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)
- The DNA damage response (DDR) is a complex network of cellular pathways that ensures the faithful maintenance of our genomes upon a wide array of genomic insults. To elucidate the functional architecture of this network, we conducted unbiased genetic interaction screens using the Cas12a genome editor to disrupt 233 DDR genes frequently mutated in cancer and other genetic diseases, either individually or in pairwise combinations. This approach enabled us to assess the phenotypic effects induced by the disruption of >27,000 DDR gene pair combinations under unperturbed cell growth conditions. From this analysis, we identified over 750 high-confidence positive (buffering) or negative (synthetic lethal/sick) gene-gene interactions, along with multiple connections between previously unlinked DDR pathways and modules, allowing us to define novel aspects of the cellular response to spontaneous, DNA replication-associated DNA damage. Among the identified genetic interactions, we uncovered profound synthetic lethal interactions between genes encoding 1) the translesion polymerase REV1-Pol ζ complex and the MCM8-MCM9-HROB DNA helicase complex; 2) Fanconi Anemia (FA) proteins and the mitotic DNA repair factors GEN1, CIP2A, and RHINO; and 3) the DNA translocase SMARCAL1 and components of the FANCM complex, suggesting novel opportunities for targeted therapies in tumors carrying mutations in these genes. Additionally, we identified robust suppressor interactions between the gene encoding the nuclease APOLLO and the core non-homologous end joining (NHEJ) genes , , and , suggesting that NHEJ impairs the fitness of APOLLO-deficient cells. This work provides a functional map of the DDR network and demonstrates the power of Cas12a-based screens for identifying synthetic lethal and buffering interactions with therapeutic potential. - Source: PubMed
Publication date: 2026/06/08
Hayward Samuel BVaitsiankova AlinaLama-Diaz TomasChou JuihsuanTaglialatela AngeloHuang Jen-WeiWijesekarahanthi YodharaudshaniHeyza Joshua RLeuzzi GiuseppeChen ChuanyuanWong NancyLhakhang TenzinFu XiBuendia Alejandro LGheorghe VeronicaAnvar Nazanin EsmaeiliSchmidt Jens CNussenzweig AndreRabadan RaulCostanzo VincenzoGuérois RaphaëlHart TraverCiccia Alberto
- Source: PubMed
- 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
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: 2026/06/23
Li ChuxuanTo ColinAdeleke Temitope MMcKinzey David RGao YangTrakselis Michael A