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
- Autophagy is a highly conserved cellular process that plays a dual role during viral infection, contributing to antiviral defense while also being exploited by viruses to support their replication. However, the molecular mechanisms by which white spot syndrome virus (WSSV) influences host autophagy remain poorly understood. In this study, we identified LvTM9SF4, a phylogenetically conserved nine-transmembrane protein with predominantly expressed in the shrimp intestine, as a host factor that physically interacts with the WSSV structural protein VP24. Functional assays showed that RNAi-mediated knockdown of LvTM9SF4 significantly suppressed WSSV infection and enhanced shrimp survival after WSSV challenge in Pacific white shrimp (Litopenaeus vannamei). Subcellular localization analyses revealed substantial colocalization of LvTM9SF4 with the autophagy marker LC3B. Transcriptomic analysis further suggested that LvTM9SF4 knockdown affected autophagy-related pathways and genes, among which LvAtg2 exhibited the most substantial downregulation. Meanwhile, silencing LvAtg2 inhibited WSSV infection and improved shrimp survival, producing phenotypes similar to those observed following LvTM9SF4 knockdown. All the results indicated that LvTM9SF4 may participate in autophagy-related processes during WSSV infection, and that LvAtg2 may represent a potential downstream effector associated with this host-virus interaction. This study provides new insights into antiviral immunity in crustaceans and highlights potential host-targeted strategies against WSSV. - Source: PubMed
Publication date: 2026/07/14
Li AixinLi ShihaoYang ZhanyuanZhang XiaojunSun MingzheJin SongjunYuan JianboLi Fuhua - 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