Ask about this productRelated genes to: SNX5 antibody
- Gene:
- SNX5 NIH gene
- Name:
- sorting nexin 5
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2016-10-05
Related products to: SNX5 antibody
Related articles to: SNX5 antibody
- Epigenetic modifications, especially DNA methylation, play an increasingly important role in oral cancer. However, their specific contributions to the progression of oral squamous cell carcinoma (OSCC) remain unclear. The present study used the Shiny Methylation Analysis Resource Tool (SMART) database (https://smart.embl.de/smart/change_mode.cgi) to identify methylation‑driven genes associated with OSCC. Among the identified candidates, integrin subunit α4 (ITGA4) exhibited significantly elevated methylation levels in head and neck cancers. A methylation‑specific PCR assay showed that ITGA4 is highly methylated in OSCC cells compared with normal immortalized human normal oral keratinocyte (iNOK) cells. Additionally, the mRNA expression levels of ITGA4 were significantly lower in OSCC cell lines compared with normal iNOK cells. ITGA4 overexpression markedly inhibited the cell proliferation, migratory ability and capacity of colony formation and induced apoptosis in FaDu and YD‑15 cells. In proteomic analysis, ITGA4 suppressed the expression of Sorting Nexin 5 (SNX5), a protein linked to cancer progression. siRNA‑mediated knockdown of SNX5 importantly inhibited cell proliferation, migration, and colony formation in FaDu and YD‑15 cells. Moreover, in a chick chorioallantoic membrane xenograft model, overexpression of ITGA4 or small interfering SNX5 significantly inhibited OSCC tumor growth and angiogenesis . Collectively, these findings demonstrated that ITGA4 acts as a tumor suppressor in OSCC by downregulating SNX5 and suggested that ITGA4 may serve as a valuable prognostic biomarker and potential therapeutic target for OSCC. - Source: PubMed
Publication date: 2026/04/24
Tien Nguyen Ngoc ThuyChoe Han-CheolAhn Sang-Gun - Atherosclerosis (AS) is a leading cardiovascular disease driven by lipid metabolism dysregulation and immune maladaptation. Although macrophage autophagy modulates plaque stability, the specific autophagy-related genes governing AS progression, particularly in spatial and immune contexts, remain poorly defined. This study aimed to systematically identify and characterize key macrophage autophagy-associated genes in AS using an integrated multi-omics approach. - Source: PubMed
Publication date: 2026/02/26
Cao WenqiWang BingyangWang YuxueLi YunyanYang HanningSun YueXu LirongLu Yongping - Alveolar bone resorption during the socket healing process compromises subsequent restoration outcomes. Recent clinical evidence suggests that dental implant placement can effectively prevent such bone loss, yet the mechanisms remain elusive. In this study, combined multi-dataset screening pinpointed sorting nexin 5 (Snx5) as a potential regulator of mechanotransduction, whose expression was downregulated in early peri-implant bone remodeling zones following implant placement. Functional studies showed that loss of Snx5 abolished the additional osteogenic enhancement normally induced by mechanical stimulation. In vivo, Snx5 deficiency disrupted the mechanosensitive activation of LepR MSCs and compromised implant-induced osteogenesis. Mechanistically, Snx5 facilitates the recycling of phosphorylated EGFR (p-EGFR) back to the plasma membrane to sustain EGFR signaling. Loss of Snx5 redirects EGFR trafficking toward late endosomes and lysosomal degradation, thereby weakening its signaling. These findings uncover a previously unrecognized role for Snx5 in mediating the osteogenic fate of peri-implant BMSCs in response to mechanical cues, expanding the functional repertoire of the Snx family. Collectively, these findings highlight Snx5 as a novel regulator of mechanosensitive bone remodeling and suggest that its downregulation may contribute to peri-implant bone adaptation. This study provides new insights into how the mechanical microenvironment regulates bone repair and highlights Snx5 as a promising molecular target for modulating skeletal mechano-responsiveness in clinical bone regeneration. - Source: PubMed
Publication date: 2026/02/20
Jiang XueWeng YutengFeng YanhuizhiHuang JieWang HaichengWang Zuolin - Tuberculosis (TB) remains one of the leading causes of death from a single infectious agent worldwide, yet the host pathways that regulate antigen presentation and lung inflammation during (Mtb) infection are incompletely defined. Sorting nexin 5 (SNX5) is a protein best known for roles in endosomal trafficking, antigen processing, and antiviral host defense, but its contribution to immunity during Mtb infection is unknown. Here, we show that SNX5-deficient mice exhibit markedly increased mortality following low-dose aerosol infection despite unchanged pulmonary bacterial burden compared to wild-type mice. mice developed exacerbated lung inflammation without major alterations in immune cell recruitment. In macrophages, did not affect phagocytosis, vacuolar maturation, intracellular bacterial control, or global transcriptional responses to Mtb, but was required for efficient MHC class II antigen presentation. deficiency reduced antigen degradation, limited peptide loading onto MHC-II and impaired activation of antigen-specific CD4 T cells without altering surface MHC-II abundance or expression of costimulatory molecules. Together, these findings identify SNX5 as a previously unrecognized regulator of MHC-II peptide loading that shapes inflammatory outcomes during pulmonary Mtb infection, highlighting a role for the endosomal sorting machinery in immunity to intracellular pathogens. - Source: PubMed
Publication date: 2026/02/02
Dias Beatriz R SNaqvi Kubra FEktnitphong Victoria AAlvarez-Arguedas SamuelRahlwes Kathryn CCampos Priscila CShiloh Michael U - Mammary carcinomas are aggressive neoplasms and a significant cause of mortality in female cats. Despite surgical removal, feline mammary carcinoma (FMC) often recurs or metastasizes. Specific tumour biomarkers are necessary for early detection, prognosis and therapy selection. This study aims to identify candidate biomarkers for FMC by comparing tissue proteomic profiles among grades of 31 FMC cats and six normal mammary tissues (control) using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Candidate proteins identified by LC-MS/MS were validated by Western blotting and LC-MS/MS. Prognostic values of candidate proteins were evaluated using immunohistochemistry and survival analysis. Protein-chemotherapy drug interaction networks were also evaluated. Among the 268 differential proteins observed, dermatopontin (DPT) expression was significantly downregulated, while sorting nexin 5 (SNX5) expression was elevated in cancerous tissues compared to controls (p < 0.05). Immunohistochemistry results revealed a significant association of DPT and SNX5 with stages (DPT, p < 0.0001; SNX5, p = 0.046) and grades of FMC (DPT, p < 0.0001; SNX5, p = 0.04). Low DPT expression was associated with poor overall survival (p = 0.02), along with Stage 4 FMC (p = 0.0001), high mitotic count (p = 0.003) and the presence of lymphovascular invasion (p = 0.003). Moreover, protein-chemotherapy drug interaction showed a relationship of DPT with doxorubicin, lapatinib and neratinib. This study identified DPT and SNX5 as potential diagnostic and therapeutic targets for FMC, with DPT emerging as a promising prognostic biomarker. - Source: PubMed
Publication date: 2025/12/19
Aruvornlop PruetthaPloypetch SekkarinSakcamduang WalasineeSirivisoot SirintraKasantikul TanitRoytrakul SittirukPhaonakrop NarumonArya Nlin