Ask about this productRelated genes to: Mcm10 antibody
- Gene:
- MCM10 NIH gene
- Name:
- minichromosome maintenance 10 replication initiation factor
- Previous symbol:
- -
- Synonyms:
- PRO2249, CNA43, DNA43
- Chromosome:
- 10p13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-22
- Date modifiied:
- 2015-08-25
Related products to: Mcm10 antibody
Related articles to: Mcm10 antibody
- Faithful DNA replication requires precise control of replication fork progression to maintain genome integrity; yet, the mechanisms that restrain excessive fork acceleration remain unclear. We identify SUDS3 as a condensate-associated regulator of replication speed. SUDS3 forms dynamic nuclear condensates during S phase and under replication stress. These condensates spatially partition replication-associated factors, particularly MCM10, thereby limiting their accessibility to replication-associated chromatin. Loss of SUDS3 disrupts this spatial regulation and leads to aberrantly accelerated fork progression. Under replication stress, unchecked fork acceleration in SUDS3-deficient cells results in defective fork protection, excessive single-stranded DNA accumulation, ATR-CHK1 hyperactivation, and increased genome instability. Consequently, SUDS3 deficiency sensitizes cells to replication-targeting chemotherapeutic agents, a phenotype rescued by wild-type SUDS3 but not by condensate-defective mutant. Together, our findings reveal a condensate-based mechanism that constrains replication dynamics and establish SUDS3 condensates as critical safeguards of genome stability and potential vulnerabilities in replication-stressed cancers. - Source: PubMed
Publication date: 2026/07/18
Zhou ZhifenHuang KunlingLi RuofeiChen YuxiLin SongDeng ShengchengHe ZibinChen JuanLu JunLiu YunyingMa WenbinWu SuLiu FengSongyang Zhou - - Source: PubMed
Publication date: 2026/04/11
Tian QiusiBao ZhijunZhao YifeiZhang Qun - To investigate the expression and predictive value of minichromosome maintenance proteins MCM2, MCM4, and MCM10 in hepatocellular carcinoma (HCC) for postoperative recurrence, and to develop an integrated predictive model. - Source: PubMed
Publication date: 2026/03/21
He BinTang Ke - OBJECTIVES: Gastric cancer (GC) remains a major global health challenge, with chemotherapy resistance significantly hindering treatment efficacy. A significant proportion of chemotherapeutics impact DNA replication, yet the mechanisms by which tumors evade this lethality remain incompletely understood. Notably, minichromosome maintenance 10 replication initiation factor (MCM10) is pivotal in initiating DNA replication, holding promise in mediating acquired chemotherapy resistance. This work aims to elucidate the driving roles of MCM10 GC pathogenesis and chemotherapeutic resistance. METHODS: The expression pattern of MCM10 and its clinical relevance in GC patients were investigated by adopting single-cell RNA-seq data and in-house GC tissue microarray. Functional roles were evaluated through bioinformatic analyses and experimental assays, including in vivo xenograft formation assay and patient-derived organoid (PDO) models. The transcriptional regulation of MCM10 by the YAP1-TEAD4 complex was examined via Yap1−/−;Taz−/− transgenic mice models and functional rescue assays. Candidates for targeting MCM10 were predicted by virtual screening and further validated by cellular thermal shift assay (CETSA). RESULTS: MCM10 was the most upregulated MCM family member in GC cell lines, and its elevated levels correlated with poor patient prognosis. Bioinformatic analysis linked MCM10 to DNA replication and DNA damage repair, a finding confirmed by functional assays showing that MCM10 depletion induced DNA damage accumulation and impaired DNA replication. MCM10 was further proven to promote GC cell malignancy and tumorigenesis by activating Wnt/β-catenin signaling in GC cell lines, clinical samples, and xenograft models. Critically, MCM10 conferred resistance to chemotherapeutic agents by enhancing cancer cell stemness acquisition and DNA damage response. Mechanistically, YAP1/TEAD4 was identified as the transcriptional activator of MCM10, as TEAD4 silencing downregulated MCM10. TEAD4 overexpression failed to rescue the tumor-suppressing effects in MCM10-depleted cells. Furthermore, Momordin Ic was identified as a promising MCM10-targeted inhibitor, which effectively attenuated GC cell malignancy and chemoresistance. CONCLUSION: MCM10 drives gastric tumorigenesis by enhancing DNA replication and maintaining cancer stemness, positioning it as a key mediator of YAP1-TEAD4 oncogenic signaling. These findings establish MCM10 as a promising therapeutic target to overcome chemotherapy resistance in GC. - Source: PubMed
Publication date: 2026/02/27
Xie FudaLeung Hoi WingLyu YangYu PeiyaoFeng TiejunChen BonanWu JialinTham JensonFang CanbinCheung Alvin H KChow ChitJiang JianhuiHu JintaoZhang FengbinZhu ChaoweiZhong KeliSun MeihengZhang GeYu SifanXu DazhiWang ShouyuHuang BingZhuang KangminLuo XiaobeiLi AiminGuo QingGao ChanchanZhang BinMa YuanWu William KkAn LiweiWong Chi ChunYu JunTo Ka FaiKang Wei - This study was conducted to elucidate the molecular and metabolic differences in ileal development according to birth weight in neonatal piglets. A total of 126 neonatal piglets born from Yorkshire × Landrace × Duroc crossbred sows were used, and the top 5% (H group, 1.77 ± 0.02 kg) and bottom 5% (L group, 0.72 ± 0.03 kg) of birth weights were selected for analysis. Ileal tissues were collected for transcriptomic (RNA-seq) and targeted metabolomic (GC-MS) analyses, and selected genes were validated using RT-qPCR. A total of 112 differentially expressed genes (DEGs) were identified, among which RFC3, PCNA, MCM3, MCM10, AURKA, AURKB, CCNB2, CCNA2, CCNF, and SI were significantly upregulated in the H group ( < 0.05). These genes were mainly involved in pathways related to DNA replication, cell division, and nutrient digestion and absorption. In addition, metabolomic analysis revealed that pyruvic acid concentrations were significantly higher in the H group ( < 0.05), indicating the activation of energy metabolic pathways. These results indicate that high-birth-weight piglets possess a genetic foundation for enhanced cellular proliferation and energy metabolism, and they further highlight potential molecular targets for improving growth performance and intestinal development in low-birth-weight piglets. - Source: PubMed
Publication date: 2026/01/11
Lee HyunseoKim GyuseongChoi WonvinKim Minju