MCM9 antibody - N-terminal region (ARP36660_P050)
- Known as:
- MCM9 (anti-) - N-terminal region (ARP36660_P050)
- Catalog number:
- arp36660_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MCM9 antibody - N-terminal region (ARP36660_P050)
Related genes to: MCM9 antibody - N-terminal region (ARP36660_P050)
- Gene:
- MCM9 NIH gene
- Name:
- minichromosome maintenance 9 homologous recombination repair factor
- Previous symbol:
- MCMDC1, C6orf61
- Synonyms:
- MGC35304, dJ329L24.3, FLJ20170
- Chromosome:
- 6q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-18
- Date modifiied:
- 2015-08-25
Related products to: MCM9 antibody - N-terminal region (ARP36660_P050)
Related articles to: MCM9 antibody - N-terminal region (ARP36660_P050)
- Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with sex differences, possibly linked to testosterone; however, the relationship remains unclear. This study aimed to clarify the genetic correlation and polygenic overlap between ADHD and testosterone traits, identify shared genomic loci, and investigate the underlying biological mechanisms through functional annotation. Genomic data on ADHD and three testosterone traits (total testosterone [TT], bioavailable testosterone [BT], and sex hormone-binding globulin [SHBG]) were obtained from publicly accessible genome-wide association studies. Employing the MiXeR bivariate causal mixture model, we quantified the polygenic overlap between ADHD and these testosterone traits. Subsequently, we applied the conjunctional false discovery rate (conjFDR) method to identify genomic loci and performed functional annotation with the Functional Mapping and Annotation tool to aid biological interpretation. Using MiXeR, we found negative correlations between TT and ADHD, and SHBG and ADHD, but a positive correlation between BT and ADHD. Over one-third of testosterone-associated variants were predicted to affect ADHD. Using the conjFDR approach, we identified 22-51 genomic loci shared between testosterone traits and ADHD, including MCM9 and MANBA. Functional enrichment analysis highlighted the predominant involvement of these mapped genes in signal transduction pathways, synapses, cell differentiation, and neurogenesis. In conclusion, we reported a substantial polygenic overlap between ADHD and testosterone traits, identified multiple shared genomic loci implicating common biological mechanisms, and highlighted the association of glutamatergic synapses and neurogenesis with ADHD and testosterone levels. - Source: PubMed
Publication date: 2026/06/03
Lu WenHe XiaoyanLei PuLiu YixinZhan XianyanMa QingyanYan BinMa XiancangYang JianGao Yuan - Human aneuploid conception, a leading cause of infertility, pregnancy loss, and congenital disorders (e.g. Down's syndrome), arises from errors in chromosome segregation during oocyte meiosis or embryonic mitosis. While advanced maternal age is a well-established risk factor, significant inter-individual variation exists among younger women, suggesting a substantial role for maternal genetic determinants. - Source: PubMed
Publication date: 2026/05/13
Ha SiyaoLiu WenyiYuan PingYuan ShangyaCao ChunweiMeng AnmingChen Hui - The minichromosomal maintenance MCM8 and MCM9 proteins form a heterohexameric complex that acts to unwind or remodel duplex DNA in DNA recombination and repair pathways. Mutations or absence of MCM8/9 have been linked to infertility, sex-specific deficiencies, and several cancers. Recently, HROB has been identified as a critical cofactor of MCM8/9; however, the mechanism underlying activation of MCM8/9 DNA binding and unwinding remain unclear. Here, we present dynamic structures of MCM8/9 with DNA, HROB and ATP analogs using cryo-electron microscopy. DNA binding induces a pronounced rotational rearrangement between the N-terminal DNA binding and C-terminal AAA ATPase domains, reorganizing DNA-binding loops into a staircase configuration that supports DNA engagement. Remarkably, HROB associates with both halves of the heterohexamer and drives a similar rotation prior DNA binding for localizing MCM8/9 to sites of crosslink damage and unwinding, culminating in a unified mechanistic model for MCM8/9 helicase function and its activation by HROB. - Source: PubMed
Publication date: 2026/04/29
Li ChuxuanTo ColinAdeleke Temitope MMcKinzey David RGao YangTrakselis Michael A - MCM8 and MCM9 form a hexameric helicase critical for homologous recombination (HR). While their variants are strongly associated with premature ovarian insufficiency (POI), with many clustering within their AAA+ ATPase domains, the requirement for their helicase activity remains unknown. Here, we show that MCM8-9's helicase activity is essential for ovarian reserve preservation and POI prevention. Using a series of helicase-deficient mouse models, we demonstrate that this activity is dispensable for meiotic recombination but critically required for mitotic HR and primordial germ cell (PGC) development. The two distinct ATPase active sites of MCM8-9 exhibit marked functional asymmetry, a property regulated by residues within their Walker B motifs. Despite this asymmetry, both ATPase active sites are equally essential for MCM8-9's function in HR, PGC development, ovarian reserve preservation, and POI prevention. Our findings establish a direct mechanistic link between compromised MCM8-9 helicase activity and POI pathogenesis through its essential role in PGC development. - Source: PubMed
Publication date: 2026/05/05
Jiao XiaofeiLi ZhifangTang ZhenghuiXu JunLu Lin-YuLiu Yidan - Familial prostate cancer (PCa) accounts for nearly 20% of all PCa cases and is associated with increased genetic susceptibility and earlier disease onset. However, early detection and risk stratification in genetically predisposed individuals remain challenging. Circulating cell-free DNA (cfDNA) provides a minimally invasive source of tumor-derived genomic and epigenomic information. Integrating multi-omic cfDNA analyses may enhance the discovery of biomarkers relevant to familial PCa biology. We conducted a pilot feasibility study employing whole-genome, strand-specific sequencing of cfDNA from eight patients with familial PCa. A unified analytical pipeline was used to jointly profile genomic alterations and epigenomic features. Variant calling, methylation mapping, and allele-specific methylation (ASM) analysis were performed to identify somatic mutations, characterize epigenetic dysregulation, and explore potential interactions between genetic and epigenetic mechanisms. Sequencing revealed 18,878 genetic variants, including 2276 potentially pathogenic alterations. We identified 26 recurrent high-impact mutations, such as stop-gain and start-loss variants, in genes including , , and . Epigenomic profiling demonstrated widespread gene-specific hypermethylation, consistent with transcriptional repression in these loci. ASM events were detected in , , , , and , suggesting coordinated interactions between somatic variation and epigenetic regulation in familial PCa. This proof-of-concept study highlights the feasibility and potential of integrating whole-genome and epigenome profiling of cfDNA to decode the molecular architecture of familial prostate cancer. By jointly capturing genomic alterations and epigenetic signatures, including allele-specific methylation, this multi-omic liquid biopsy approach supports a high-resolution exploration of biologically relevant molecular features. Moreover, this integrated profiling strategy provides a minimally invasive and clinically scalable tool that may substantially improve risk assessment. These findings offer a promising foundation for future validation studies in larger cohorts, with the aim of advancing multi-omic cfDNA analysis as a next-generation technology in the field of precision oncologic epigenetics. - Source: PubMed
Publication date: 2026/04/03
Truda AnnaCordella AngelaDe Leo IleniaDi Palo ArmandoIorio RobertaMarino SimonaLa Rocca RobertoCollà Ruvolo ClaudiaPotenza NicolettaRavo MariaMarchese Giovanna