Affinage

MAU2

MAU2 chromatid cohesion factor homolog · UniProt Q9Y6X3

Length
613 aa
Mass
69.1 kDa
Annotated
2026-04-28
62 papers in source corpus 17 papers cited in narrative 17 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAU2 (Scc4) is a TPR-domain protein that heterodimerizes with NIPBL (Scc2) to form the cohesin loader complex, which is essential for loading cohesin onto chromosomes and establishing sister chromatid cohesion (PMID:10882066, PMID:16682347, PMID:22628566). Structurally, MAU2 forms a TPR superhelix that envelops an extended N-terminal peptide of NIPBL; it functions as a chromatin adaptor directing cohesin loading to specific genomic sites including centromeres and nucleosome-free regions generated by chromatin remodelers, while NIPBL catalyzes the loading reaction itself (PMID:26038942, PMID:26212329, PMID:25173104). Transcription factors including steroid receptors form ternary complexes with NIPBL/MAU2 to recruit cohesin to enhancers, linking the loader to transcriptional regulation (PMID:40377219). Heterozygous loss-of-function MAU2 variants cause Cornelia de Lange syndrome, with in-frame mutations disrupting NIPBL interaction and truncating variants causing MAU2 haploinsufficiency with secondary NIPBL reduction (PMID:41912533).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 2000 High

    The fundamental question of how cohesin reaches chromosomes was answered by demonstrating that the Scc2/Scc4 (NIPBL/MAU2) complex is required not for cohesin assembly but specifically for its loading onto chromatin.

    Evidence Genetic epistasis, co-immunoprecipitation, and chromatin binding assays in S. cerevisiae

    PMID:10882066

    Open questions at the time
    • Mechanism of loading catalysis unknown
    • Mammalian orthologs not yet identified
    • How the loader is targeted to specific chromosomal loci unresolved
  2. 2004 Medium

    Before its cohesin-loading role was established in metazoans, C. elegans mau-2 was found to function cell-autonomously in neurons for axon guidance, suggesting developmental roles potentially independent of cohesion.

    Evidence GFP localization, cell-autonomous rescue, genetic epistasis with slt-1 in C. elegans

    PMID:15539489

    Open questions at the time
    • Whether axon guidance role is cohesin-dependent or independent was not tested
    • No biochemical interaction with worm Scc2 ortholog demonstrated in this study
  3. 2006 High

    Conservation of the Scc2/Scc4 cohesin-loading partnership was established across metazoans: human MAU2 binds NIPBL via N-terminal regions and is required for cohesin chromatin association, with depletion causing precocious sister chromatid separation.

    Evidence Co-immunoprecipitation, chromatin fractionation, siRNA knockdown in HeLa cells; morpholino knockdown in Xenopus; genetic and biochemical analysis in S. pombe

    PMID:16682347 PMID:16682348 PMID:16802858

    Open questions at the time
    • Direct biochemical reconstitution of human cohesin loading not yet achieved
    • Cell-cycle regulation of loading not fully defined
  4. 2009 High

    Genome-wide mapping resolved how the loader determines cohesin distribution: Scc2/Scc4 co-localizes with cohesin at CARs, and its chromatin association is independent of cohesin, establishing the loader as an upstream determinant of cohesin positioning.

    Evidence ChIP-chip genome-wide mapping in S. cerevisiae

    PMID:19797771

    Open questions at the time
    • Whether loader sites and cohesin final positions diverge in metazoans was unclear
    • Mechanism of loader recruitment to specific loci not identified
  5. 2011 Medium

    The clinical relevance of the NIPBL-MAU2 interaction was demonstrated when CdLS patient NIPBL missense mutations were shown to specifically disrupt MAU2 binding, fine-mapping the interaction domain.

    Evidence Interaction domain mapping and co-immunoprecipitation with patient-derived NIPBL mutations

    PMID:21934712

    Open questions at the time
    • No MAU2 mutations in CdLS patients identified at this time
    • Functional consequence for cohesin loading not directly measured
  6. 2012 High

    Biochemical reconstitution demonstrated that purified human NIPBL/MAU2 complex directly loads cohesin onto prereplication-complex-containing DNA in vitro, establishing the sufficiency of the heterodimer for catalyzing loading.

    Evidence In vitro cohesin loading assay with purified proteins and Xenopus extract depletion/rescue

    PMID:22628566

    Open questions at the time
    • Whether MAU2 contributes catalytically or only as an adaptor not resolved
    • Role of chromatin context in vitro only partially recapitulated
  7. 2014 High

    The chromatin context for loader recruitment was identified: RSC chromatin remodeling complex creates nucleosome-free regions that recruit Scc2/Scc4, linking chromatin architecture to cohesin loading site selection.

    Evidence ChIP-seq, nucleosome mapping, genetic epistasis, gene expression analysis in S. cerevisiae

    PMID:25173104

    Open questions at the time
    • Whether equivalent remodelers recruit NIPBL/MAU2 in mammals not established
    • Direct physical interaction between RSC and Scc2/Scc4 not demonstrated
  8. 2015 High

    Crystal structures of the Scc4-Scc2 N-terminal complex revealed the molecular architecture: MAU2 is a TPR superhelix enveloping an extended NIPBL peptide; a conserved surface patch on MAU2 mediates centromere recruitment, while the catalytic activity resides in NIPBL body/hook domains, establishing MAU2 as a chromatin adaptor rather than a catalytic subunit.

    Evidence X-ray crystallography, electron microscopy, in vitro cohesin loading assay, mutagenesis in yeast

    PMID:26038942 PMID:26212329

    Open questions at the time
    • Full-length Scc2/Scc4 structure not resolved
    • How the conserved surface patch recognizes centromeric chromatin features unknown
  9. 2016 Medium

    Dissection of MAU2 functional domains showed that a small N-terminal region is essential for viability and cohesion, and that MAU2 cannot engage cohesin without NIPBL, clarifying the obligate dependency within the heterodimer.

    Evidence Random insertion/dominant negative screen, cohesin loading assay, ChIP, co-immunoprecipitation in S. cerevisiae

    PMID:27280786

    Open questions at the time
    • Which specific contacts on the N-terminal region mediate its essential function not mapped
    • Whether findings extend to mammalian MAU2 not tested
  10. 2020 High

    A surprising separation of function was uncovered: an alternative NIPBL isoform lacking the MAU2-binding domain can still load cohesin, demonstrating that MAU2-independent cohesin loading occurs and reframing MAU2 as a regulatory rather than absolutely essential loading subunit.

    Evidence Engineered NIPBL truncation cell lines, co-immunoprecipitation, cohesin ChIP, CdLS patient variant analysis

    PMID:32433956

    Open questions at the time
    • Whether MAU2-independent loading is sufficient for all genomic loci or only a subset unclear
    • Relative contribution of MAU2-dependent vs -independent loading in vivo not quantified
  11. 2025 High

    The NIPBL-MAU2 heterodimer was shown to serve as a platform for transcription factor-directed cohesin recruitment: steroid receptors bind NIPBL LxxLL motifs to form ternary complexes that target cohesin to enhancers, and MAU2 loss-of-function variants were established as a direct genetic cause of Cornelia de Lange syndrome.

    Evidence LxxLL motif mutagenesis, co-immunoprecipitation, ChIP-seq, reporter assays, patient variant functional analysis, heterozygous Mau2 KO mouse model, DNA methylation episignature profiling

    PMID:40377219 PMID:41912533

    Open questions at the time
    • Ternary complex structure relies partly on computational prediction and awaits direct structural validation
    • Full spectrum of transcription factors that recruit NIPBL/MAU2 to enhancers not defined
    • Whether CdLS pathology is primarily due to cohesin loading deficits or transcriptional dysregulation remains unresolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the precise mechanism by which MAU2 recognizes and adapts to distinct chromatin environments (centromeres, enhancers, nucleosome-free regions), the quantitative contribution of MAU2-dependent versus MAU2-independent cohesin loading across the genome, and whether MAU2 has cohesin-independent functions in development.
  • No full-length human NIPBL/MAU2 structure available
  • MAU2 chromatin receptor identity unknown
  • Cohesin-independent developmental roles not formally excluded

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 4
Localization
GO:0005694 chromosome 5 GO:0005634 nucleus 2
Pathway
R-HSA-1640170 Cell Cycle 3 R-HSA-1643685 Disease 3 R-HSA-4839726 Chromatin organization 2
Partners
NIPBLSMC1ASMC3
Complex memberships
NIPBL/MAU2 cohesin loader complex

Evidence

Reading pass · 17 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 Scc2p (NIPBL ortholog) forms a complex with Scc4p (MAU2 ortholog) in budding yeast; in scc2 or scc4 mutants, cohesin complexes form normally but fail to bind centromeres and chromosome arms, establishing that the Scc2/Scc4 complex is required for loading cohesin onto chromosomes. Genetic epistasis, co-immunoprecipitation, chromatin binding assays in S. cerevisiae Molecular cell High 10882066
2006 Human MAU2 (Scc4) is associated with NIPBL (Scc2), is bound to chromatin from telophase until prophase, and is required for association of cohesin with chromatin during interphase; siRNA depletion of MAU2 causes precocious sister-chromatid separation and prometaphase arrest. Co-immunoprecipitation, chromatin fractionation, siRNA knockdown, fluorescence microscopy in HeLa cells Current biology : CB High 16682347
2006 Metazoan MAU2 orthologs (human MAU2, Drosophila MAU-2) interact with NIPBL/delangin/Nipped-B via N-terminal regions of both proteins; siRNA knockdown of human MAU2 causes precocious sister chromatid separation and impaired cohesin loading onto chromatin; MAU2 knockdown in Xenopus embryos phenocopies NIPBL knockdown. PSI-BLAST homology, protein-protein interaction mapping, siRNA knockdown, antisense morpholino in Xenopus PLoS biology High 16802858
2006 Fission yeast Ssl3 (Scc4/MAU2 ortholog) forms a complex with Mis4 (Scc2/NIPBL ortholog) and is required in G1 for cohesin binding to chromosomes but is dispensable in G2 after cohesion is established. Genetic screen, co-immunoprecipitation, chromatin immunoprecipitation in S. pombe Current biology : CB High 16682348
2009 Budding yeast Scc2/Scc4 co-localizes with cohesin at cohesin-associated regions (CARs) genome-wide; pericentromeric Scc2/Scc4 enrichment is kinetochore-dependent; Scc2/Scc4 association with CARs is independent of cohesin, indicating the loader directly determines cohesin distribution. ChIP-chip genome-wide mapping in S. cerevisiae Genes & development High 19797771
2012 Human Scc2/Scc4 (NIPBL/MAU2) complex was purified and shown to interact with human cohesin and the Smc1-Smc3 heterodimer (but not individual Smc subunits); both complexes load onto dsDNA containing prereplication complexes in vitro, and this loading is blocked by geminin or depletion of Scc2/Scc4. In vitro cohesin loading assay, purified protein reconstitution, co-immunoprecipitation, Xenopus extract depletion/rescue Proceedings of the National Academy of Sciences of the United States of America High 22628566
2014 The Scc2-Scc4 cohesin loader complex in budding yeast is recruited to broad nucleosome-free regions by the RSC chromatin remodeling complex; inactivation of either Scc2-Scc4 or RSC has similar effects on nucleosome positioning, gene expression, and sister chromatid cohesion. Genetic epistasis, ChIP-seq, nucleosome mapping, gene expression analysis in S. cerevisiae Nature genetics High 25173104
2014 Neural crest cell-specific inactivation of Mau2 in mice causes craniofacial defects; Mau2 single homozygous mutants showed a more severe phenotype than Nipbl;Mau2 double homozygous mutants, suggesting MAU2/NIPBL interaction may restrict NIPBL's role in gene expression regulation beyond cohesin loading. Conditional knockout (Cre-lox) mouse model, histology, immunofluorescence Genesis (New York, N.Y. : 2000) Medium 24700590
2015 Crystal structure of Scc4 (MAU2 ortholog) bound to the N terminus of Scc2 reveals Scc4 is a TPR array that envelops an extended Scc2 peptide; a conserved surface patch on Scc4 is required for recruitment of Scc2/Scc4 to centromeres and for building pericentromeric cohesion. X-ray crystallography, yeast mutagenesis, ChIP, sister chromatid cohesion assay eLife High 26038942
2015 Crystal structure of Scc4 (MAU2 ortholog) bound to Scc2 N-terminus shows Scc4 is a TPR superhelix enveloping an extended Scc2 N-terminus; EM reveals the Scc2-Scc4 loader has three domains (head, body, hook); the body and hook domains catalyze cohesin loading onto circular DNA in vitro, while Scc4 functions as a chromatin adaptor for loading onto chromatinized DNA. X-ray crystallography, electron microscopy, in vitro cohesin loading assay, deletion mutagenesis Cell reports High 26212329
2016 A small N-terminal region of Scc4 (MAU2 ortholog) in budding yeast is required for cell viability, cohesion, cohesin loading, and Scc4 chromatin binding; Scc4 cannot bind cohesin in the absence of Scc2, revealing that Scc2 is required for Scc4-cohesin interaction. Random insertion/dominant negative genetic screen, cohesin loading assay, ChIP, co-immunoprecipitation in S. cerevisiae G3 (Bethesda, Md.) Medium 27280786
2011 Specific NIPBL missense mutations found in Cornelia de Lange syndrome patients map to the MAU2-interacting domain of NIPBL and result in markedly reduced MAU2 binding, fine-mapping the minimal interaction domain between NIPBL and MAU2. Interaction domain mapping, co-immunoprecipitation, patient mutation analysis European journal of human genetics : EJHG Medium 21934712
2020 A MAU2 variant causing CdLS (deletion of seven amino acids) impairs the interaction between MAU2 and the NIPBL N-terminus; NIPBL lacking the N-terminal MAU2-binding domain (via alternative translation initiation) can still bind DNA and mediate cohesin loading, demonstrating that cohesin loading can occur independently of functional NIPBL/MAU2 complexes. Patient variant analysis, engineered cell lines with NIPBL truncation, co-immunoprecipitation, cohesin ChIP, alternative translation initiation mapping Cell reports High 32433956
2013 NIPBL/MAU2 heterodimer localizes to chromosomal axes from zygotene to mid-pachytene in mammalian meiotic germ cells and relocalizes to chromocenters in spermatocytes; localization pattern is consistent with a role as loading factor for cohesin and condensin I but not Smc5/6. Immunofluorescence on meiotic chromosome spreads from mouse germ cells, co-localization with SMC complex subunits Chromosoma Medium 24287868
2004 C. elegans mau-2 encodes a conserved protein that functions cell-autonomously within neurons for axonal migration guidance; MAU-2::GFP localizes to the cytoplasm of neurons; mau-2 interacts genetically with slt-1 (Slit ortholog) in guiding AVM axon, indicating mau-2 participates in guidance by a slt-1-independent mechanism. GFP fusion protein localization, cell-autonomous rescue experiments, genetic epistasis with slt-1 in C. elegans Development (Cambridge, England) Medium 15539489
2025 NIPBL contains two clusters of LxxLL motifs: one interacts with MAU2 and is necessary for maintenance of the NIPBL-MAU2 heterodimer; the second binds steroid receptor ligand-binding domains. AlphaFold2 modeling and molecular docking reveal a GR-NIPBL-MAU2 ternary complex at enhancers, and multiple transcription factors interact with NIPBL-MAU2 to localize cohesin at enhancers. LxxLL motif mutagenesis, co-immunoprecipitation, AlphaFold2/molecular docking, ChIP-seq, transcriptional reporter assays Nucleic acids research Medium 40377219
2025 Heterozygous MAU2 pathogenic variants cause a Cornelia de Lange syndrome subtype; in-frame variants impair NIPBL-MAU2 interaction, whereas truncating variants cause MAU2 haploinsufficiency and secondary reduction of NIPBL; heterozygous Mau2 knockout mice recapitulate short stature and microcephaly, confirming MAU2 disruption as causally sufficient for CdLS-related phenotypes. Patient variant functional analysis, NIPBL-MAU2 interaction assays, DNA methylation episignature profiling, heterozygous Mau2 KO mouse model Nature communications High 41912533

Source papers

Stage 0 corpus · 62 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 612 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 110 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 104 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 63 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
2006 A screen for cohesion mutants uncovers Ssl3, the fission yeast counterpart of the cohesin loading factor Scc4. Current biology : CB 55 16682348
2009 The Scc2/Scc4 cohesin loader determines the distribution of cohesin on budding yeast chromosomes. Genes & development 54 19797771
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 50 24859325
2020 MAU2 and NIPBL Variants Impair the Heterodimerization of the Cohesin Loader Subunits and Cause Cornelia de Lange Syndrome. Cell reports 49 32433956
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
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 45 28181380
2019 Maize Dek15 Encodes the Cohesin-Loading Complex Subunit SCC4 and Is Essential for Chromosome Segregation and Kernel Development. The Plant cell 40 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
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
2004 mau-2 acts cell-autonomously to guide axonal migrations in Caenorhabditis elegans. Development (Cambridge, England) 22 15539489
2013 Localisation of the SMC loading complex Nipbl/Mau2 during mammalian meiotic prophase I. Chromosoma 21 24287868
2017 Casticin impairs cell growth and induces cell apoptosis via cell cycle arrest in human oral cancer SCC-4 cells. Environmental toxicology 20 29098808
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 19 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 14 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 8 32424009
2017 The Arabidopsis homolog of Scc4/MAU2 is essential for embryogenesis. Journal of cell science 8 28137757
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