ArticleThe Journal of experimental medicine1998
Acidic sphingomyelinase (ASM) is necessary for fas-induced GD3 ganglioside accumulation and efficient apoptosis of lymphoid cells.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 150 citations in OpenAlex.
- Gene Therapy Targeting GD3 Synthase Protects Against MPTP-Induced Parkinsonism and Executive Dysfunction.The European journal of neuroscience · 2025Article
- Targeted deletion of GD3 synthase protects against MPTP-induced neurodegeneration.Genes, brain, and behavior · 2017Article
- Keratin impact on PKCδ- and ASMase-mediated regulation of hepatocyte lipid raft size - implication for FasR-associated apoptosis.Journal of cell science · 2016Article
- Glycosphingolipids and cell death: one aim, many ways.Apoptosis : an international journal on programmed cell death · 2015Review
- Re-configuration of sphingolipid metabolism by oncogenic transformation.Biomolecules · 2014Review
- Sphingolipids: key regulators of apoptosis and pivotal players in cancer drug resistance.International journal of molecular sciences · 2014Review
- Podocyte pathology and nephropathy - sphingolipids in glomerular diseases.Frontiers in endocrinology · 2014Review
- Article
- Anti-ganglioside anti-idiotypic vaccination: more than molecular mimicry.Frontiers in oncology · 2012Article
- Caspase-8 and caspase-7 sequentially mediate proteolytic activation of acid sphingomyelinase in TNF-R1 receptosomes.The EMBO journal · 2011Article
- Production of multiple brain-like ganglioside species is dispensable for fas-induced apoptosis of lymphoid cells.PloS one · 2011Article
- Article
- Different mechanisms are involved in apoptosis induced by melanoma gangliosides on human monocyte-derived dendritic cells.Glycobiology · 2009Article
- Acidic sphingomyelinase downregulates the liver-specific methionine adenosyltransferase 1A, contributing to tumor necrosis factor-induced lethal hepatitis.The Journal of clinical investigation · 2004Article
- Glycosphingolipids and cell death.Glycoconjugate journal · 2004Review
- Ceramide: second messenger or modulator of membrane structure and dynamics?The Biochemical journal · 2003Review
- Defective TNF-alpha-mediated hepatocellular apoptosis and liver damage in acidic sphingomyelinase knockout mice.The Journal of clinical investigation · 2003Article
- Acetylation suppresses the proapoptotic activity of GD3 ganglioside.The Journal of experimental medicine · 2002Article
- O-acetylation of GD3: an enigmatic modification regulating apoptosis?The Journal of experimental medicine · 2002Article
- Ceramide in apoptosis: a revisited role.Neurochemical research · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Ceramides deriving from sphingomyelin hydrolysis are important mediators of apoptotic signals originating from Fas (APO-1/CD95). However, definitive evidence for the role played by individual sphingomyelinases is still lacking. We have analyzed lymphoblastoid cell lines derived from patients affected by Niemann Pick disease (NPD), an autosomal recessive disorder caused by loss-of-function mutations within the acidic sphingomyelinase (ASM) gene. NPD lymphoblasts, which display normal neutral sphingomyelinase activity, fail to activate ASM in response to Fas cross-linking, unlike normal lymphoblasts. NPD lymphoblasts also fail to accumulate GD3 ganglioside, a downstream mediator of ceramide-induced cell death (De Maria, R., L. Lenti, F. Malisan, F. D'Agostino, B. Tomassini, A. Zeuner, M.R. Rippo, R. Testi. 1997. Science. 277:1652-1655), and display a substantially inefficient apoptosis after Fas cross-linking. Inefficient apoptosis is due to lack of ASM activity, because proximal signaling from Fas in NPD lymphoblasts is not impaired and apoptosis can be efficiently triggered by passing the ASM defect with exogenous ceramides. Moreover, mannose receptor-mediated transfer of ASM into NPD lymphoblasts rescues their ability to transiently activate ASM, accumulate GD3, and rapidly undergo apoptosis after Fas cross-linking. These results provide definitive genetic evidence for the role of ASM in the progression of apoptotic signals originating from Fas.
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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.