VPS28 Antibody
- Known as:
- VPS28 Antibody
- Catalog number:
- XW-7975
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- VPS28 Antibody
Related genes to: VPS28 Antibody
- Gene:
- VPS28 NIH gene
- Name:
- VPS28 subunit of ESCRT-I
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-13
- Date modifiied:
- 2019-01-31
Related products to: VPS28 Antibody
Related articles to: VPS28 Antibody
- Antisense oligonucleotide (ASO) therapeutics silence gene expression through RNase H-mediated mRNA degradation or steric blockade, yet their clinical efficacy is limited by inefficient intracellular trafficking, with <1% of internalized ASOs escaping endosomes to access target RNA. A deeper understanding of the cellular mechanisms governing ASO trafficking and activity is therefore critical. Here, we identify the endosomal sorting complex required for transport-I (ESCRT-I) as a previously unrecognized regulator of ASO pharmacological activity. Using human hepatocyte-derived cell models and FDA-approved ASO drugs inotersen and mipomersen, we demonstrate that suppression of specific ESCRT-I subunits, VPS23 and VPS28, markedly enhances ASO-mediated target silencing, whereas depletion of other subunits has minimal effect. Mechanistically, VPS23 functions as a central ESCRT-I component linking endosomal trafficking to intracellular glucose homeostasis. Loss of VPS23 reduces expression of the glucose transporter GLUT2, lowers intracellular glucose levels, and possibly enables ASO endosomal escape without altering cellular uptake or RNase H1-dependent activity. VPS23 suppression disrupts endosomal morphology, decreases ASO retention in late endosomes, and enhances cytosolic availability of ASOs. Notably, this regulatory effect extends beyond ASOs to small interfering RNA (siRNA) therapeutics, indicating a broader role for ESCRT-I in RNA drug biology. Together, these findings uncover a metabolic-endosomal axis controlling nucleic acid drug efficacy and provide new mechanistic insight into intracellular determinants of RNA-based therapeutics. - Source: PubMed
Publication date: 2026/08/04
Nguyen Le Tra GiangTawfik Sherouk MJin JingDurwin AndreaArmanios BeshoyZhong Xiao-Bo - Heat stress limits dairy production. The temperature-humidity index (THI), combining temperature and relative humidity, is widely used to assess heat stress. However, in Chinese Holstein cattle, the phenotypic responses of milk traits and genotype-environment interaction mechanisms under different THI conditions are understudied. Based on 63,334 records from 7240 cows (milk yield, fat percentage, protein percentage), matched with meteorological data and 113,297 SNPs, we employed a random-effects GWAS to examine SNP effects across a continuous THI gradient, comparing results with conventional, temperature-, and humidity-interaction GWAS. As THI increased, all traits declined with distinct patterns. Random regression GWAS identified 149 significant SNP × THI interactions (5 for MY, 86 for FP, 58 for PP), distributed across BTA5, BTA6, BTA14, and BTA20. Candidate gene annotation identified 52 candidate genes near significant SNPs, of which 50 core candidate genes were supported in both temperature and humidity GWAS. The most robustly supported core candidate genes include , , , , , , , , , and -of which , , and have been functionally validated in milk production traits, whereas others represent novel candidates requiring further investigation. Temperature and THI-GWAS showed high consistency, while humidity-GWAS detected both overlapping and specific signals. Incorporating THI as a continuous environmental gradient identifies environment-dependent regulatory signals not captured by conventional GWAS, providing candidate genes that may contribute to future breeding strategies after further validation. - Source: PubMed
Publication date: 2026/08/03
Ou KangliZheng KunTeng JunLi YanZhang QinNing ChaoWang Dan - Mosquito-borne orthoflavivirus, such as Japanese encephalitis virus (JEV), Dengue virus (DENV), and Zika virus (ZIKV), pose a serious global health threat. As obligate intracellular parasites, they often hijack the host ubiquitin system to modify their own proteins, thereby regulating the viral life cycle, host adaptation, transmission, and pathogenesis. Despite its critical roles, the precise molecular mechanisms and functional significance of viral protein ubiquitination in orthoflavivirus infection remain incompletely understood. Here, we identify JEV prM as a novel target for host-specific ubiquitination, which occurs exclusively in vertebrate hosts but not in mosquitoes. Ubiquitin conjugation at the evolutionarily conserved lysine residues (K107/108/116) in multiple mosquito-borne orthoflaviviruses (USUV, MVEV, and WNV) confers differential adaptation between vertebrate hosts and mosquito vectors. Mechanistically, prM ubiquitination serves as a recruitment signal for the ESCRT-I subunit TSG101, an early-acting component of the ESCRT machinery, which in turn serves as an adaptor to recruit downstream ESCRT components (VPS28, CHMP2A, and CHMP4B), thereby driving viral particle budding. These findings elucidate a novel mechanism by which viral protein ubiquitination regulates JEV infection and host adaptation, and provide important insights into the adaptive evolution of orthoflaviviruses across different hosts and vectors. - Source: PubMed
Publication date: 2026/07/08
Li ChenxiGuo WenzhuangZhao WenZhang LinjieTang ChenyangLi JingjingShi JingSun MinganLi Yanhua - Breast cancer (BC) is a highly heterogeneous malignancy and remains the leading cause of cancer-related mortality among women worldwide. Although advances in molecular classification and targeted therapies have improved outcomes for certain subtypes, robust prognostic biomarkers applicable across clinical contexts are still lacking. The CRISPR-Cas9 system offers a powerful platform for identifying cancer cell vulnerabilities and may facilitate the development of clinically relevant prognostic models. - Source: PubMed
Publication date: 2026/05/14
Xiao Wen-TaoHe Jun-YanYang DongXun Yi - During open mitosis, reassembly of the nuclear envelope requires the coordinated recruitment of the ESCRT machinery, initiated by the chromatin-associated factor BAF1 and the nuclear-envelope-associated factor LEM2. Because telomeres are enriched at the reforming envelope, we investigated whether ESCRT factors contribute to telomere integrity. Reduction in the pivotal nuclear ESCRT factor CHMP7 caused DNA damage, heterochromatin disorganization, and telomere defects, including sister telomere associations and telomere free ends. Extending this analysis, we found that additional ESCRT components, including TSG101, VPS28, CHMP4B, and the ESCRT-associated factor AKTIP/Ft1, also contribute to telomere integrity, although with different strengths. Genetic interaction analyses suggest that CHMP7 converges in a common pathway with CHMP4B and AKTIP/Ft1, while it functions in parallel routes to TNKS1, a telomere-specific regulator of the shelterin TRF1. More genetic analyses indicated that BAF1 and LEM2 contribute to safeguarding of telomeres during nuclear envelope reassembly. Because defects in nuclear envelope dynamics and chromatin-membrane coupling are hallmarks of disorders associated with nuclear deformation and fragility, including aging and cancer, our findings contribute a new angle into these conditions and suggest potential targets for selectively modulating telomere maintenance pathways. - Source: PubMed
Publication date: 2026/01/29
Burla RominaLa Torre MattiaMaccaroni KliziaTacconi StefanoFidaleo MarcoDini LucianaSaggio Isabella