Ask about this productRelated genes to: ZNF549 antibody
- Gene:
- ZNF549 NIH gene
- Name:
- zinc finger protein 549
- Previous symbol:
- -
- Synonyms:
- FLJ34917
- Chromosome:
- 19q13.43
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-15
- Date modifiied:
- 2014-11-19
Related products to: ZNF549 antibody
Related articles to: ZNF549 antibody
- Chromatin accessibility and transcription levels during oocyte growth are important for oocyte maturation and subsequent development. However, chromatin accessibility changes in porcine oocytes during growth are unclear. The present study demonstrated that porcine oocytes derived from large follicles (LFO) exhibited higher developmental capacity than those derived from small follicles (SFO). Assay for transposase-accessible chromatin using sequencing (ATAC-seq) analysis identified 1117 and 1694 uniquely accessible chromatin peaks in LFO and SFO, respectively. Motif analysis of differential peaks revealed the top 10 significantly enriched transcription factor (TF)-binding motifs in LFO versus SFO, with only one increased peak (Spi1 binding site) and nine decreased peaks (NFYA, ATOH1, ZNF549, Foxn1, HAND2, THRB, NHLH2, FoxP1, and FoxP2 binding sites). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis identified key processes in the regulation of oocyte growth and maturation. Integration of ATAC-seq and RNA sequencing data revealed the top 10 hub genes involved in chromatin remodeling (MYSM1 and EZH2), histone modification (MYSM1, RNF2, USP1, EZH2, and MIER1), and transcription regulation (MYSM1, ASXL3, and MIER1), as well as those involved in metabolic processes and signal transduction (DOCK7, FGGY, DTL, and DNAJC6). All these genes exhibited increased expression levels in LFO versus SFO. In conclusion, the study demonstrated the dynamic nature of chromatin accessibility during porcine oocyte growth and revealed the TFs and genes closely associated with oocyte growth and maturation. These findings provide new insight into porcine oocyte growth and offer a potential strategy to enhance the in vitro developmental ability of SFO. - Source: PubMed
Publication date: 2025/02/01
Cheng YazhuoLi JingyuShang JiyongJia XilongBi YelingGu JiaxuJiang NanHuan YanjunLi YouweiSun Mingju - Intervertebral disc degeneration (IDD) leads to low back pain (LBP). This study aimed to determine the regulation of IDD by competing endogenous RNAs (ceRNAs). We obtained the GSE63492, GSE124272, and GSE129789 datasets from the Gene Expression Omnibus database. The changes of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs in IDD were characterized. The significantly changed mRNAs were subjected to protein-protein interaction analysis using the STRING database, and its functions and involved pathways were analyzed using the DAVID database and gene set enrichment analysis (GSEA). The significant changed lncRNAs, miRNAs and mRNAs were linked in a ceRNA network based on their interactions - predicted by Starbase and miRWalk. Differentially methylated loci of significantly changed mRNAs in early and advanced IDD were compared using the GSE129789 dataset. We identified 245 significantly changed mRNAs, 133 lncRNAs, and 228 miRNAs between patients with IDD and normal individuals. GSEA suggested that 17 pathways related to cell proliferation were activated while 35 cell signaling and immune-related pathways were suppressed in IDD. The following ceRNA network in IDD was built: LINC00665/hsa-miR-7-5p/FZD3, ZNF549; LINC00665/hsa-let-7e-5p/FZD3, ACVR2B; TRG-AS1/hsa-miR-574-5p/ACVR2B, P3H2; TRG-AS1/ hsa-let-7e-5p/FZD3, ACVR2B; and ZNF571-AS1/let-7e-5p/ACVR2B, FZD3. A lncRNA-miRNAmRNA ceRNA network which might regulate the progression of IDD was developed. - Source: PubMed
Fan XutaoChen GuowuMa FengyuQi BaoLiang YanhuGopng PihaoMeng Chunyang - Colon adenocarcinoma (COAD) is the most common type of gastrointestinal cancer and is still the third leading cause of cancer-related mortality worldwide. Therefore, finding new and promising drugs to eradicate cancer may be a feasible method to treat COAD patients. Cys2-His2 zinc finger proteins (ZFPs) is one of the largest transcription factor family and many of them are highly involved in regulation of cell differentiation, proliferation, apoptosis, and neoplastic transformation. In this study, we identified a tumor-inhibiting factor, ZNF549, which expressed lowly in COAD tissues and COAD cell lines (HT29, HCT116, SW480, LoVo, and SW620). Overexpression of ZNF549 inhibit the ability of COAD cell proliferation and migration. On the contrary, decreasing the ZNF549 expression level promote the ability of COAD cell proliferation and migration. Through bioinformatics analysis, we found that ZNF549 was a potential target of hsa-miR-708-5p (miR-708-5p). Furthermore, we verified the possibility of miR-708-5p targeting the ZNF549 gene, and miR-708-5p inhibited the expression of ZNF549 by luciferase reporter assays, qRT-PCR and western blot assays. Moreover, the relationship between miR-708-5p and phosphatidylinositol 3-kinase/AKt (PI3K/AKt) signal pathway was elucidated. Overexpression and inhibition of miR-708-5p resulted in increased and decreased expression of p-AKt and p-PI3K in HCT116 cells, respectively. RT-qPCR and western blot assays results demonstrated that miR-708-5p regulated COAD cells development by promoting the process of Epithelial-mesenchymal transition (EMT) through PI3K/AKt signaling pathway. In summary, our findings demonstrated that ZNF549, the target gene of miR-708-5p, functions as a tumor suppressor to inhibit COAD cell lines proliferation and migration through regulate the PI3K/AKt signal pathway. - Source: PubMed
Publication date: 2020/10/07
Zhao ZhidongQin Xianju - Smoking is a common risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Although COPD patients have higher risk of lung cancer compared to non-COPD smokers, the molecular links between these diseases are not well-defined. This study aims to identify genes that are downregulated by cigarette smoke and commonly repressed in COPD and lung cancer. - Source: PubMed
Publication date: 2020/05/25
Tessema MathewosTassew Dereje DYingling Christin MDo KieuPicchi Maria AWu GuodongPetersen HansRandell ScottLin YongBelinsky Steven ATesfaigzi Yohannes - Epigenetic changes, including DNA methylation, disrupt normal cell function, thus contributing to multiple steps of carcinogenesis. Nasopharyngeal carcinoma (NPC) is endemic in southern China and is highly associated with Epstein-Barr virus (EBV) infection. Significant changes of the host cell methylome are observed in EBV-associated NPC with cancer development. Epigenetic marks for NPC diagnosis are urgently needed. In order to explore DNA methylation marks, we investigated DNA methylation of candidate genes in EBV-associated nasopharyngeal carcinoma. - Source: PubMed
Publication date: 2017/07/17
Zhao WeilinMo YingxiWang ShuminMidorikawa KaoruMa NingHiraku YusukeOikawa ShinjiHuang GuangwuZhang ZheMurata MarikoTakeuchi Kazuhiko