Results 1 to 10 of about 775,217 (268)

S1P Lyase Deficiency in the Brain Promotes Astrogliosis and NLRP3 Inflammasome Activation via Purinergic Signaling

open access: yesCells, 2023
Astrocytes are critical players in brain health and disease. Brain pathologies and lesions are usually accompanied by astroglial alterations known as reactive astrogliosis.
Shah Alam   +6 more
doaj   +1 more source

Sphingosine‐1‐phosphate‐lyase deficiency affects glucose metabolism in a way that abets oncogenesis

open access: yesMolecular Oncology, 2022
Sphingosine‐1‐phosphate (S1P), a bioactive signaling lipid, is involved in several vital processes, including cellular proliferation, survival and migration, as well as neovascularization and inflammation.
Sumaiya Y. Afsar   +3 more
doaj   +1 more source

Sphingolipid metabolism in the development and progression of cancer: one cancer's help is another's hindrance

open access: yesMolecular Oncology, 2021
Cancer development is a multistep process in which cells must overcome a series of obstacles before they can become fully developed tumors. First, cells must develop the ability to proliferate unchecked.
Antonia Piazzesi   +2 more
doaj   +1 more source

Neurodegeneration Caused by S1P-Lyase Deficiency Involves Calcium-Dependent Tau Pathology and Abnormal Histone Acetylation

open access: yesCells, 2020
We have shown that sphingosine 1-phosphate (S1P) generated by sphingosine kinase 2 (SK2) is toxic in neurons lacking S1P-lyase (SGPL1), the enzyme that catalyzes its irreversible cleavage.
Shah Alam   +4 more
doaj   +1 more source

Phospholipase D3 degrades mitochondrial DNA to regulate nucleotide signaling and APP metabolism

open access: yesNature Communications, 2023
Phospholipase D3 (PLD3) polymorphisms are linked to late-onset Alzheimer’s disease (LOAD). Being a lysosomal 5’-3’ exonuclease, its neuronal substrates remained unknown as well as how a defective lysosomal nucleotide catabolism connects to AD ...
Zoë P. Van Acker   +11 more
doaj   +1 more source

Analytical and computational workflow for in-depth analysis of oxidized complex lipids in blood plasma

open access: yesNature Communications, 2022
Oxidized lipids are prominent bioactive agents, and yet their molecular repertoire remains largely unknown. Here, the authors apply bioinformatics and LC-MS/MS to uncover the diversity and specificity of modified lipids in human blood plasma of lean and ...
Angela Criscuolo   +9 more
doaj   +1 more source

Special Issue on “Sphingolipids: From Pathology to Therapeutic Perspectives”

open access: yesCells, 2020
It is an honor for us to dedicate this Special Issue to our dearest friend Lina Obeid, who was not only a pioneer in the field of sphingolipids, but also a remarkable personality [...]
Gerhild van Echten-Deckert
doaj   +1 more source

Membrane lipids and their degradation compounds control GM2 catabolism at intralysosomal luminal vesicles

open access: yesJournal of Lipid Research, 2019
The catabolism of ganglioside GM2 is dependent on three gene products. Mutations in any of these genes result in a different type of GM2 gangliosidosis (Tay-Sachs disease, Sandhoff disease, and the B1 and AB variants of GM2 gangliosidosis), with GM2 as ...
Susi Anheuser   +2 more
doaj   +1 more source

When Is a Reaction Network a Metabolism? Criteria for Simple Metabolisms That Support Growth and Division of Protocells

open access: yesLife, 2021
With the aim of better understanding the nature of metabolism in the first cells and the relationship between the origin of life and the origin of metabolism, we propose three criteria that a chemical reaction system must satisfy in order to constitute a
Paul G. Higgs
doaj   +1 more source

Membrane lipids regulate ganglioside GM2 catabolism and GM2 activator protein activity[S]

open access: yesJournal of Lipid Research, 2015
Ganglioside GM2 is the major lysosomal storage compound of Tay-Sachs disease. It also accumulates in Niemann-Pick disease types A and B with primary storage of SM and with cholesterol in type C.
Susi Anheuser   +3 more
doaj   +1 more source

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