Ask about this productRelated genes to: SEC61G antibody
- Gene:
- SEC61G NIH gene
- Name:
- SEC61 translocon gamma subunit
- Previous symbol:
- -
- Synonyms:
- SSS1
- Chromosome:
- 7p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-14
- Date modifiied:
- 2019-04-15
Related products to: SEC61G antibody
Related articles to: SEC61G antibody
- Lung adenocarcinoma (LUAD) is the predominant pathological subtype of non-small cell lung cancer. Its considerable tumor heterogeneity and drug resistance present major clinical obstacles, resulting in unfavorable patient outcomes. Protein palmitoylation is known to be a key factor in tumorigenesis; however, its cell-specific expression patterns and prognostic value in LUAD remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/06
Liu HaixiaoHu YueWang LingyunLi ChanglinLi DongtaoMeng LinghanZheng GuangdaRen JuanxiaShang LuBao Yanju - Lung cancer is the predominant contributor to cancer-induced mortality, with non-small cell lung cancer (NSCLC) constituting the majority. However, the intricacies of tumorigenesis and progression in this context remain incompletely understood. - Source: PubMed
Publication date: 2026/02/26
Zhang KunpengXia WenqiangLi YiShi BowenYang Weiwei - SEC61G is an oncogene in hepatocellular carcinoma (HCC), a common malignant tumor worldwide. MicroRNAs (miRNAs) regulation of oncogenes are available therapeutic strategies being investigated in HCC, but the effective miRNA delivery remains a challenge. Here, we investigated the potential therapeutic effects of miRNA-loaded engineered exosomes in patients with HCC. MiRNAs that could bind to SEC61G were screened using Targetscan, and were verified using HepG2 cells viability after transfecting miRNAs mimic. Five miRNAs binding to SEC61G,among which, miR-651-3p and miR-488-3p mimic significantly inhibited HepG2 cells viability (p < 0.05) and decreased SEC61G protein expression. Then, dual-luciferase reporter assay also confirmed SEC61G as a target of miR-488-3p in HCC. After that, miR-488-3p-loaded engineered exosomes (Exo-miR-488-3p) were isolated from the supernatant of 488-3p-overexpressed cells and identified via nanoparticle tracking analysis, transmission electron microscopy and western blot. In vitro experiments showed that exo-miR-488-3p significantly inhibited proliferation, colony formation, migration and invasion of HepG2 cells than corresponding negative control. In addition, Exo-miR-488-3p tended to induce HepG2 cells apoptosis, though this relationship was not statistically significant. In conclusion, exo-miR-488-3p inhibits the malignant cytological activities in HCC, a possible strategy in the treatment of HCC. - Source: PubMed
Publication date: 2026/02/09
Gao HuijieHe ZhaobinYang ShengbiaoWang XiqiangYan QisenGao ChaoLiu NaiqingZhang ZhaoyangNiu WeiboNiu JunPeng Cheng - Ischemic stroke (IS) continues to pose a significant threat to human health. Few studies have explored the connection between ferroptosis-related genes and immune infiltration in the context of IS. Initially, 303 differentially expressed genes were identified, from which four characteristic genes were distinguished, all validated for their excellent diagnostic efficacy. Animal experiments confirmed significant brain injury and Ferroptosis post-ischemia-reperfusion in rats, with increased expression of Sdcbp, Ppia, and Sec61g, but no change in Rpl22. Furthermore, these key genes were closely associated with levels of immune infiltration. Notably, Rpl22 and Ppia were regulated by nine common transcription factors. Sdcbp and Rpl22 were most abundantly expressed in Microglia, and Ppia in Oligodendrocytes, while Sec61g exhibited lower overall expression, all showing high activity in immune metabolic pathways. Bioinformatics analysis and experimental verification indicate that Sdcbp, Ppia, and Sec61g are associated with ferroptosis and immune infiltration in IS, and hold promise as therapeutic targets for IS treatment. - Source: PubMed
Publication date: 2025/12/18
Huang FanZhu MingjingWang HuihuiDu ZilongWu QianqianHe YongjingLiang YilinHu WanxiangXie Lu - Vascular dementia (VaD) is the second most common type of dementia, yet its pathogenesis is not fully understood, and effective diagnostic and therapeutic tools are lacking. While endoplasmic reticulum stress (ERS) is associated with VaD and is recognised as a promising target, the exact mechanism remains unclear. This study analysed differentially expressed ERS-related genes in VaD to identify potential diagnostic markers and provide a new perspective for further in-depth research on the role of ERS in VaD. VaD gene expression data (GSE186798) from human patients were obtained from the GEO database for analysis. After intersecting the obtained genes with those in the GeneCards and Molecular Signatures Databases (MSigDB), key ERS-related genes for the diagnosis of VaD were identified as hub genes using bioinformatics and machine learning techniques. Two hub genes, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-Alpha (PPARGC1A) and SEC61 Translocon Subunit Gamma (SEC61G), exhibited good diagnostic ability for VaD and were validated in the GSE122063 dataset using receiver operating characteristic (ROC) curve analysis. GeneMANIA analysis indicated a robust association between VaD pathophysiology and ERS responses. Hub genes regulated by microRNAs, transcription factors, and chemicals were computationally predicted, and immune cells with varying dysregulation were also observed. In an in vivo bilateral common carotid artery stenosis (BCAS) mouse model, quantitative real-time PCR (qRT-PCR) and Western blotting analyses confirmed the significant downregulation of the hub genes' expression levels. These hub genes may serve as potential diagnostic biomarkers for VaD. - Source: PubMed
Publication date: 2026/01/13
Zhao YilongXing WenJiang LinglingLiu XiangrongQu HuiChen WeiqiWang Yilong