Ask about this productRelated genes to: ZNF644 antibody
- Gene:
- ZNF644 NIH gene
- Name:
- zinc finger protein 644
- Previous symbol:
- -
- Synonyms:
- KIAA1221, BM-005, MGC60165, MGC70410
- Chromosome:
- 1p22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-08
- Date modifiied:
- 2014-11-19
Related products to: ZNF644 antibody
Related articles to: ZNF644 antibody
- Tail docking, serving as an important management intervention in animal husbandry, plays a significant role in regulating tail fat deposition and improving production performance and health status in fat-tailed sheep. This study systematically revealed the reprogramming effects of tail docking on the epigenetic landscape and transcriptome of fat-tailed sheep by integrating whole-genome bisulfite sequencing (WGBS) and RNA m6A methylated immunoprecipitation sequencing (MeRIP-seq). At the DNA level, the tail-docked group exhibited a pronounced trend of hypomethylation across multiple functional genomic regions, including promoters, exons, and introns. Differentially methylated regions (DMRs) were significantly enriched in pathways related to tissue development and stress response, such as the Hippo signaling pathway and adherens junctions. Pyrosequencing validation of the promoter region of the key gene DGAT1 further confirmed the reliability of the WGBS data. At the RNA level, RNA m6A modifications showed an overall up-regulated pattern: the tail-docked group displayed higher numbers of m6A peaks, greater total peak length, and increased genomic coverage compared to the control group, along with better overall prediction of modification sites. Genes associated with differential m6A peaks were closely related to processes such as stem cell pluripotency and cytoskeleton regulation. qPCR validation of several methylation-related enzyme genes (e.g., METTL3, FTO, YTHDF1) yielded results consistent with the sequencing trends. Through integrated analysis of DNA methylation and RNA methylation, we identified 143 genes with concurrent changes in methylation and mRNA expression, among which 41 genes were regulated by both DNA and RNA methylation. These genes were primarily enriched in the adherens junction pathway. Notably, two core genes CITED4 and ZNF644 showed significant changes across all three levels: DNA methylation, RNA methylation, and mRNA expression. This study systematically elucidates the epigenetic mechanism by which tail docking stress induces coordinated DNA hypo-methylation and RNA m6A hyper-methylation to regulate transcriptomic reprogramming in response to environmental intervention. The findings provide novel insights into the molecular basis of trait formation in livestock. - Source: PubMed
Publication date: 2026/02/04
Zhang JianMa YannanSong Shuzhen - Coding mutations can cause neurodevelopmental disorders (NDDs), including autism. Yet, predicting which non-coding (e.g., 5' untranslated region [UTR]) mutations are functional is challenging. We tested assays of various throughput for the assessment of 997 mutations from NDD families. A massively parallel reporter assay (MPRA) using polysomes from cell lines identified >100 altering translation, with a subset subsequently altering endogenous protein production in patient lymphoblastoid cell lines. Next, since UTR function varies by cell type, we optimized Cre-dependent MPRAs, enabling assessment in neurons in vivo. We demonstrate that neurons have different principles of regulation by 5' UTRs and discover mutations altering translational activity. Finally, we tested whether polysome-MPRAs predict changes in canonical open reading frame (ORF) protein production. Only for mutations altering UTR structure was there a reasonable correlation. Overall, we benchmarked a variety of approaches for assessing impacts of 5' UTR mutation and identified functional 5' UTR mutations from known NDD genes, including LRRC4 and ZNF644. - Source: PubMed
Publication date: 2025/12/03
Plassmeyer Stephen PFlorian Colin PChase RebeccaKasper Michael JMueller ShaynaLiu YatingMcFarland White KelliSierra-Cortez LlaelynFischer Anthony DJungers Courtney FDjuranovic Slavica PavlovicDjuranovic SergejDougherty Joseph D - To investigate the variants in 18 disease-causing genes associated with nonsyndromic myopia in 83 Chinese individuals diagnosed with early-onset high myopia(eo-HM). - Source: PubMed
Publication date: 2025/09/08
Liu YangZhang Shao-ChiZhang WenXue Zhong-QiQin Yi-XuanPiao Shun-YuLi Wen-JingJi Meng-LiZhuang Wen-Juan - Patient-derived xenograft (PDX) models are crucial for tumor biology and therapeutic response evaluations. The metabolic, transcriptomic, and proteomic changes in PDX models derived from pancreatic ductal adenocarcinoma (PDAC) during serial passaging remain poorly understood. - Source: PubMed
Publication date: 2025/07/02
Guo PengfeiFang HaizongShi HanZhang JunrongSong GeFan ChongjiuQiu XinyuLin XianchaoWen ShiFeng JianghuaHuang HeguangTeng Tianhong - mutations cause a variety of neurodevelopmental disorders including autism. Recent whole genome sequencing from individuals with autism has shown that many mutations also occur in untranslated regions (UTRs) of genes, but it is difficult to predict from sequence alone which mutations are functional, let alone causal. Therefore, we developed a high throughput assay to screen the transcriptional and translational effects of 997 variants from 5'UTR patient mutations. This assay successfully enriched for elements that alter reporter translation, identifying over 100 potentially functional mutations from probands. Studies in patient-derived cell lines further confirmed that these mutations can alter protein production in individuals with autism, and some variants fall in genes known to cause syndromic forms of autism, suggesting a diagnosis for these individual patients. Since UTR function varies by cell type, we further optimized this high throughput assay to enable assessment of mutations in neurons . First, comparing to results, we demonstrate neurons have different principles of regulation by 5'UTRs, consistent with a more robust mechanism for reducing the impact of RNA secondary structure. Finally, we discovered patient mutations specifically altering the translational activity of additional known syndromic genes and in neurons of the brain. Overall our results highlight a new approach for assessing the impact of 5'UTR mutations across cell types and suggest that some cases of neurodevelopmental disorder may be caused by such variants. - Source: PubMed
Publication date: 2023/11/03
Plassmeyer Stephen PFlorian Colin PKasper Michael JChase RebeccaMueller ShaynaLiu YatingWhite Kelli McFarlandJungers Courtney FDjuranovic Slavica PavlovicDjuranovic SergejDougherty Joseph D