Ask about this productRelated genes to: Mcm10 Blocking Peptide
- 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 Blocking Peptide
Related articles to: Mcm10 Blocking Peptide
- DNA replication initiation requires activation of the CMG helicase to establish the replisome. This process involves the extrusion of single-stranded DNA (ssDNA) from the central channel of MCM double hexamers, allowing the two CMG helicases to pass each other; however, the factors that mediate this process in human cells remain unclear. We show that degron-mediated depletion of either MCM10 or RECQL4 alone causes mild replication defects, whereas simultaneous depletion of both proteins severely impairs CMG activation. ChIP-seq analyses demonstrate that RECQL4 localizes to replication initiation zones (IZs) independently of MCM10, whereas MCM10 recruitment to IZs is enhanced upon RECQL4 depletion, consistent with partially redundant roles during CMG activation. Rescue experiments further indicate that RECQL4 cooperates with MCM10 through direct interaction, and that their ssDNA-binding activity underlies their functional overlap. We propose that MCM10 and RECQL4 act cooperatively and redundantly to promote CMG activation. - Source: PubMed
Publication date: 2026/09/04
Bektash AtabekZhu XiaoxuanHatoyama YukiToyoda AtsushiKanemaki Masato T - 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