Ask about this productRelated genes to: ZNF791 antibody
- Gene:
- ZNF791 NIH gene
- Name:
- zinc finger protein 791
- Previous symbol:
- -
- Synonyms:
- FLJ90396
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-17
- Date modifiied:
- 2016-10-05
Related products to: ZNF791 antibody
Related articles to: ZNF791 antibody
- Genomic imprinting is an epigenetic process that results in parent-of-origin effects on mammalian development and growth. Research on genomic imprinting in domesticated animals has lagged due to a primary focus on orthologs of mouse and human imprinted genes. This emphasis has limited the discovery of imprinted genes specific to livestock. To identify genomic imprinting in pigs, we generated parthenogenetic porcine embryos alongside biparental normal embryos, and then performed whole-genome bisulfite sequencing and RNA sequencing on these samples. In our analyses, we discovered a maternally methylated differentially methylated region within the orthologous ZNF791 locus in pigs. Additionally, we identified both a major imprinted isoform of the ZNF791-like gene and an unannotated antisense transcript that has not been previously annotated. Importantly, our comparative analyses of the orthologous ZNF791 gene in various eutherian mammals, including humans, non-human primates, rodents, artiodactyls, and dogs, revealed that this gene is subjected to genomic imprinting exclusively in domesticated animals, thereby highlighting lineage-specific imprinting. Furthermore, we explored the potential mechanisms behind the establishment of maternal DNA methylation imprints in porcine and bovine oocytes, supporting the notion that integration of transposable elements, active transcription, and histone modification may collectively contribute to the methylation of embedded intragenic CpG island promoters. Our findings convey fundamental insights into molecular and evolutionary aspects of livestock species-specific genomic imprinting and provide critical agricultural implications. - Source: PubMed
Publication date: 2025/01/15
Ahn JinsooHwang In-SulPark Mi-RyungRosa-Velazquez MilcaCho In-CheolRelling Alejandro EHwang SeongsooLee Kichoon - It has been reported that long noncoding RNA (lncRNA) KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) played an important role in myocardial infarction (MI). However, the regulatory network behind KCNQ1OT1 in MI is largely unknown. Quantitative real time polymerase chain reaction (qRT-PCR) was applied to detect the enrichment of KCNQ1OT1, microRNA-130a-3p (miR-130a-3p) and zinc finger 791 (ZNF791). The viability and apoptosis of AC16 cells were measured by (4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was conducted to assess the inflammation and oxidative stress status of AC16 cells. The targeted relationship between miR-130a-3p and KCNQ1OT1 or ZNF791 was predicted by StarBase bioinformatic database, and dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were carried out to verify these predictions. Hydrogen peroxide (H O ) stimulation caused a significant upregulation in the expression of KCNQ1OT1, while the level of miR-130a-3p showed an opposite phenomenon. KCNQ1OT1 was a crucial downstream component in H O -mediated toxic effects, and KCNQ1OT1 accelerated H O -induced toxic effects in AC16 cells. KCNQ1OT1 could sponge miR-130a-3p and down-regulate its expression. MiR-130a-3p exerted opposite effects to KCNQ1OT1, and the depletion of miR-130a-3p attenuated the protective effects of KCNQ1OT1 intervention on AC16 cells exposed to H O . MiR-130a-3p could bind to ZNF791, and ZNF791 served as the target of miR-130a-3p to promote H O -induced injury of AC16 cells. ZNF791 was modulated by KCNQ1OT1/miR-130a-3p signaling in H O -treated AC16 cells. In all, lncRNA KCNQ1OT1 deteriorated H O -mediated injury in cardiomyocytes through upregulating ZNF791 via serving as a molecular sponge for miR-130a-3p. - Source: PubMed
Publication date: 2022/08/21
Xin HongLi ChengliangCai TianzhiCao JinlongWang Meixue - The aim of this study was to elucidate the potential function of microRNA-488-3p (miRNA-488-3p) in the pathogenesis of acute myocardial infarction (AMI). - Source: PubMed
Zheng H-FSun JZou Z-YZhang YHou G-Y