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
- The early developmental stages of fish exhibit the highest mortality and greatest environmental sensitivity throughout their life cycle. This period encompasses a series of crucial biological events, including morphogenesis, organ differentiation, and nutritional mode transition from fertilized eggs to newly hatched larvae. Although largemouth bass (Micropterus nigricans) is a commercially important fish species in China, the molecular regulatory mechanisms governing its endogenous nutritional stage remain largely unexplored. To elucidate the molecular basis of this critical period, we performed transcriptomic profiling across six consecutive developmental stages (Multicellular, Blastula, Gastrula, Neurula, Organogenesis, and 5 day post hatching larvae). Our results reveal stage-specific transcriptional programs: the multicellular-to-blastula transition is characterized by stage-specific enrichment of by cell cycle and DNA replication pathways, with MCM complex (mcm2-5) upregulation accelerating proliferation; the blastula-to-gastrula transition features activation of bmp4, fgfr2, and lft1 for germ layer induction; the neurula stage exhibits transcriptional bursts and enrichment of neural tube-related pathways; organogenesis involves simultaneous activation of focal adhesion (col1a1b, col4a5, tnc) and Wnt signaling (wnt1, wnt4, wnt3a) pathway; and 5 dph larvae show visual function maturation, with light transduction genes (gnat1, gnat2, gucy2f, pde6b) identified as hub genes. Mfuzz analysis further reveals sustained upregulation of Cluster 14 (igf2r、napin、vamp7、il1b、aco2) indicating functional maturation, while Cluster 29 (mcm10, espl1, cep152, cep44, cep295) confirms declining cell division activity. Collectively, this study provides a transcriptomic resource for understanding largemouth bass embryonic development and offers molecular insights for improving hatchery practices. - Source: PubMed
Publication date: 2026/08/31
Hua JixiangTao YifanSun HuiZhu TaideWang XiaoyiHuang XiaochenWang WenLu SiqiLu JianQiang Jun - 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