ArticleMolecular neurodegeneration2017
Tetraspanin 6: a pivotal protein of the multiple vesicular body determining exosome release and lysosomal degradation of amyloid precursor protein fragments.
Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 91 citations in OpenAlex.
- Valosin-containing protein is cargo in Amyloid Precursor Protein extracellular vesicles.Cell communication and signaling : CCS · 2026Article
- The 'sugar' side of extracellular vesicle-glycome: a panorama from basic characteristics, deciphering technologies, functions, to applications.Journal of nanobiotechnology · 2026Review
- Unveiling the role of extracellular vesicles in HIV infection: molecular mechanisms, viral persistence, and therapeutic opportunities.FEMS microbiology reviews · 2026Review
- Redefining the Limits of Nanodevices-Based Drug Delivery Systems: Extracellular Vesicles.Pharmaceutics · 2025Review
- Sex-specific associations of gene expression with Alzheimer's disease neuropathology and ante-mortem cognitive performance.Nature communications · 2025Article
- Tetraspanins affect membrane structures and the trafficking of molecular partners: what impact on extracellular vesicles?Biochemical Society transactions · 2025Review
- Extracellular vesicles: cargo loading, degradation and secretory pathways, and their intersection with autophagy.Extracellular vesicles and circulating nucleic acids · 2025Review
- The role of Caveolin-1 in tumor-derived extracellular vesicle biology and its implications.Frontiers in cell and developmental biology · 2025Review
- The Role of Cardiac Troponin and Other Emerging Biomarkers Among Athletes and Beyond: Underlying Mechanisms, Differential Diagnosis, and Guide for Interpretation.Biomolecules · 2024Review
- Research on the TSPAN6 regulating the secretion of ADSCs-Exos through syntenin-1 and promoting wound healing.Stem cell research & therapy · 2024Article
- New insights into the role of tetraspanin 6, 7, and 8 in physiology and pathology.Cancer medicine · 2024Review
- Identification of crucial inflammaging related risk factors in multiple sclerosis.Frontiers in molecular neuroscience · 2024Article
- TSPAN6 reinforces the malignant progression of glioblastoma via interacting with CDK5RAP3 and regulating STAT3 signaling pathway.International journal of biological sciences · 2024Article
- The Regulation of Exosome Generation and Function in Physiological and Pathological Processes.International journal of molecular sciences · 2023Review
- Context-specific regulation of extracellular vesicle biogenesis and cargo selection.Nature reviews. Molecular cell biology · 2023Review
- Phospholipase D3 degrades mitochondrial DNA to regulate nucleotide signaling and APP metabolism.Nature communications · 2023Article
- Biological Role and Aberrant Overexpression of Syntenin-1 in Cancer: Potential Role as a Biomarker and Therapeutic Target.Biomedicines · 2023Review
- Review
- The versatile roles of testrapanins in cancer from intracellular signaling to cell-cell communication: cell membrane proteins without ligands.Cell & bioscience · 2023Review
- The Potential Roles of Exosomes Carrying APP and Tau Cleavage Products in Alzheimer's Disease.Journal of clinical medicine · 2023Review
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 6 countries.
Funding
Abstract
backgroundThe mechanisms behind Aβ-peptide accumulation in non-familial Alzheimer's disease (AD) remain elusive. Proteins of the tetraspanin family modulate Aβ production by interacting to γ-secretase.
methodsWe searched for tetraspanins with altered expression in AD brains. The function of the selected tetraspanin was studied in vitro and the physiological relevance of our findings was confirmed in vivo.
resultsTetraspanin-6 (TSPAN6) is increased in AD brains and overexpression in cells exerts paradoxical effects on Amyloid Precursor Protein (APP) metabolism, increasing APP-C-terminal fragments (APP-CTF) and Aβ levels at the same time. TSPAN6 affects autophagosome-lysosomal fusion slowing down the degradation of APP-CTF. TSPAN6 recruits also the cytosolic, exosome-forming adaptor syntenin which increases secretion of exosomes that contain APP-CTF.
conclusionsTSPAN6 is a key player in the bifurcation between lysosomal-dependent degradation and exosome mediated secretion of APP-CTF. This corroborates the central role of the autophagosomal/lysosomal pathway in APP metabolism and shows that TSPAN6 is a crucial player in APP-CTF turnover.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.