Ask about this productRelated genes to: MCM8 antibody
- Gene:
- MCM8 NIH gene
- Name:
- minichromosome maintenance 8 homologous recombination repair factor
- Previous symbol:
- C20orf154
- Synonyms:
- MGC4816, MGC12866, MGC119522, MGC119523, dJ967N21.5, REC
- Chromosome:
- 20p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2015-08-25
Related products to: MCM8 antibody
Related articles to: MCM8 antibody
- Meiotic DNA double-strand break (DSB) formation and repair by homologous recombination is crucial for ensuring proper chromosome segregation. In mice, the mini-chromosome maintenance family protein, MCM8, has been proposed to function in meiotic recombination and its loss leads to infertility, but the underlying mechanisms are poorly understood. Here we used cytological and genomic assays to infer the role of MCM8 during meiotic recombination in mouse spermatocytes. We show that MCM8-deficient spermatocytes exhibit increased levels of SPO11-dependent DSBs at recombination hotspots during early prophase. DSBs are resected normally and accumulate strand-exchange proteins. However, downstream recombination intermediates are barely detected and recombination intermediate-associated MutSgamma foci do not form efficiently. Consistent with a role in early recombination intermediate processing, MCM8 binds to displacement loop (D-loop) structures . We propose that MCM8 controls meiotic recombination in at least two ways. MCM8 participates in regulating meiotic DSB number. Further, MCM8 plays a role in the formation and/or stability of post-resection recombination intermediates, steps that are critical for DSB repair via recombination and for efficient synapsis of homologous chromosomes during mouse meiosis. - Source: PubMed
Publication date: 2026/03/30
Surarapu Lava KumarTilton KevinStritto Maria Rosaria DelloAcharya AnanyaMenendez Andrea MartonLu MinShaheen NajmaLiang ShunIyer MythriCejka PetrPratto FlorenciaJain Devanshi - Primary liver cancer ranks among the most prevalent and refractory malignant tumors globally. This investigation delves into the role of Epstein-Barr virus nuclear antigen 2-binding protein (EBP2) in hepatocellular carcinoma (HCC). Significantly, EBP2 exhibits marked overexpression in HCC tissues, a finding that correlates with advanced tumor staging and unfavorable prognostic outcomes. In HCC cells, EBP2 silencing led to attenuated proliferation, enhanced apoptosis, and reduced migratory capacity, coupled with reversal of epithelial-mesenchymal transition (EMT). In vivo studies further demonstrated that EBP2 depletion potently suppressed tumor growth in xenograft models. Mechanistically, EBP2 interacts with CENPA to transcriptionally upregulate minichromosome maintenance protein family member 8 (MCM8), thereby stabilizing the MCM8/MCM9 complex and enhancing homologous recombination-mediated DNA repair. Functional rescue experiments revealed that MCM8 overexpression abrogated the suppressive effects of EBP2 knockdown on HCC cell proliferation and migration. In parallel, EBP2 regulates HMGB1 expression through the CENPA/YY1 transcriptional complex, thereby participating in the progression of HCC. Collectively, these findings highlight EBP2 as a crucial regulator of HCC progression via the dual axes-EBP2-CENPA-MCM8 and EBP2-CENPA/YY1-HMGB1, offering a promising therapeutic target for HCC intervention. - Source: PubMed
Publication date: 2026/04/04
Ma EnsiXing HaoSun ChaoZhang QuanbaoShen ConghuanZhan YangyangLi JianhuaLi LiXue HongyuanLi RuidongTeng FeiTao Yifeng - The Homologous Recombination Factor With OB-Fold (HROB) plays a role in homologous recombination and DNA replication, where it enhances the MCM8-MCM9 helicase complex activity. Recent findings link biallelic germline HROB variants to primary gonadal insufficiency (hypergonadotropic hypogonadism), a phenotype also associated with MCM8/MCM9 deficiency. Here, we describe a family where two individuals with biallelic HROB variants presented with hypergonadotropic hypogonadism and colonic polyposis. Exome sequencing identified three unique HROB variants: a likely pathogenic nonsense variant (c.1267C>T [p.(Gln423*)]) in exon four, and two missense variants (c.1363C>G [p.(Leu455Val)] and c.1318A>G [p.(Ser440Gly)]) in exon five. RNA analysis and protein mapping indicate that the nonsense variant is likely pathogenic, whereas the missense variants remain of uncertain significance. Mutational signature analysis of polyposis tissue did not reveal signatures directly linked to HROB deficiency, yet a review of published cases and analyses of cohorts with unexplained polyposis/cancer identified additional individuals with HROB variants exhibiting hypergonadotropic hypogonadism or colonic polyposis. These findings reinforce the association between biallelic germline HROB variants and hypergonadotropic hypogonadism and suggest a potential role in colonic polyposis predisposition. We recommend incorporating HROB into diagnostic gene panels for hypergonadotropic hypogonadism, especially in cases where colonic polyposis is also present. Furthermore, we emphasize the importance of additional studies to comprehensively characterize HROB's phenotypic impact and assess its contribution to disease risk. - Source: PubMed
Publication date: 2026/03/25
Helderman Noah CTops Carli MLegebeke JelmerYang TingGay Marcos DíazTerlouw DianthaLashley Lisa E E L OAretz StefanSommer Anna KTerradas MarionaValle Laurade Voer Richarda MAlexandrov Ludmil BMorreau Hansvan Wezel TomNielsen Maartje - Oxidized low-density lipoprotein (oxLDL), formed by LDL oxidative modification, drives pathogenesis in cardiovascular diseases and cancers through ER stress, inflammation, and protein aggregation. Stromal-derived factor 2-like 1 (SDF2L1), an ER-resident chaperone, may modulate these processes, but its role in oxLDL-related pathologies remains unclear. - Source: PubMed
Publication date: 2026/03/04
Tian HuapingZhao TujingHuang XiaoyiLi HongjingYe LinLi ZhengLi RunzeLiao RuilinXu HaojueZou LiangShi YiHuang Lulin - Colorectal cancer (CRC) ranks among the top three in both incidence and mortality rates of malignant tumors worldwide. For patients with advanced colon cancer, radical surgery is challenging, and chemotherapy drugs are prone to inducing drug resistance, resulting in a five-year survival rate of only 13.1%. Therefore, in-depth analysis of the occurrence, development, and drug resistance mechanisms of colon cancer is of great clinical significance for optimizing treatment strategies and improving patient prognosis. As one of the homologous recombination repair proteins, minichromosomal maintenance protein 8 (MCM8) not only participates in DNA replication initiation, homologous recombination repair, and genome stability maintenance in normal cells, but also has been reported to be abnormally highly expressed in multiple tumors (e.g. glioblastoma, cholangiocarcinoma, bladder cancer) to promote malignant progression. - Source: PubMed
Publication date: 2026/01/16
Qian SiyiZeng LongwuChen FuxinTian YuxuanZhao BinjieLiu QiangZhang Bin