Ask about this productRelated genes to: TM9SF4 Blocking Peptide
- Gene:
- TM9SF4 NIH gene
- Name:
- transmembrane 9 superfamily member 4
- Previous symbol:
- -
- Synonyms:
- KIAA0255, dJ836N17.2
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-19
- Date modifiied:
- 2016-04-12
Related products to: TM9SF4 Blocking Peptide
Related articles to: TM9SF4 Blocking Peptide
- Cytolethal Distending Toxin (CDT) is the only exotoxin that () can secrete. CDT (CDT) triggers DNA damage responses, leading to irreversible cell cycle arrest and apoptosis, playing an important role in the pathogenic process of . Currently, research on the host cell receptors of CDT remains limited. Screening and identification of host cell receptors that interact with CDT are crucial for systematically elucidating the cytotoxic mechanisms induced by this toxin. - Source: PubMed
Publication date: 2026/03/19
Lei LiXu ShiyuYang ZhenPan XingyuXu JialiDu SenyanZhao QinHuang XiaoboCao SanjieWu RuiWang YipingYan QiguiWen Yiping - The objective is to explore the potential pathogenesis and therapeutic mechanism of Yinchenhao decoction (YCHD) in intrahepatic cholestasis of pregnancy (ICP) by focusing on the regulatory role of exosomal miR-370-3p on target genes TM9SF4 and KIT. Exosomes were isolated from the serum samples of normal pregnant women (control), patients with ICP, HTR-8/SVneo cells, and Sprague-Dawley (SD) pregnant rats via differential centrifugation. Characterization of these exosomes was performed using electron microscopy, nanoparticle tracking analysis (NTA), and western blotting. Quantitative reverse transcription PCR (qRT-PCR) and the bioinformatics tool starBase were used to identify miR-370-3p as a candidate miRNA. Dual-luciferase reporter assays were used to confirm that TM9SF4 and KIT are direct targets of miR-370-3p. An in vitro ICP cell model was established using HTR-8/SVneo cells to investigate the interactions between miR-370-3p and its targets. An animal model was established to validate the targeted regulation of miR-370-3p on TM9SF4 and KIT, as well as the therapeutic effect of YCHD . The exosomal miR-370-3p expression was significantly upregulated, whereas the TM9SF4 and KIT expressions were downregulated as demonstrated by qRT-PCR and western blot analyses. RNA pull-down assays confirmed a direct negative regulatory relationship between miR-370-3p and both TM9SF4 and KIT at the molecular level. Finally, the therapeutic potential of YCHD was verified by its ability to reverse the altered expression patterns of miR-370-3p, TM9SF4, and KIT in the animal ICP model. Our study demonstrates that YCHD protects against ICP through the miR-370-3p/TM9SF4/KIT axis, suggesting miR-370-3p as a potential therapeutic target for ICP. - Source: PubMed
Publication date: 2025/07/26
Jiang HongxiuYu WenjingTao XingranYan QiaoZhou GuanlunChen ChaoHan Guorong - - Source: PubMed
Publication date: 2025/05/06
Zhu RenzhongTian ChuanxinGao NanLi ZhiqiangYang ShengZhang YueZhou MingJin KangpengZhang ChuanSun Yueming - The transmembrane 9 superfamily protein member 4 (TM9SF4) is a transmembrane protein upregulated in multiple cancers; however, its role in hepatocellular carcinoma (HCC) remains unknown. - Source: PubMed
Publication date: 2025/04/23
Ma YahuiGuo LinglingZhang BoWang TingFeng Qingchun - Colorectal cancer (CRC) ranks among the primary causes of human mortality globally. Numerous studies have highlighted the significant role of PLOD3 in the progression of various cancers. However, the exact function and underlying mechanisms of PLOD3 in CRC remains incompletely understood. To investigate the expression of PLOD3, qRT‒PCR, immunohistochemistry and western blotting were utilized to analyze the expression of PLOD3 in CRC tissues and adjacent normal tissues. Functional assays were conducted to assess the roles of PLOD3 both in vitro and in vivo. To elucidate the potential mechanism of PLOD3 in CRC, a range of techniques, including coimmunoprecipitation, immunofluorescence, CHX pulse-chase, and ubiquitination assays were used. As the results indicated, hypomethylation of the PLOD3 promoter leads to its over- expression in CRC, and elevated PLOD3 levels are associated with a poor prognosis. Both in vitro and in vivo models demonstrated that PLOD3 enhances CRC cell proliferation, invasion, and migration. Furthermore, through mechanistic studies, TM9SF4 was identified as a protein that interacts with PLOD3 and contributes to CRC progression by promoting autophagy. Additionally, PLOD3 could be secreted by CRC cells and secreted PLOD3 could promote CRC cells migration and invasion. These results demonstrated that PLOD3 promotes CRC progression through the PLOD3/TM9SF4 axis and could be a potential biomarker and treatment target for CRC. - Source: PubMed
Publication date: 2025/03/25
Zhu RenzhongTian ChuanxinGao NanLi ZhiqiangYang ShengZhang YueZhou MingJin KangpengZhang ChuanSun Yueming