ArticleJournal of Korean medical science2010
GD3 accumulation in cell surface lipid rafts prior to mitochondrial targeting contributes to amyloid-β-induced apoptosis.
Article in Journal of Korean medical science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Higher Magnetic Field NMR Renders Resolution Enhancement on Ganglioside GD3 Catalyzed AβbioRxiv : the preprint server for biology · 2026Article
- The good, the bad, and the unknown nature of decreased GD3 synthase expression.Frontiers in molecular neuroscience · 2024Article
- Potential neuroprotection byNeural regeneration research · 2022Article
- Cholesterol and Sphingolipid Enriched Lipid Rafts as Therapeutic Targets in Cancer.International journal of molecular sciences · 2021Review
- Ganglioside Synthesis by Plasma Membrane-Associated Sialyltransferase in Macrophages.International journal of molecular sciences · 2020Article
- Hemodynamic shear stress induces protective autophagy in HeLa cells through lipid raft-mediated mechanotransduction.Clinical & experimental metastasis · 2018Article
- Apoptosis in Alzheimer's disease: an understanding of the physiology, pathology and therapeutic avenues.Neurochemical research · 2014Review
- Involvement of sphingolipids in ethanol neurotoxicity in the developing brain.Brain sciences · 2013Article
- Trans-activity of plasma membrane-associated ganglioside sialyltransferase in mammalian cells.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal apoptosis induced by amyloid β-peptide (Aβ) plays an important role in the pathophysiology of Alzheimer's disease (AD). However, the molecular mechanism underlying Aβ-induced apoptosis remains undetermined. The disialoganglioside GD3 involves ceramide-, Fas- and TNF-α-mediated apoptosis in lymphoid cells and hepatocytes. Although the implication of GD3 has been suggested, the precise role of GD3 in Aβ-induced apoptosis is still unclear. Here, we investigated the changes of GD3 metabolism and characterized the distribution and trafficking of GD3 during Aβ-induced apoptosis using human brain-derived TE671 cells. Extracellular Aβ-induced apoptosis in a mitochondrial-dependent manner. GD3 level was negligible in the basal condition. However, in response to extracellular Aβ, both the expression of GD3 synthase mRNA and the intracellular GD3 level were dramatically increased. Neosynthesized GD3 rapidly accumulated in cell surface lipid microdomains, and was then translocated to mitochondria to execute the apoptosis. Disruption of membrane lipid microdomains with methyl-β-cyclodextrin significantly prevented both GD3 accumulation in cell surface and Aβ-induced apoptosis. Our data suggest that rapidly accumulated GD3 in plasma membrane lipid microdomains prior to mitochondrial translocation is one of the key events in Aβ-induced apoptosis.
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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.