MCM2 Antibody
- Known as:
- MCM2 Antibody
- Catalog number:
- 32134
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- MCM2 Antibody
Related genes to: MCM2 Antibody
- Gene:
- MCM2 NIH gene
- Name:
- minichromosome maintenance complex component 2
- Previous symbol:
- CCNL1, CDCL1
- Synonyms:
- D3S3194, KIAA0030, BM28, cdc19, DFNA70
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-30
- Date modifiied:
- 2017-08-14
- Gene:
- MCM7 NIH gene
- Name:
- minichromosome maintenance complex component 7
- Previous symbol:
- MCM2
- Synonyms:
- CDC47, PPP1R104
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-13
- Date modifiied:
- 2016-10-05
Related products to: MCM2 Antibody
Related articles to: MCM2 Antibody
- During eukaryotic DNA replication initiation, inactive MCM2-7 double-hexamers assembled at replication origins must be converted into two active CMG helicases, yet how this transition is coupled to origin DNA unwinding in vivo remains unclear. Here, we identify a DNA-bound intermediate with an extended genomic footprint that forms during helicase activation. Genome-wide mapping of initial strand separation reveals that DNA unwinding initiates near the N-terminal interface of opposing MCM2-7 hexamers. At these sites, the origin DNA exhibits a conserved AT-rich/GC-rich/AT-rich sequence architecture centred under the helicase complex, which is associated with an elevated DNA melting probability. We further show that restricting hexamer splitting delays release of the Cdc45-loading factor Sld3, demonstrating that mechanical transitions during helicase activation are tightly coupled to complex disassembly. Finally, we provide in vivo evidence that single-stranded DNA is ejected through a specialised DNA exit gate at the Mcm2/5 interface during helicase activation, which is dispensable for ongoing DNA synthesis. Together, these findings establish a mechanistic framework for how replication origins are remodelled to initiate DNA replication and reveal key intermediates and DNA transactions during helicase activation. - Source: PubMed
Publication date: 2026/07/23
Weekes ChristopherWillerding LiaKhadayate Sanjay PLiebl KorbinianMossler AudreyMontoya AlexRauthe VanessaKarimi Mohammad MZacharias MartinUlrich Helle DSpeck ChristianReuter L Maximilian - Aberrant activation of DNA replication programs is essential for Glioblastoma cell proliferation, but the upstream mechanisms that maintain replication competence remain poorly defined. Here, we identify TRIM28 as a multilayered regulator of DNA replication in Glioblastoma. TRIM28 was highly expressed in Glioblastoma tissues, increased with tumor grade, and predicted poor prognosis. The enrichment analysis linked TRIM28-high tumors to DNA replication-related pathways, and TRIM28 depletion impaired BrdU incorporation and CldU-labeled replication activity in Glioblastoma cells. Integrated analyses of Glioblastoma datasets identified MCM7, a core component of the MCM2-7 replicative helicase complex, as a TRIM28-associated replication factor. MCM7 was upregulated in Glioblastoma, positively correlated with TRIM28, and associated with unfavorable clinical outcome. Mechanistically, TRIM28 occupied the MCM7 promoter and enhanced its transcriptional activity, as supported by public ChIP-seq data, promoter reporter assays, and ChIP-qPCR validation. In parallel, TRIM28 interacted with MCM7 and promoted its K63-dependent ubiquitination. These findings reveal a TRIM28-MCM7 axis that supports DNA replication-associated proliferation through transcriptional activation and K63-dependent post-translational regulation. - Source: PubMed
Publication date: 2026/06/15
Hu XiaosongYang LiCui Hongjuan - Eukaryotic DNA replication requires the precise assembly of MCM2-7 single hexamers (SHs) into head-to-head double hexamers (DHs) at replication origins. While DH formation is well-characterized in budding yeast, the underlying mechanisms in human cells remain poorly understood. Here, we report cryo-electron microscopy structures of endogenous human MCM2-7 SH isolated from G1-phase cells. In these structures, human MCM2-7 adopts a latched spiral conformation in an autoinhibited state where the carboxyl-terminal extension (CTE) of MCM5 occupies the central channel, and MCM3-CTE is capable of locking the MCM2-5 gate to occlude DNA entry. Systematic functional analysis demonstrates that the six CTEs of MCM2-7 play distinct roles in SH stability, MCM loading, and DH formation on chromatin. Surprisingly, unlike in yeast, the human MCM3-CTE is dispensable for cell viability but ensures efficient genome-wide replication initiation. Our findings establish how human MCM2-7 enables flexible yet precise MCM loading via its CTEs, providing a framework for understanding the regulation of DNA replication initiation in higher eukaryotes. - Source: PubMed
Publication date: 2026/05/14
Fan XinyuLam Wai HeiYu DaqiJiang HuadongHui Yan ChitZhang QiongdanLi WeiranLi JianLin ZiyangYin ZhanWu WenxiongZhang YingyiLiu NanKanemaki Masato TDang ShangyuZhai Yuanliang - Chromatin loading of the hexameric replicative helicase MCM2-7 complex requires coordinated interactions with the origin recognition complex (ORC), CDC6, and CDT1. MCM2-7 not bound to DNA forms a single hexamer (SH) with an open DNA entry gate between MCM2 and MCM5. Two MCM2-7 SHs can be loaded sequentially to form the double hexamer (DH) that encircles the DNA duplex. Activated MCM2-7 then unwinds DNA and initiates DNA replication. Our cryoelectron microscopy analyses show that a fraction of human MCM2-7 without DNA exists as DH. Unexpectedly, we find that the MCM3 winged helix domain (WHD) docks on MCM2 in both DNA-free DH and SH, creating a safety latch across the DNA entry gate to block DNA entry into the central channel. The safety latch can be opened by ORC-CDC6 binding. Perturbing this latch by structure-based or disease-related mutations of MCM3 causes replication defects and DNA damage checkpoint activation. Shortening the MCM3 linker between the helicase domain and WHD alleviates the cell cycle defects of the latch-strengthening mutation. Our findings uncover a regulated step in MCM2-7 loading with implications for human diseases. - Source: PubMed
Publication date: 2026/02/20
Liu YusongYang MengquanLu PingGao HaishanHe MaozhouWang YitaoQi AoCao TingZhang QiuqinQi ShutaoShi YigongYu Hongtao - The Magnoliaceae family represents one of the most ancient angiosperm lineage and provides key insights into early flowering plant evolution. Woonyoungia septentrionalis is an endangered dioecious tree endemic to the karst regions of Southwest China, with small and fragmented populations threatened by habitat loss and low reproductive success. Here, we generated a high-quality chromosome-scale genome assembly of W. septentrionalis with an assembled genome size of 2.62 Gb and 98.9 % completeness based on BUSCO. Repetitive elements occupy 81.23 % of the genome, dominated by long terminal repeat retrotransposons. Ks-based analysis revealed an ancestral whole-genome duplication event around 65 Mya shared with Magnolia species. Phylogenomic analyses indicated that W. septentrionalis represents the earliest diverging lineage within Magnolia sensu lato, reflecting its distinct evolutionary position. Comparative and transcriptomic analyses identified gene family expansions and sex-biased regulatory networks, including hub genes such as MCM2-MCM7, and transcription factors SPL, TCP, and ERF, which may be involved in floral organ differentiation and dioecy formation. This reference genome provides a valuable resource for exploring the molecular basis of reproductive specialization and evolutionary diversification in Magnoliaceae, and supports conservation efforts for this endangered species. - Source: PubMed
Publication date: 2025/11/30
Cai MengxianZhang WenqingChen ZhengrenPeng YangWang ZenghuiOu JingZeng Tuo