Ask about this productRelated genes to: SFRS14 antibody
- Gene:
- SUGP2 NIH gene
- Name:
- SURP and G-patch domain containing 2
- Previous symbol:
- SFRS14
- Synonyms:
- KIAA0365
- Chromosome:
- 19p13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-09
- Date modifiied:
- 2015-11-13
Related products to: SFRS14 antibody
Related articles to: SFRS14 antibody
- Research on genes affecting tumors without lymph node metastasis is limited, hence this study employed both bioinformatic and experimental approaches to identify specific genes associated with lung cancer adenocarcinoma (LUAD) before lymph node metastasis occurs. Expression profiles of mRNAs and lncRNAs and LUAD clinical data were downloaded from the Cancer Genome Atlas (TCGA) using R software to identify differentially expressed genes (DEGs) associated with N0 and N + status. TargetScan, miRTarBase, and miRDB databases were used to identify interactions between miRNAs and mRNAs. The DIANA database and lncBase tool were used to find the association between lncRNA and miRNA. After selecting some genes, the expression of candidate genes was confirmed by real-time RT-PCR technique. Following the knockdown LINC00894 gene using the shRNA technique, its effect on invasion, migration, and apoptosis in the calu-3 cell line was investigated. In total, we found 321 specific DEGs not only in N0 vs. normal but also in N0 Vs. N + in LUAD, most of which were lncRNA and we identified a ceRNA network containing nine lncRNAs with the highest degree of connectivity. Among them, in addition to bioinformatic analyses, LINC00894 and YEATS2-AS1 were significantly increased in tumor tissues compared to normal tissues (P = 0.0001). also, SUGP2 that was shared in both lncRNA-related ceRNA subnetworks was significantly upregulated (P = 0.0001). Additionally, following the knockdown of LINC00894 in Calu-3 cell line, a significant decrease in migration and invasion was observed, but early apoptosis was significantly increased in the shLINC00894(48 h) group (P = 0.007). The findings of the present study show that lncRNAs play an important role in the N0 status of LUAD. Moreover, LINC00894, YEATS2-AS1, and SUGP2 can act as biomarkers in patients with N0 LUAD. - Source: PubMed
Publication date: 2025/03/27
Alipour MarzyehMoghanibashi MehdiNaeimi SirousMohamadynejad Parisa - - Source: PubMed
Publication date: 2024/12/02
Qiu HuiqingYuan MengweiGuo ZiyuLiang JiayiLi YangGao YanHe ShaMa Xiaowei - Pathogenic variants in HFE and non-HFE genes have been identified in hemochromatosis in different patient populations, but there are still a certain number of patients with unexplained primary iron overload. We recently identified in Chinese patients a recurrent p.(Arg639Gln) variant in SURP and G-patch domain containing 2 (SUGP2), a potential mRNA splicing-related factor. However, the target gene of SUGP2 and affected iron-regulating pathway remains unknown. We aimed to investigate the pathogenicity and underlying mechanism of this variant in hemochromatosis. RNA-seq analysis revealed that SUGP2 knockdown caused abnormal alternative splicing of CIRBP pre-mRNA, resulting in an increased normal splicing form of CIRBP V1, which in turn increased the expression of BMPER by enhancing its mRNA stability and translation. Furthermore, RNA-protein pull-down and RNA immunoprecipitation assays revealed that SUGP2 inhibited splicing of CIRBP pre-mRNA by a splice site variant at CIRBP c.492 and was more susceptible to CIRBP c.492 C/C genotype. Cells transfected with SUGP2 p.(Arg639Gln) vector showed up-regulation of CIRBP V1 and BMPER expression and down-regulation of pSMAD1/5 and HAMP expression. CRISPR-Cas9 mediated SUGP2 p.(Arg622Gln) knock-in mice showed increased iron accumulation in the liver, higher total serum iron, and decreased serum hepcidin level. A total of 10 of 54 patients with hemochromatosis (18.5%) harbored the SUGP2 p.(Arg639Gln) variant and carried CIRBP c.492 C/C genotype, and had increased BMPER expression in the liver. Altogether, the SUGP2 p.(Arg639Gln) variant down-regulates hepcidin expression through the SUGP2/CIRBP/BMPER axis, which may represent a novel pathogenic factor for hemochromatosis. - Source: PubMed
Publication date: 2024/05/27
Li YanmengXu AnjianLiu SusuZhang WeiZhou DonghuOuYang QinZi HuaduanZhang BeiZhang NingGeng WeiZhou YimingDuan WeijiaWang XiaomingZhao XinyanOu XiaojuanFan ChangfaJia JidongHuang Jian - Mammalian spermatogenesis is a highly ordered process that is determined by chromatin-associated moderators which still remain poorly understood. Through a multi-control group proteomics strategy, we confirmed that Sugp2 was a chromatin-associated candidate protein, and its signal arose along spermatogenesis. The expression results showed that Sugp2, which is mainly expressed in the testis, had two transcripts, encoding one protein. During spermatogenesis, Sugp2 was enriched in the nucleus of male germ cells. With the depletion of Sugp2 by CRISPER-Cas9 technology, we found that Sugp2 controlled a network of genes on metal ion and ATP binding, suggesting that alternative splicing regulation by Sugp2 is involved in cellular ion and energy metabolism during spermatogenesis, while it had a little effect on meiotic progression and male fertility. Collectively, these data demonstrated that, as a chromatin-associated protein, Sugp2 mediated the alternative splicing regulatory network during spermatogenesis. - Source: PubMed
Publication date: 2021/10/18
Zhan JunfengLi JianboWu YuerongWu PanfengYu ZiqiCui PengZhou MofanXu YuminJin TingyuDu ZiyeLuo MengchengLiu Cong - Hereditary hemochromatosis (HH) is widely recognized and clinical manifestations of hemochromatosis-related (HFE-related) HH is well studied in European populations. Less is known about the clinical and laboratory characteristics of non-HFE related HH in Asian population. We aimed to explore the relationship between genotype and clinical phenotype in Chinese patients with non-HFE related hereditary hemochromatosis. - Source: PubMed
Publication date: 2021/09/28
Wu LiyanZhang WeiLi YanmengZhou DonghuZhang BeiXu AnjianWu ZhenWu LinaLi ShuxiangWang XiaomingZhao XinyanWang QianyiLi MinWang YuYou HongHuang JianOu XiaojuanJia Jidong