Ask about this productRelated genes to: ZFP62 antibody
- Gene:
- ZFP62 NIH gene
- Name:
- ZFP62 zinc finger protein
- Previous symbol:
- -
- Synonyms:
- FLJ34231, ZET, ZNF755
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-28
- Date modifiied:
- 2016-10-25
Related products to: ZFP62 antibody
Related articles to: ZFP62 antibody
- The mechanism of brain aging is not fully understood. Few studies have attempted to identify molecular changes using bioinformatics at the subregional level in the aging brain. This study aimed to identify the molecular signatures and key genes involved in aging, depending on the brain region. Differentially expressed genes (DEGs) associated with aging of the cerebral cortex (CX), hippocampus (HC), and cerebellum (CB) were identified based on five datasets from the Gene Expression Omnibus (GEO). The molecular signatures of aging were explored using functional and pathway analyses. Hub genes of each brain region were determined by protein-protein interaction network analysis, and commonly expressed DEGs (co-DEGs) were also found. Gene-microRNAs (miRNAs) and gene-disease interactions were constructed using online databases. The expression levels and regional specificity of the hub genes and co-DEGs were validated using animal experiments. In total, 32, 293, and 141 DEGs were identified in aging CX, HC, and CB, respectively. Enrichment analysis indicated molecular changes related to leukocyte invasion, abnormal neurotransmission, and impaired neurogenesis due to inflammation as the major signatures of the CX, HC, and CB. Itgax is a hub gene of cortical aging. Zfp51 and Zfp62 were identified as hub genes involved in hippocampal aging. Itgax and Cxcl10 were identified as hub genes involved in cerebellar aging. S100a8 was the only co-DEG in all three regions. In addition, a series of molecular changes associated with inflammation was observed in all three brain regions. Several miRNAs interact with hub genes and S100a8. The change in gene levels was further validated in an animal experiment. Only the upregulation of Zfp51 and Zfp62 was restricted to the HC. The molecular signatures of aging exhibit regional differences in the brain and seem to be closely related to neuroinflammation. Itgax, Zfp51, Zfp62, Cxcl10, and S100a8 may be key genes and potential targets for the prevention of brain aging. - Source: PubMed
Publication date: 2023/03/23
Su XieXie LuLi JingTian XinyueLin BingChen Menghua - The COVID-19 pandemic is an acute and rapidly evolving global health crisis. To better understand this disease's molecular basis and design therapeutic strategies, we built upon the recently proposed concept of an integrated cell, iCell, fusing three omics, tissue-specific human molecular interaction networks. We applied this methodology to construct infected and control iCells using gene expression data from patient samples and three cell lines. We found large differences between patient-based and cell line-based iCells (both infected and control), suggesting that cell lines are ill-suited to studying this disease. We compared patient-based infected and control iCells and uncovered genes whose functioning (wiring patterns in iCells) is altered by the disease. We validated in the literature that 18 out of the top 20 of the most rewired genes are indeed COVID-19-related. Since only three of these genes are targets of approved drugs, we applied another data fusion step to predict drugs for re-purposing. We confirmed with molecular docking that the predicted drugs can bind to their predicted targets. Our most interesting prediction is artenimol, an antimalarial agent targeting ZFP62, one of our newly identified COVID-19-related genes. This drug is a derivative of artemisinin drugs that are already under clinical investigation for their potential role in the treatment of COVID-19. Our results demonstrate further applicability of the iCell framework for integrative comparative studies of human diseases. - Source: PubMed
Publication date: 2023/01/11
Xenos AlexandrosMalod-Dognin NoëlZambrana CarmePržulj Nataša - Recurrent deletions of the long arm of chromosome 5 were detected in 23/200 cases of T-cell acute lymphoblastic leukemia. Genomic studies identified two types of deletions: interstitial and terminal. Interstitial 5q deletions, found in five cases, were present in both adults and children with a female predominance (chi-square, P=0.012). Interestingly, these cases resembled immature/early T-cell precursor acute lymphoblastic leukemia showing significant down-regulation of five out of the ten top differentially expressed genes in this leukemia group, including TCF7 which maps within the 5q31 common deleted region. Mutations of genes known to be associated with immature/early T-cell precursor acute lymphoblastic leukemia, i.e. WT1, ETV6, JAK1, JAK3, and RUNX1, were present, while CDKN2A/B deletions/mutations were never detected. All patients had relapsed/resistant disease and blasts showed an early differentiation arrest with expression of myeloid markers. Terminal 5q deletions, found in 18 of patients, were more prevalent in adults (chi-square, P=0.010) and defined a subgroup of HOXA-positive T-cell acute lymphoblastic leukemia characterized by 130 up- and 197 down-regulated genes. Down-regulated genes included TRIM41, ZFP62, MAPK9, MGAT1, and CNOT6, all mapping within the 1.4 Mb common deleted region at 5q35.3. Of interest, besides CNOT6 down-regulation, these cases also showed low BTG1 expression and a high incidence of CNOT3 mutations, suggesting that the CCR4-NOT complex plays a crucial role in the pathogenesis of HOXA-positive T-cell acute lymphoblastic leukemia with terminal 5q deletions. In conclusion, interstitial and terminal 5q deletions are recurrent genomic losses identifying distinct subtypes of T-cell acute lymphoblastic leukemia. - Source: PubMed
Publication date: 2016/05/05
La Starza RobertaBarba GianlucaDemeyer SofiePierini ValentinaDi Giacomo DanikaGianfelici ValentinaSchwab ClaireMatteucci CaterinaVicente CarmenCools JanMessina MonicaCrescenzi BarbaraChiaretti SabinaFoà RobinBasso GiuseppeHarrison Christine JMecucci Cristina - ZT3, isolated from a murine muscle cell cDNA library by a low-stringency hybridization, encodes a zinc finger domain containing factor with a transcript of 5.0 kb. A 3' 2.5 kb partial nucleotide sequence contains an ORF of 1.5 kb where 17 canonical C2H2 zinc finger domains organized in tandem were identified. It maps on mouse chromosome 11, close to two mutations which affect skeletal formation. ZT3 expression depends upon differentiation of myogenic cells in culture, since it is upregulated with myogenin and inhibited in scr-transfected C2C12 cells. ZT3 is not expressed in NIH3T3 or C3H10T1/2 fibroblasts, but is induced when fibroblasts are myogenically converted by transfection with the muscle regulatory genes (MRFs). Its expression is also upregulated in the rhabdomyosarcoma cell line RD induced to myogenic differentiation by TPA treatment. In postimplantation embryos, ZT3 is diffusely expressed but higher expression is detectable in the neural tube and encephalic vesicles, in the somites and, at a high level, in the limb buds as they form. During further development ZT3 is expressed in many tissues of neuroectodermal and mesodermal origin, but its expression decreases during fetal development and in the adult it is restricted to skeletal and cardiac muscle and to spleen. This pattern of expression suggests a possible role played by ZT3 in differentiating skeletal muscle. Its expression in other tissues is compatible with the suggestion that members of this class of DNA-binding factors play different roles during post-implantation development and in the adult life. - Source: PubMed
Polimeni MGiorgi SDe Gregorio LDragani T AMolinaro MCossu GBouché M