Ask about this productRelated genes to: ZNF200 Blocking Peptide
- Gene:
- ZNF200 NIH gene
- Name:
- zinc finger protein 200
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2014-11-19
Related products to: ZNF200 Blocking Peptide
Related articles to: ZNF200 Blocking Peptide
- Rare genetic variation is considered a potential source of heritability in individuals with sporadic Alzheimer disease and related dementias (ADRD). The Variant-set test for association using annotation information (STAAR) framework leverages multiple functional annotations of genetic variants and combines association statistics from multiple variant aggregation-based methods, including burden, sequence kernel association test (SKAT), and aggregated Cauchy association test (ACAT-V), into a single measure of significance. Using whole-genome sequencing data from the Alzheimer's Disease Sequencing Project (ADSP), we comprehensively examined the association of rare genetic variation with ADRD in 23,454 individuals (37% individuals affected by ADRD) and with cognitively healthy elder status in 13,292 individuals (13% cognitively healthy elders) from diverse populations via the STAAR framework. We identified several genes significantly associated with ADRD or cognitively healthy status. However, our analysis revealed several limitations within the STAAR framework incorporating ultra-rare variants with dichotomous outcomes. To enhance the robustness of the framework, we proposed several computational refinements, including creating a burden of ultra-rare variants and employing more precise annotations to match the expected mechanism. After implementing the proposed modifications, the association with ADRD for ZNF200 was no longer statistically significant (α = 1 × 10), while TBX19, PLXNB2, CARD11, and LINC01880 remained significantly associated with cognitively healthy status. We identified and addressed the computational limitations in the STAAR framework that could lead to potential spurious results for ultra-rare variant aggregates with an extremely low cumulative minor-allele count. Our proposed refinements produced more robust results for associations with rare variants in the context of dichotomous outcomes. - Source: PubMed
Publication date: 2026/01/20
Wang DongyuAbbruzzese SabrinaHeard-Costa NancyRampersaud AndyMartin EdenNaj AdamAkgun BilcagKunkle BrianSeshadri SudhaPeloso Gina DeStefano Anita LLi ZilinLi XihaoChoi Seung Hoan - Protein arginine methyltransferase 3 (PRMT3), a type I arginine methyltransferase is localized predominantly in the cytoplasm and regulates different cellular functions. Nevertheless, PRMT3 also exhibits regulatory functions in the nucleus by interacting with the liver X receptor alpha (LXRα) and catalyzes asymmetric dimethylation modifications at arginine 3 of histone 4 (H4R3me2a). However, very little is known about the regulation of the versatile global regulator PRMT3 and how PRMT3 is translocated to the nucleus. In this study, we identified ZNF200, a hitherto uncharacterized protein, as a potential binding partner of PRMT3 through yeast two-hybrid screening. We confirmed the interaction of PRMT3 with ZNF200 using immunoprecipitation and in vitro pull-down experiments. GST pull-down experiments and molecular docking studies revealed that the N-terminal zinc finger domain of PRMT3 binds to the C-terminal zinc finger regions of ZNF200. Furthermore, the evolutionary conservation of the Znf domain of PRMT3 correlates with the emergence of ZNF200 in mammals. We found that ZNF200 stabilizes PRMT3 by inhibiting its proteasomal degradation. ZNF200, a nuclear-predominant protein, promotes the nuclear translocation of PRMT3, leading to the global increase of H4R3me2a modifications. These findings imply that ZNF200 is a critical regulator of the steady-state levels and nuclear and epigenetic functions of PRMT3. - Source: PubMed
Gupta SomleeVerma MamtaKadumuri Rajashekar VarmaChutani NamitaKhan Mohd Imran KChavali SreenivasDhayalan Arunkumar - Neutrophils contribute to host defense through different mechanisms, including the formation of neutrophil extracellular traps (NETs). The genetic background and underlying mechanisms contributing to NET formation remain unclear. - Source: PubMed
Publication date: 2021/02/24
Donkel Samantha JPortilla Fernández ElianaAhmad ShahzadRivadeneira Fernandovan Rooij Frank J AIkram M ArfanLeebeek Frank W Gde Maat Moniek P MGhanbari Mohsen - Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome, or the congenital absence of uterus and vagina, is the most severe anomaly of the female reproductive tract. It affects 1 in 5,000 females, and is the second most common cause of primary amenorrhea. The etiology remains unknown in most patients, although four single gene defects and some repetitive copy number variants (CNVs) have been identified. Translocations in MRKH patients are very rare, and reported only in three patients previously without breakpoint mapping. We have identified the fourth MRKH translocation patient and are the first to characterize the breakpoints mapped by molecular methods. - Source: PubMed
Publication date: 2016/07/30
Williams Lacey SKim Hyung-GooKalscheuer Vera MTuck J MatthewChorich Lynn PSullivan Megan EFalkenstrom AllisonReindollar Richard HLayman Lawrence C - We previously identified a panel of genes associated with outcome of ovarian cancer. The purpose of the current study was to assess whether variants in these genes correlated with ovarian cancer risk. - Source: PubMed
Publication date: 2010/01/27
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