Ask about this productRelated genes to: TSG101 Blocking Peptide
- Gene:
- TSG101 NIH gene
- Name:
- tumor susceptibility 101
- Previous symbol:
- TSG10
- Synonyms:
- VPS23
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-20
- Date modifiied:
- 2016-10-05
Related products to: TSG101 Blocking Peptide
Related articles to: TSG101 Blocking Peptide
- Parasitic extracellular vesicles (EVs) play crucial roles in the growth and development of parasites. However, we remain unaware of the EVs from the plerocercoids of Spirometra mansoni. In this study, firstly, the plerocercoids of S. mansoni were cultured in vitro to enrich EVs, which were then characterized using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blotting. Next, the protein components and miRNAs of EVs were subsequently analysed using data-independent acquisition (DIA) and high-throughput sequencing, respectively. The results showed that EVs derived from the plerocercoids exhibit a typical double-layered membrane structure as spherical or elliptical vesicles ranging from 80 to 150 nm in diameter. The molecular markers HSP70, TSG101, HSP90, CD81, and β-Actin were significantly expressed in these EVs. Micro-proteomic analysis revealed 2,729 proteins, with functional annotation indicating that EV proteins are enriched primarily in pathways such as intracellular transport/secretion, cellular processes, and signal transduction. High-throughput miRNA sequencing revealed that the identified EVs contained 37 known miRNAs and 118 novel miRNAs. Functional enrichment analysis indicated that miRNAs primarily participate in host interactions by regulating DNA integration, apoptosis, cholesterol metabolism, and cAMP signaling pathways. Immunological analysis demonstrated that the antiserum against EVs elicited a mixed Th1/Th2 immune response, which was predominantly Th1-type. In this study, S. mansoni plerocercoid-derived EVs were successfully isolated and characterized. Systematic profiling of EV components via microproteomics and high-throughput miRNA sequencing provides a foundation for further investigations into the functional mechanisms of EVs. - Source: PubMed
Publication date: 2026/06/18
Song Xuan XuanGao FeiGuan Gu JinZhou Yan YanZhang Xi - To investigate whether mesenchymal stem cell-derived exosomes (MSC‑Exo) regulate ferroptosis by modulating the JAK2/STAT3 signaling pathway to alleviate hypoxia/re-oxygenation (H/R)-induced oligodendrocyte injury. - Source: PubMed
Meng Yuan-CuiWang ChaoZhu Yan-Ping - Spinal cord injury (SCI) is a severe condition with high disability. We aimed to explore the role and mechanism of M2-EVs in SCI-induced inflammation in rats, providing novel treatment methods for SCI. Primary macrophages were differentiated into M2 macrophages. M2-EVs were extracted, followed by morphology detection and measurement of CD63, TSG101, and Calnexin. SCI rats were injected with M2-EVs, followed by assessment of hind limb motor ability, pathological changes, nerve cell morphology, and proinflammatory factor expression. LPS-stimulated spinal astrocytes were treated with M2-EVs. Cell viability, ROS levels, LDH and MDA contents, the expression of lncRNA FTX, FTX, KDM3A, and KLF3, the binding of FTX to KDM3A, and KDM3A enrichment and H3K9me2 on the KLF3 promoter were detected. Results exhibited that M2-EVs treatment increased BBB score, recovered the damaged spinal cord structure, reduced neuronal loss and proinflammatory factor expression. M2-EVs treatment increased cell viability and decreased inflammation. Mechanistically, M2-EVs delivered FTX into cells. FTX bound to KDM3A and inhibited KLF3 expression via blocking H3K9me2 demethylation. KDM3A and KLF3 overexpression partially reversed the inhibitory effect of M2-EVs on inflammation in SCI. In conclusion, M2-EVs suppress SCI inflammation by delivering FTX into cells and inhibiting the KDM3A/KLF3 axis. - Source: PubMed
Publication date: 2026/06/16
Li JunjieLiang ShuhanLuo JinxinRao Yaojian - Tumor-produced extracellular vesicles (EVs) are key players in cancer progression by transferring their bioactive cargo (nucleic acids, lipids, proteins) to target cells leading to increase their proliferation, migration and invasive properties. EVs are involved in virus-associated carcinogenesis. Cervical cancer is due to a persistent infection with a high-risk human papillomavirus (HPV) whose integration into the cellular genome causes the continuous and deregulated expression of viral oncoproteins E6/E7, responsible for the carcinogenesis process. This study aimed to isolate EVs of HPV-infected cells, to explore their viral material content, to determine whether viral cargo can impact the proliferative status of HPV-lacking recipient cells. - Source: PubMed
Publication date: 2026/06/16
Arslan SergenBarbaud AlexandreBernauer JasonAvoscan LaureTissot MarionPrétet Jean-LucGobbo JessicaGarrido CarmenLascombe IsabelleFauconnet Sylvie - Function of CENPJ/CPAP is essential for centriole duplication and cilia biogenesis. Recently, we showed that CPAP is also an integral Endosomal Sorting Complexes Required for Transport (ESCRT)-0-like protein that recruits ESCRT-I protein TSG101 to early endosome (EE) and positively regulates multi-vesicular body (MVB) formation. Sequential recruitment of the ESCRT protein complexes and AAA+ ATPase VPS4B to EE facilitates MVB biogenesis. VPS4B is critical for ESCRT-III disassembly/recycling and contributes to membrane fission in several cellular processes. Here, we report that CPAP is critical for the protein stability and EE localization of VPS4B, and this function is independent from its role as an ESCRT-0. Other VPS4B-dependent cellular processes such as exosome release, cytokinesis, and retroviral budding are also compromised under CPAP deficiency. Interaction with CPAP prevents the proteasome degradation of VPS4B. The stability and EE localization of VPS4B can be attributed to two different C-terminal domains in CPAP. Overall, these observations provide evidence that CPAP is critical for VPS4B function and suggest that distinct pools of CPAP may be involved in its ESCRT-0 and VPS4B stabilization roles. - Source: PubMed
Publication date: 2026/06/02
Gudi RadhikaVasu Chenthamarakshan