ZNF239 antibody - N-terminal region (ARP35784_P050)
- Known as:
- ZNF239 (anti-) - N-terminal region (ARP35784_P050)
- Catalog number:
- arp35784_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ZNF239 antibody - N-terminal region (ARP35784_P050)
Related genes to: ZNF239 antibody - N-terminal region (ARP35784_P050)
- Gene:
- ZNF239 NIH gene
- Name:
- zinc finger protein 239
- Previous symbol:
- -
- Synonyms:
- MOK2, HOK-2
- Chromosome:
- 10q11.22-q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-06
- Date modifiied:
- 2014-11-19
Related products to: ZNF239 antibody - N-terminal region (ARP35784_P050)
Related articles to: ZNF239 antibody - N-terminal region (ARP35784_P050)
- Osteoporosis is a common age-related disease with disabling consequences, the early diagnosis of which is difficult due to its long and hidden course, which often leads to diagnosis only after a fracture. In this regard, great expectations are placed on advanced developments in machine learning technologies aimed at predicting osteoporosis at an early stage of development, including the use of large data sets containing information on genetic and clinical predictors of the disease. Nevertheless, the inclusion of DNA markers in prediction models is fraught with a number of difficulties due to the complex polygenic and heterogeneous nature of the disease. Currently, the predictive power of neural network models is insufficient for their incorporation into modern osteoporosis diagnostic protocols. Studies in this area are sporadic, but are widely demanded, as their results are of great importance for preventive medicine. This leads to the need to search for the most effective machine learning approaches and optimise the selection of genetic markers as input parameters to neural network models. - Source: PubMed
Publication date: 2024/01/24
Yalaev B INovikov A VMinniakhmetov I RKhusainova R I - The identification of significant DNA markers of primary osteoporosis may gain new insights by studying genome regions involved in mechanisms of epigenetic regulation through interactions with microRNAs. - Source: PubMed
Publication date: 2024/10/01
Yalaev BulatDeev RomanTyurin AntonSalakhov RamilSmirnov KirillEremkina AnnaMokrysheva NataliaMinniakhmetov IldarKhusainova Rita - Hepatocellular carcinoma (HCC) is a common malignant primary cancer with high mortality. Previous studies have demonstrated that RNA binding proteins (RBPs) are involved in the biological processes of cancers, including hepatocellular cancer. - Source: PubMed
Publication date: 2020/12/09
Wang LiZhou NaQu JialinJiang ManZhang Xiaochun - In this study, we found that gene expression of the human β-galactoside α2,6-sialyltransferase (hST6Gal I) was specifically increased during differentiation of human MG-63 osteoblastic cells by serum starvation (SS). In parallel, a distinct increase in binding to SNA, the α2,6-sialyl-specific lectin, was observed in serum-starved cells, as demonstrated by FACS analysis. 5'-Rapid amplification of cDNA ends analysis demonstrated that the increase of hST6Gal I transcript by SS is mediated by P1 promoter. To elucidate transcriptional regulation of hST6Gal I in SS-induced MG-63 cells, we functionally characterized the P1 promoter region of the hST6Gal I gene. The 5'-deletion analysis of P1 promoter region revealed that the 189 bp upstream region of transcription start site is critical for transcriptional activity of hST6Gal I gene in SS-induced MG-63 cells. This region contains the predicted binding sites for several transcription factors, including AREB6, FOXP1, SIX3, HNF1, YY2, and MOK2. The mutagenesis analysis for these sites and chromatin immunoprecipitation assay demonstrated that the YY2 binding site at -98 to -77 was essential for the SS-induced hST6Gal I gene expression during differentiation of MG-63 cells. - Source: PubMed
Publication date: 2020/10/27
An So-YoungLee MiriYoon Hyun-KyoungAbekura FukushiKim Kyoung-SookKim Dong-HyunKim Hyeon-JunLee KichoonKim Cheorl-HoLee Young-Choon - The "thrifty genotype" hypothesis proposes that the high prevalence of type 2 diabetes (T2D) in Native Americans and admixed Latin Americans has a genetic basis and reflects an evolutionary adaptation to a past low calorie/high exercise lifestyle. However, identification of the gene variants underpinning this hypothesis remains elusive. Here we assessed the role of Native American ancestry, socioeconomic status (SES) and 21 candidate gene loci in susceptibility to T2D in a sample of 876 T2D cases and 399 controls from Antioquia (Colombia). Although mean Native American ancestry is significantly higher in T2D cases than in controls (32% v 29%), this difference is confounded by the correlation of ancestry with SES, which is a stronger predictor of disease status. Nominally significant association (P<0.05) was observed for markers in: TCF7L2, RBMS1, CDKAL1, ZNF239, KCNQ1 and TCF1 and a significant bias (P<0.05) towards OR>1 was observed for markers selected from previous T2D genome-wide association studies, consistent with a role for Old World variants in susceptibility to T2D in Latin Americans. No association was found to the only known Native American-specific gene variant previously associated with T2D in a Mexican sample (rs9282541 in ABCA1). An admixture mapping scan with 1,536 ancestry informative markers (AIMs) did not identify genome regions with significant deviation of ancestry in Antioquia. Exclusion analysis indicates that this scan rules out ~95% of the genome as harboring loci with ancestry risk ratios >1.22 (at P < 0.05). - Source: PubMed
Publication date: 2012/04/17
Campbell Desmond DParra Maria VDuque ConstanzaGallego NataliaFranco LilianaTandon ArtiHünemeier TábitaBortolini CátiraVillegas AlbertoBedoya GabrielMcCarthy Mark IPrice AlkesReich DavidRuiz-Linares Andrés