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
- Peripheral artery disease (PAD) is a chronic ischemic condition characterized by vascular occlusion and metabolic-immune dysregulation. To elucidate the molecular mechanisms underlying PAD and the therapeutic effects of Kaempferol, we integrated bulk transcriptomics, single-cell RNA sequencing, network pharmacology, and experimental validation. Transcriptomic analysis identified 1,144 differentially expressed genes in PAD, highlighting extensive transcriptional remodeling. WGCNA revealed distinct gene modules significantly correlated with PAD, suggesting key networks associated with vascular inflammation and immune dysregulation. Network pharmacology identified kaempferol as the core active component of Ruan Jian Qing Mai formula that is clinically effective in treating PAD, targeting 87 PAD-related genes enriched in immune and inflammatory pathways, predominantly expressed in macrophages. Integration of kaempferol-associated targets from RNA-seq and multi-database prediction uncovered 70 overlapping targets implicated in macrophage activation, lipid metabolism, and atherosclerosis signaling. CIBERSORTx and single-cell analysis further pinpointed macrophages as major cellular mediators, with kaempferol-target genes (e.g., TNF, SYK, LCK, IL4I1) specifically enriched in macrophages. Macrophages were stratified into high-inflammatory and low-inflammatory subsets; PAD lesions exhibited prominent enrichment of high-inflammatory macrophages, which concurrently displayed elevated inflammatory signatures and enhanced ferroptosis transcriptional activity, and represented the primary cellular population responsive to kaempferol. In silico gene knockout analysis further verified that SYK and SNX5 serve as core immune signaling regulators in macrophages, while TNF and LCK lack macrophage-specific immune regulatory functions. Functional experiments confirmed that kaempferol significantly suppressed LPS-induced M1 macrophage polarization and inflammatory cytokine expression in RAW264.7 cells. Ferroptosis scoring revealed enhanced ferroptosis susceptibility in PAD macrophages, with kaempferol-target genes correlating positively with ferroptosis drivers. Molecular docking further validated strong binding affinities between kaempferol and key macrophage-related targets (IL4I1, LCK, TNF, SYK). Using a zebrafish vascular regeneration injury model, we further verified that high-dose kaempferol rescues impaired angiogenesis under vascular ischemic damage. Collectively, these multi-omics and experimental findings uncover macrophage polarization and ferroptosis modulation as central mechanisms mediating kaempferol's therapeutic efficacy in PAD, providing mechanistic insights and potential molecular targets for precision intervention. - Source: PubMed
Publication date: 2026/09/03
Qiao Zi-JunWang Miao-MiaoLuo Wang-ShengYu Bo-LanLiu TaoZhu PingHu CanLi JiLiang Zhi-QiangChen Jian - - Source: PubMed
Publication date: 2026/08/20
Han YonggangLiu YunchaoZhang BaoxuYin Gangfeng - 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 Mycobacterium tuberculosis (Mtb) infection are incompletely defined. Sorting nexin 5 (SNX5) is a protein implicated in endosomal trafficking, antigen processing, and antiviral host defense, but its contribution to antibacterial immunity is unknown. Here, we show that SNX5-deficient mice exhibit increased mortality following low-dose aerosol Mtb infection despite unchanged pulmonary bacterial burden compared with wild-type mice. Snx5-/- mice developed exacerbated lung inflammation without major alterations in immune cell recruitment. In macrophages, Snx5 did not affect phagocytosis, vacuolar maturation, intracellular bacterial control, or global transcriptional responses to Mtb but was required for efficient major histocompatibility complex (MHC) class II antigen presentation. Snx5 deficiency was associated with reduced endolysosomal proteolysis and impaired MHC class II antigen presentation in vitro, resulting in reduced activation of antigen-specific CD4+ T cells without altering surface MHC class II abundance or costimulatory molecule expression. Together, these findings identify SNX5 as a regulator of MHC class II antigen presentation that influences inflammatory outcomes during pulmonary Mtb infection. - Source: PubMed
Dias Beatriz R SNaqvi Kubra FEktnitphong Victoria AAlvarez-Arguedas SamuelRahlwes Kathryn CCampos Priscila CShiloh Michael U - Interferon-induced antiviral proteins act on the first line of defense against viruses, including influenza A virus (IAV). Among those, the short isoform of nuclear receptor coactivator 7 (NCOA7-AS) has been shown to inhibit IAV entry and more especially the fusion between endosomal and viral membranes. Ectopic expression of NCOA7-AS leads to the increased acidification of the endolysosomal pathway, putatively through NCOA7-AS interaction with the vacuolar ATPase (V-ATPase). However, the precise mechanism of action of NCOA7-AS is not fully understood. Here, we identified the cellular partners of NCOA7-AS by mass spectrometry, including the V-ATPase subunits known to interact with NCOA7-AS. A point mutation disrupting the interaction with the V-ATPase led to loss of antiviral activity against IAV, demonstrating that V-ATPase engagement is required for the antiviral phenotype. Moreover, sorting nexin (SNX) 1/2/5/6 were identified as novel partners of NCOA7-AS. These proteins are involved in retrograde transport of cellular cargoes from endosomes to the trans-Golgi network. We revealed that SNX5/6 interacted directly with NCOA7-AS and were essential for NCOA7-AS antiviral activity against IAV. Interestingly, crystal structures of NCOA7-AS/SNX5 complexes showed that the SNX5-interaction motif in NCOA7-AS was similar to those found in known cargoes of SNX5/6. In addition, we could pinpoint several critical residues that were important for binding and antiviral activity. Collectively, our study identifies novel essential partners for NCOA7-AS antiviral activity and the structural basis for their interaction. - Source: PubMed
Publication date: 2026/07/28
Arnaud-Arnould MaryRebendenne AntoineTauziet MarineUrbach SergeEl Koulali KhadijaRicci Emiliano PWencker MélanieMoncorgé OlivierBlaise MickaëlGoujon Caroline - Predicting how fast a patient with Alzheimer's disease will decline over the next year remains a challenge. Existing blood transcriptomic studies have not established whether probe selection is reproducible, whether the signal is transcriptional or reflects immune cell shifts, or whether they generalise across platforms. We applied five steps to 96 ADNI-GO whole-blood microarray samples (Affymetrix HG-U219; 12-month MMSE change): PyImpetus Markov Blanket selection, Elastic Net with leave-one-out cross-validation (LOOCV), SHAP attribution, MCP-counter cell-type deconvolution, and cross-platform mapping into AddNeuroMed (GSE63060, = 329, Illumina). Feature selection preceded cross-validation without constituting data leakage. The same six probes emerged across four independent runs (Jaccard J = 0.214, = 0.03): , , , , , and an transcript. The panel achieved LOOCV MAE = 1.388 and R = 0.247, outperforming the full-probe baseline by 14.9%. All probes survived immune cell correction with signs intact. replicated in AddNeuroMed (r = -0.170, = 0.002). The exploratory six-probe blood RNA panel predicts 12-month cognitive decline (LOOCV R = 0.247) with transcriptional origin confirmed by cell-type deconvolution and cross-platform evidence for . External testing in ADNI-2 ( = 91, R = -0.222) showed that generalisation depends on visit-timepoint matching, indicating clinical utility cannot yet be claimed and defining conditions for prospective validation. Code and a research prototype tool are publicly available. - Source: PubMed
Publication date: 2026/07/02
Syed Asif HassanAlhayyani Sultan