Ask about this productRelated genes to: Snx10 Blocking Peptide
- Gene:
- SNX10 NIH gene
- Name:
- sorting nexin 10
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7p15.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2014-11-18
Related products to: Snx10 Blocking Peptide
Related articles to: Snx10 Blocking Peptide
- The intake of industrial trans-fatty acids (iTFAs), particularly elaidic acid (EA), has been implicated in non-alcoholic fatty liver disease (NAFLD), yet the underlying mechanisms remain incompletely understood. Functional chaperone-mediated autophagy (CMA) is essential for maintaining cellular lipid homeostasis. We found that EA exposure reduced the protein level of the CMA rate-limiting component LAMP-2A and induced lipid accumulation in hepatocytes. Importantly, treatment with the CMA activator QX77 significantly alleviated EA-induced lipid accumulation, supporting a functional role for CMA in this process. Cathepsin A (CTSA) is a critical enzyme that promotes the degradation of the LAMP-2A protein. Our data showed that EA upregulated sorting nexin 10 (SNX10), which in turn facilitated CTSA maturation, leading to decreased LAMP-2A abundance. We further investigated the upstream regulatory mechanism of SNX10 from the perspective of competitive endogenous RNA (ceRNA). Bioinformatics analysis and dual-luciferase reporter assays confirmed the existence of the GAS5/miR-27b-3p/SNX10 axis. Long chain non-coding RNA (LncRNA) GAS5 upregulated SNX10 expression by competitively binding to miR-27b-3p. Together, these findings suggested CMA disruption as a possible contributor to EA-induced lipid accumulation and identified the GAS5/miR-27b-3p/SNX10 ceRNA network as a potential regulatory mechanism for CMA. - Source: PubMed
Publication date: 2026/05/25
Chen YuelinFeng JunzhuLang LingxiPeng HuanhuanGuo JinGuan ShuangLu Jing - Osteopetrosis is a heterogeneous group of bone diseases with increased bone density as a result of defective osteoclast function or differentiation. The clinical presentations range from the early, often lethal, infantile malignant forms to the mild autosomal dominant forms. This review provides recent updates in preclinical findings regarding molecular genetics, diagnosis, and novel therapeutic approaches in osteopetrosis. - Source: PubMed
Publication date: 2026/05/07
Donati SimoneAurilia CinziaPalmini GaiaFalsetti IreneMarini FrancescaGiusti FrancescaZonefrati RobertoRanaldi FrancescoIantomasi TeresaBrandi Maria Luisa - The infection cycle of the Influenza A Virus (IAV) typically requires host factors to regulate replication and proliferation. However, the roles of these factors remain undiscovered. This study focuses on Sorting Nexin 10 (SNX10), which is involved in regulating membrane trafficking and endosomal stabilization. Our previous study identified that SNX10 facilitates the replication of human coronavirus OC43 through enhancing clathrin-mediated endocytosis. In our present study, we found that SNX10 significantly promoted IAV infection in host cells. The conditional knockout of in mice lungs prolonged survival following IAV challenge. Mechanistically, SNX10 facilitated the production of acidic endosomal vesicles and promoted the accumulation of pro-viral autophagic structures, a process supported by the specific interaction between SNX10 and the viral NP and M2 protein of IAV. Blocking SNX10-mediated acidic endosomal vesicles and autophagosome formation demonstrated antiviral effects. Moreover, IAV infection increased SNX10 protein levels by suppressing its ubiquitination, suggesting that SNX10 could serve as a potential host-derived antiviral drug target. - Source: PubMed
Publication date: 2026/04/12
Chen LizhuLi HaobinGuo HuiyiLiang JinlongZhong YingyuanHe XuchengWu WenjiaoLiu Shuwen - - Source: PubMed
Publication date: 2026/02/16
Hao Haiping - Acute lung injury (ALI) is a common complication of sepsis in connection with excessive inflammation and accumulation of oxidative stress. Sorting nexin 10 (SNX10) is a sorting nexin family member involved in inflammatory processes. This study aimed to explore the function of SNX10 in ALI. The cecal ligation and puncture (CLP) model was established to induce ALI in C57BL/6J mice. CLP mice exhibited elevated levels of SNX10 expression in the lung tissues. Mice were intratracheally injected with 50 μL adenovirus (108 PFU) containing short hairpin RNA plasmid targeting SNX10. SNX10 knockdown mice showed remission of CLP-induced pulmonary edema, hemorrhage, inflammatory infiltration, and thickened alveolar septum. SNX10 downregulation reduced reactive oxygen species (ROS) levels, increased superoxide dismutase activity and glutathione content, and decreased malondialdehyde content in the lung tissues. SNX10 knockdown decreased the phosphorylation of NF-κB p65 and its nuclear translocation, thus inhibiting the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6. Furthermore, SNX10 downregulation inhibited the NLRP3, p20 caspase 1, and ASC protein levels and the levels of IL-18 and IL-1β. A549 cells were treated with lipopolysaccharide (LPS) (10 μg/mL) for 24 h to simulate the inflammatory condition and SNX10 was knocked down using small interfering RNA. SNX10 knockdown cells showed increased viability and less ROS accumulation. Consistent with the in vivo results, the NF-κB/NLRP3 pathway and the secretion of inflammatory cytokines were inhibited after SNX10 knockdown in A549 cells. In summary, SNX10 downregulation mitigated sepsis-induced oxidative stress and pulmonary inflammation by inhibiting the NF-κB/NLRP3 pathway. - Source: PubMed
Publication date: 2026/02/16
Wei MinYang JianYu ZejiaLi ShanXie HuiYuan ShiyangHuang QiujieZhang HuiFeng Jun