bind delangin/Nipped-B (NIPBL orthologs), with the interaction domain mapped to the N-terminal regions of both proteins. siRNA knockdown of human MAU2 in HeLa cells causes precocious sister chromatid separation and impaired cohesin loading onto chromatin. MAU2 regulates chromosome segregation in C. elegans embryos by RNAi. Protein-protein interaction mapping (pulldown), siRNA knockdown, RNAi in C. elegans, Xenopus morpholino knockdown PLoS biology High 16802858
2006 Fission yeast Ssl3 (Scc4 ortholog) forms a complex with Mis4 (Scc2 ortholog) and is required in G1 for cohesin binding to chromosomes but is dispensable in G2 when cohesion is already established, demonstrating that the Scc2/Scc4 loading complex is functionally conserved in S. pombe. Co-immunoprecipitation, chromatin immunoprecipitation, genetic analysis in S. pombe Current biology : CB High 16682348
2009 The Scc2/Scc4 loader determines the nonrandom chromosomal distribution of cohesin. Both Scc2 and Scc4 co-localize with cohesin at cohesin-associated regions (CARs), including pericentromeric regions where enrichment is kinetochore-dependent. Scc2/Scc4 association with CARs is independent of cohesin itself. Chromatin immunoprecipitation (ChIP) genome-wide mapping in budding yeast Genes & development High 19797771
2012 Purified human Scc2/Scc4 (NIPBL/MAU2) heterodimer interacts with human cohesin and the Smc1-Smc3 heterodimer (but not Smc1 or Smc3 alone) and loads cohesin onto dsDNA containing prereplication complexes in vitro. Loading requires pre-RC formation and is blocked by geminin. In vitro cohesin loading assay, co-immunoprecipitation of purified human proteins, Xenopus extract depletion/complementation Proceedings of the National Academy of Sciences of the United States of America High 22628566
2014 The Scc2-Scc4 cohesin loader complex is recruited to broad nucleosome-free regions by the RSC chromatin remodeling complex, and the loader helps maintain these nucleosome-free regions. Inactivation of either Scc2-Scc4 or RSC produces similar effects on nucleosome positioning, gene expression, and sister chromatid cohesion, placing the loader downstream of RSC in chromatin organization. Genetic epistasis, nucleosome mapping (MNase-seq), gene expression analysis, chromatin immunoprecipitation in budding yeast Nature genetics High 25173104
2015 Crystal structure of Scc4 (MAU2 ortholog) bound to the N-terminal peptide of Scc2 reveals that Scc4 is a TPR-repeat superhelix that envelops an extended Scc2 N-terminal peptide. A conserved surface patch on Scc4 is required for recruitment of Scc2/Scc4 to centromeres and for building pericentromeric cohesion, establishing the molecular basis for Scc4-dependent localization of cohesin loading. X-ray crystallography, yeast genetics (centromere recruitment assays, cohesion assays), mutagenesis eLife High 26038942
2015 Crystal structure of Scc4 bound to the Scc2 N-terminus shows Scc4 is a TPR superhelix entrapping an extended Scc2 N-terminal segment. EM analysis reveals the Scc2-Scc4 complex has three domains (head=Scc2N-Scc4, body, hook). In vitro cohesin loading assays show the body and hook domains are sufficient for loading onto circular DNA but not chromatinized DNA, suggesting Scc4 functions as a chromatin adaptor. X-ray crystallography, electron microscopy, in vitro cohesin loading assay on circular and chromatinized DNA Cell reports High 26212329
2016 A genetic screen identified functional domains in yeast Scc4 required for cohesin loading. The N-terminal region of Scc4 is dominant negative when overexpressed and essential for Scc2/Scc4 activity. Mutant alleles reduce but do not eliminate interaction of Scc4 with Scc2 or cohesin. Scc4 cannot bind cohesin in the absence of Scc2. Random insertion/dominant negative genetic screen, viability assays, cohesion assays, co-immunoprecipitation in budding yeast G3 (Bethesda, Md.) Medium 27280786
2004 C. elegans MAU-2 protein localizes to the cytoplasm of neurons, is ubiquitously expressed in embryos and predominantly in the nervous system during morphogenesis, and functions cell-autonomously in individual neurons to guide axonal migrations. Genetic interaction with slt-1 reveals mau-2 participates in AVM axon guidance through a slt-1-independent mechanism. GFP fusion protein localization, tissue-specific rescue experiments, genetic epistasis with slt-1 in C. elegans Development (Cambridge, England) Medium 15539489
2011 Specific NIPBL missense mutations that cause Cornelia de Lange syndrome map to the MAU2-interacting domain of NIPBL and result in markedly reduced MAU2 binding, establishing that disruption of the NIPBL-MAU2 interaction is a pathogenic mechanism in CdLS. Protein-protein interaction mapping, co-immunoprecipitation, clinical variant analysis European journal of human genetics : EJHG Medium 21934712
2013 NIPBL/MAU2 heterodimer localizes to chromosomal axes from zygotene to mid-pachytene in mammalian germ cells of both sexes during meiotic prophase I. In spermatocytes it relocalizes to chromocenters, while in oocytes it remains on chromosomal axes throughout prophase. Its localization pattern is consistent with a role as a loading factor for cohesin and condensin I (but not SMC5/6) during meiosis. Immunofluorescence localization in mouse spermatocytes and oocytes, co-localization with SMC complex markers Chromosoma Medium 24287868
2014 Neural crest cell-specific inactivation of Mau2 in mice strongly affects craniofacial development. Early neural crest cell proliferation and migration are only moderately affected, suggesting cohesin loading is more critical for later developmental gene regulation. Mau2 single homozygous mutants showed a more severe craniofacial phenotype than Nipbl;Mau2 double homozygous mutants, suggesting the Mau2/Nipbl interaction may also restrict Nipbl's role in gene expression regulation. Conditional gene knockout in mice (Cre-lox), phenotypic analysis of neural crest-specific knockouts Genesis (New York, N.Y. : 2000) Medium 24700590
2020 A MAU2 variant (7 amino acid in-frame deletion) causing CdLS impairs the interaction between MAU2 and the NIPBL N-terminus. However, cohesin loading can occur independently of a functional NIPBL/MAU2 complex: an NIPBL truncating mutation leads to alternative translation initiation producing an NIPBL form lacking the MAU2-binding N-terminus, which can still bind DNA and mediate cohesin loading. Patient variant characterization, co-immunoprecipitation, engineered cell lines with NIPBL truncating mutations, cohesin ChIP Cell reports High 32433956
2025 NIPBL contains two clusters of LxxLL motifs: one interacts with MAU2 and is necessary for maintaining the NIPBL-MAU2 heterodimer; the second binds the ligand-binding domains of steroid receptors. The glucocorticoid receptor (GR), NIPBL, and MAU2 form a ternary complex (modeled by AlphaFold2 and molecular docking), and this interaction is important for GR-dependent gene regulation. Multiple transcription factors interact with NIPBL-MAU2 to localize cohesin at enhancers. LxxLL motif mutagenesis, co-immunoprecipitation, AlphaFold2 structural modeling with molecular docking, transcriptional reporter assays Nucleic acids research Medium 40377219
2025 18 individuals with 15 heterozygous MAU2 variants display CdLS phenotypes. In-frame MAU2 variants predominantly impair NIPBL-MAU2 interaction, while truncating variants cause MAU2 haploinsufficiency and lead to NIPBL reduction. A heterozygous Mau2 knockout mouse model recapitulates the human phenotype (short stature, microcephaly), confirming MAU2 disruption as causal. Patient variant functional analysis, co-immunoprecipitation, Western blot, DNA methylation episignature analysis, heterozygous Mau2 knockout mouse model Nature communications High 41912533
2019 In maize, DEK15/SCC4 (MAU2 ortholog) interacts with chromatin remodeling proteins (CHB102, CHB105, CHB106) identified by yeast two-hybrid, suggesting a mechanism for cohesin loading onto chromatin via chromatin remodelers, consistent with findings in yeast. Yeast two-hybrid screen, genetic positional cloning, chromosome segregation analysis The Plant cell Low 30705131

Source papers

Stage 0 corpus · 61 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2000 Cohesin's binding to chromosomes depends on a separate complex consisting of Scc2 and Scc4 proteins. Molecular cell 616 10882066
2006 Human Scc4 is required for cohesin binding to chromatin, sister-chromatid cohesion, and mitotic progression. Current biology : CB 209 16682347
2009 Berberine suppresses in vitro migration and invasion of human SCC-4 tongue squamous cancer cells through the inhibitions of FAK, IKK, NF-kappaB, u-PA and MMP-2 and -9. Cancer letters 129 19251361
2014 The Scc2-Scc4 complex acts in sister chromatid cohesion and transcriptional regulation by maintaining nucleosome-free regions. Nature genetics 111 25173104
2009 Berberine induced apoptosis via promoting the expression of caspase-8, -9 and -3, apoptosis-inducing factor and endonuclease G in SCC-4 human tongue squamous carcinoma cancer cells. Anticancer research 105 19846952
2009 Emodin induces apoptosis of human tongue squamous cancer SCC-4 cells through reactive oxygen species and mitochondria-dependent pathways. Anticancer research 92 19331169
2006 Metazoan Scc4 homologs link sister chromatid cohesion to cell and axon migration guidance. PLoS biology 86 16802858
2008 Gypenosides induced G0/G1 arrest via CHk2 and apoptosis through endoplasmic reticulum stress and mitochondria-dependent pathways in human tongue cancer SCC-4 cells. Oral oncology 76 18674953
2009 Aloe-emodin induces cell death through S-phase arrest and caspase-dependent pathways in human tongue squamous cancer SCC-4 cells. Anticancer research 64 20032398
2015 Structural evidence for Scc4-dependent localization of cohesin loading. eLife 61 26038942
2009 Rhein induced apoptosis through the endoplasmic reticulum stress, caspase- and mitochondria-dependent pathways in SCC-4 human tongue squamous cancer cells. In vivo (Athens, Greece) 57 19414420
2009 The Scc2/Scc4 cohesin loader determines the distribution of cohesin on budding yeast chromosomes. Genes & development 56 19797771
2006 A screen for cohesion mutants uncovers Ssl3, the fission yeast counterpart of the cohesin loading factor Scc4. Current biology : CB 56 16682348
2007 Baicalein induces apoptosis in SCC-4 human tongue cancer cells via a Ca2+-dependent mitochondrial pathway. In vivo (Athens, Greece) 53 18210755
2015 Structural Studies Reveal the Functional Modularity of the Scc2-Scc4 Cohesin Loader. Cell reports 52 26212329
2014 Gallic acid inhibits migration and invasion of SCC-4 human oral cancer cells through actions of NF-κB, Ras and matrix metalloproteinase-2 and -9. Oncology reports 51 24859325
2020 MAU2 and NIPBL Variants Impair the Heterodimerization of the Cohesin Loader Subunits and Cause Cornelia de Lange Syndrome. Cell reports 49 32433956
2017 Fisetin-induced apoptosis of human oral cancer SCC-4 cells through reactive oxygen species production, endoplasmic reticulum stress, caspase-, and mitochondria-dependent signaling pathways. Environmental toxicology 47 28181380
2008 Gypenosides inhibited invasion and migration of human tongue cancer SCC4 cells through down-regulation of NFkappaB and matrix metalloproteinase-9. Anticancer research 47 18507059
2019 Maize Dek15 Encodes the Cohesin-Loading Complex Subunit SCC4 and Is Essential for Chromosome Segregation and Kernel Development. The Plant cell 41 30705131
2012 In vitro loading of human cohesin on DNA by the human Scc2-Scc4 loader complex. Proceedings of the National Academy of Sciences of the United States of America 36 22628566
2011 Induction of apoptotic death by curcumin in human tongue squamous cell carcinoma SCC-4 cells is mediated through endoplasmic reticulum stress and mitochondria-dependent pathways. Cell biochemistry and function 35 21887696
2011 Scc1 (CP0432) and Scc4 (CP0033) function as a type III secretion chaperone for CopN of Chlamydia pneumoniae. Journal of bacteriology 30 21571996
2011 Isolated NIBPL missense mutations that cause Cornelia de Lange syndrome alter MAU2 interaction. European journal of human genetics : EJHG 25 21934712
1988 2,3,7,8-Tetrachlorodibenzo-p-dioxin and polycyclic aromatic hydrocarbons suppress retinoid-induced tissue transglutaminase in SCC-4 cultured human squamous carcinoma cells. Carcinogenesis 25 2897254
2010 Capsaicin induces apoptosis in SCC-4 human tongue cancer cells through mitochondria-dependent and -independent pathways. Environmental toxicology 24 20925121
2004 mau-2 acts cell-autonomously to guide axonal migrations in Caenorhabditis elegans. Development (Cambridge, England) 24 15539489
2014 Neural crest cell-specific inactivation of Nipbl or Mau2 during mouse development results in a late onset of craniofacial defects. Genesis (New York, N.Y. : 2000) 23 24700590
2014 RAD001 enhances the radiosensitivity of SCC4 oral cancer cells by inducing cell cycle arrest at the G2/M checkpoint. Anticancer research 23 24922656
2017 Casticin impairs cell growth and induces cell apoptosis via cell cycle arrest in human oral cancer SCC-4 cells. Environmental toxicology 21 29098808
2013 Localisation of the SMC loading complex Nipbl/Mau2 during mammalian meiotic prophase I. Chromosoma 21 24287868
2017 Bufalin induced apoptosis in SCC‑4 human tongue cancer cells by decreasing Bcl‑2 and increasing Bax expression via the mitochondria‑dependent pathway. Molecular medicine reports 20 28983595
2011 Safrole induces cell death in human tongue squamous cancer SCC-4 cells through mitochondria-dependent caspase activation cascade apoptotic signaling pathways. Environmental toxicology 19 21591240
2020 Association of the NCAN-TM6SF2-CILP2-PBX4-SUGP1-MAU2 SNPs and gene-gene and gene-environment interactions with serum lipid levels. Aging 15 32568739
2018 Suppression of the long non-coding RNA MALAT-1 impairs the growth and migration of human tongue squamous cell carcinoma SCC4 cells. Archives of medical science : AMS 15 31360193
2014 Methotrexate enhances 5-aminolevulinic acid-mediated photodynamic therapy-induced killing of human SCC4 cells by upregulation of coproporphyrinogen oxidase. Journal of the Formosan Medical Association = Taiwan yi zhi 11 24485831
2020 Context-Dependent Action of Scc4 Reinforces Control of the Type III Secretion System. Journal of bacteriology 9 32424009
2016 Identification of Functional Domains in the Cohesin Loader Subunit Scc4 by a Random Insertion/Dominant Negative Screen. G3 (Bethesda, Md.) 7 27280786
1995 Differential regulation of plasminogen activation in normal keratinocytes and SCC-4 cells by fibroblasts. The Journal of investigative dermatology 7 7861005
2016 4-Hydroxybutenolide impairs cell migration, and invasion of human oral cancer SCC-4 cells via the inhibition of NF-κB and MAPK signaling pathways. International journal of oncology 6 27221634
2025 Transcription factors form a ternary complex with NIPBL/MAU2 to localize cohesin at enhancers. Nucleic acids research 5 40377219
2020 Casticin Inhibits In Vivo Growth of Xenograft Tumors of Human Oral Cancer SCC-4 Cells. In vivo (Athens, Greece) 5 32871773
2019 Purification of Tag-Free Chlamydia trachomatis Scc4 for Structural Studies Using Sarkosyl-Assisted on-Column Complex Dissociation. Biochemistry 5 31545893
2023 Clinical study and genetic analysis of Cornelia de Lange syndrome caused by a novel MAU2 gene variant in a Chinese boy. Molecular genetics & genomic medicine 4 37962004
2022 Betanin alleviates inflammation and ameliorates apoptosis on human oral squamous cancer cells SCC131 and SCC4 through the NF-κB/PI3K/Akt signaling pathway. Journal of biochemical and molecular toxicology 4 35645143
2021 Cetyltrimethylammonium Bromide Disrupts Mesenchymal Characteristics of Human Tongue Squamous Cell Carcinoma SCC4 Cells Through Modulating Canonical TGF-β/Smad/miR-181b/TIMP3 Signaling Pathway. Anticancer research 4 34848464
2017 Minichromosome Maintenance Complex is Required for Checkpoint Kinase 2 Chromatin Loading and its Phosphorylation to DNA Damage Response in SCC-4 Cells. Protein and peptide letters 4 27964702
2025 Transcription factors form a ternary complex with NIPBL/MAU2 to localize cohesin at enhancers. bioRxiv : the preprint server for biology 2 39713324
2023 In-silico, evolutionary, and functional analysis of CHUP1 and its related proteins in Bienertia sinuspersici-a comparative study across C3, C4, CAM, and SCC4 model plants. PeerJ 2 37456874
2020 Chain-Selective Isotopic Labeling of the Heterodimeric Type III Secretion Chaperone, Scc4:Scc1, Reveals the Total Structural Rearrangement of the Chlamydia trachomatis Bi-Functional Protein, Scc4. Biomolecules 2 33114427
2020 RhoA/ROCKs signaling is increased by treatment with TKI-258 and leads to increased apoptosis in SCC-4 oral squamous cell carcinoma cell line. Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology 2 33222274
2018 SCC4 cell monolayers as an alternative sublingual barrier model: influence of nanoencapsulation on carvedilol transport. Drug development and industrial pharmacy 2 30230390
2020 Rho GTPases are Involved on Regulation of Cytodifferentiation of SCC-4 Oral Squamous Cell Carcinoma Cell Line: A Preliminary Study. Asian Pacific journal of cancer prevention : APJCP 1 31983155
2020 Backbone and sidechain resonance assignments and secondary structure of Scc4 from Chlamydia trachomatis. Biomolecular NMR assignments 1 32617786
2017 Cetuximab has an inhibitory effect on cell motility in SCC-4 oral squamous cell carcinoma cell line. Cellular and molecular biology (Noisy-le-Grand, France) 1 28980916
2026 Pathogenic variants in the cohesin loader subunit MAU2 underlie a distinct Cornelia de Lange Syndrome subtype. Nature communications 0 41912533
2025 [Expression of Concern] 4‑Hydroxybutenolide impairs cell migration, and invasion of human oral cancer SCC‑4 cells via the inhibition of NF‑κB and MAPK signaling pathways. International journal of oncology 0 40878940
2025 Pathogenic variants in the cohesin loader subunit MAU2 lead to a new Cornelia de Lange Syndrome subtype. medRxiv : the preprint server for health sciences 0 41332805
2024 Insights into the association of the Chlamydia trachomatis type III secretion chaperone complex, Scc4:Scc1, from sequential expression in Escherichia coli. Protein expression and purification 0 38857716
2019 [Effects of microRNA-218 on proliferation, apoptosis and invasion of human tongue cancer cell line SCC-4 and SCC-9]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 31792476
2014 [Effects of 5-aza-2-deoxycytidine on methylation status of RECK gene and cancer cell invasion in tongue cancer SCC-4 cells]. Shanghai kou qiang yi xue = Shanghai journal of stomatology 0 25543600

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