Ask about this productRelated genes to: SNX8 antibody
- Gene:
- SNX8 NIH gene
- Name:
- sorting nexin 8
- Previous symbol:
- -
- Synonyms:
- Mvp1
- Chromosome:
- 7p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2015-08-26
Related products to: SNX8 antibody
Related articles to: SNX8 antibody
- Here, we analyzed the recycling of the Vps55/Vps68 complex in the yeast endocytic pathway. The two proteins seem to form a functional unit. Single deletions of VPS55 or VPS68 affected the turnover of the endocytic cargo protein Ste6 to the same degree. The double deletion had no additive effect on Ste6 turnover. Vps55 and Vps68 were dependent on each other for proper cellular localization. Under normal conditions, the sfGFP-tagged proteins localized to punctate structures; but, when the corresponding partner protein was missing, staining of the vacuolar lumen was observed. This suggests that the orphaned proteins are degraded in the vacuole via the multivesicular bodies (MVB) pathway. A tyrosine-based recycling signal was identified in the cytosolic tail of Vps68. This signal completely restored retromer-dependent recycling and function of a Vps10 variant devoid of its own recycling signals. In line with this finding, Vps68 recycling turned out to be dependent on both retromer and Mvp1/SNX8. This finding was unexpected, since Vps55 recycling seems to depend solely on Mvp1. In co-immunoprecipitation experiments, a weak co-immunoprecipitation signal was detected between Mvp1 and the retromer subunit Vps26, indicating a physical association between Mvp1 and retromer. - Source: PubMed
Publication date: 2026/04/15
Kölling Ralf - Patients with high-grade serous ovarian cancer (HGSOC) typically present with widespread metastasis, obscuring a temporal understanding of tumor-immune dynamics. To address this, we perform multi-site global proteomics alongside matched immunohistochemistry (IHC) for CD4⁺ and CD8⁺ tumor-infiltrating lymphocytes (TILs) in patient samples. We order the protein expression profiles using an unbiased pseudotime analysis, recapitulating clinical observations of metastatic progression, and providing a framework to explore tumor-immune dynamics from localized to metastatic disease. Metastatic progression correlates with immune cell infiltration, the recruitment of regulatory T cells (Tregs) to counterbalance γδ T cell abundance, and an increased abundance of exhausted CD8⁺ T cells. The accumulation of Tregs at metastatic sites correlates with SNX8 expression, a critical regulator of the STING pathway. In early-stage tumors, keratin-expressing cancer cells recruit Tregs via MHC class II, fostering an inflammatory phenotype with limited IFNγ production and non-clonally expanded T cells. Together, our findings reveal novel mechanisms of immune escape associated with both localized disease and metastatic progression in HGSOC. - Source: PubMed
Publication date: 2025/06/16
Egan DonaghGlennon KateTreacy AnnFabre AurelieMcCormack JanetHill SalishaMorrison RyanZhernovkov VadimLiebler DanielKolch WalterBrennan Donal - Protein palmitoylation is a reversible fatty acyl modification that undertakes important functions in multiple physiological processes. Dysregulated palmitoylations are frequently associated with the formation of cancer. How palmitoyltransferases for S-palmitoylation are involved in the occurrence and development of hepatocellular carcinoma (HCC) is largely unknown. - Source: PubMed
Publication date: 2024/12/19
Mo YaqiHan YameiChen YangFu ChunlingLi QingLiu ZhuangXiao MingmingXu Bo - Multisystem inflammatory syndrome in children (MIS-C) is a severe, post-infectious sequela of SARS-CoV-2 infection, yet the pathophysiological mechanism connecting the infection to the broad inflammatory syndrome remains unknown. Here we leveraged a large set of samples from patients with MIS-C to identify a distinct set of host proteins targeted by patient autoantibodies including a particular autoreactive epitope within SNX8, a protein involved in regulating an antiviral pathway associated with MIS-C pathogenesis. In parallel, we also probed antibody responses from patients with MIS-C to the complete SARS-CoV-2 proteome and found enriched reactivity against a distinct domain of the SARS-CoV-2 nucleocapsid protein. The immunogenic regions of the viral nucleocapsid and host SNX8 proteins bear remarkable sequence similarity. Consequently, we found that many children with anti-SNX8 autoantibodies also have cross-reactive T cells engaging both the SNX8 and the SARS-CoV-2 nucleocapsid protein epitopes. Together, these findings suggest that patients with MIS-C develop a characteristic immune response to the SARS-CoV-2 nucleocapsid protein that is associated with cross-reactivity to the self-protein SNX8, demonstrating a mechanistic link between the infection and the inflammatory syndrome, with implications for better understanding a range of post-infectious autoinflammatory diseases. - Source: PubMed
Publication date: 2024/08/07
Bodansky AaronMettelman Robert CSabatino Joseph JVazquez Sara EChou JanetNovak TanyaMoffitt Kristin LMiller Haleigh SKung Andrew FRackaityte ElzeZamecnik Colin RRajan Jayant VKortbawi HannahMandel-Brehm CaleighMitchell AntheaWang Chung-YuSaxena AditiZorn KelseyYu David J LPogorelyy Mikhail VAwad WalidKirk Allison MAsaki JamesPluvinage John VWilson Michael RZambrano Laura DCampbell Angela P Thomas Paul GRandolph Adrienne GAnderson Mark SDeRisi Joseph L - Lysosomal Storage Disorders (LSDs), which share common phenotypes, including enlarged lysosomes and defective lysosomal storage, are caused by mutations in lysosome-related genes. Although gene therapies and enzyme replacement therapies have been explored, there are currently no effective routine therapies against LSDs. During lysosome reformation, which occurs when the functional lysosome pool is reduced, lysosomal lipids and proteins are recycled to restore lysosome functions. Here we report that the sorting nexin protein SNX8 promotes lysosome tubulation, a process that is required for lysosome reformation, and that loss of SNX8 leads to phenotypes characteristic of LSDs in human cells. SNX8 overexpression rescued features of LSDs in cells, and AAV-based delivery of SNX8 to the brain rescued LSD phenotypes in mice. Importantly, by screening a natural compound library, we identified three small molecules that enhanced SNX8-lysosome binding and reversed LSD phenotypes in human cells and in mice. Altogether, our results provide a potential solution for the treatment of LSDs. - Source: PubMed
Publication date: 2024/03/22
Li XinranXiang CongZhu ShileiGuo JianshengLiu ChangWang AilianCao JinLu YanNeculai DanteXu PinglongFeng Xin-Hua