Sphingolipid Metabolism and Signaling

This study identifies S1P as a key activator of the MAP3K1-JNK pathway, which drives epithelial cell movement and eyelid morphogenesis in mice.

This study identifies that multiple cationic amphipathic drugs (CADs) share molecular similarities with chloroquine and inhibit sphingolipid biosynthesis, suggesting their potential as antiviral agents against diverse pathogens including SARS-CoV-2.

The paper characterizes S1PR1-regulated transcriptomes in aortic endothelial cells, revealing distinct subtypes and signaling mechanisms in arterial and lymphatic endothelium.

The paper shows that ATX expression from GFAP+ cells is essential for embryonic development and is reactivated in EAE, linking it to chronic inflammation.

The paper examines sphingolipid synthesis and the serine-palmitoyltransferase (SPT) complex in oligodendrocytes during myelination in postnatal rats, showing changes in SPT subunit levels and sphingolipid composition.

This paper shows that dihydroceramide desaturase deficiency causes oxidative stress by altering Rac1 membrane localization and activating Rac1-NADPH oxidase in neurons.

This study shows that endothelial S1PR1 deficiency worsens brain injury and BBB dysfunction in mice after subarachnoid hemorrhage.

This study shows that inhibiting de novo ceramide biosynthesis with L-cycloserine improves aging-related phenotypes in cultured cortical neurons.

This study shows that inhibiting nSMase2 improves myelin quality by protecting oligodendrocytes during remyelination.

This study identifies a DEGS1 mutation causing sphingolipid metabolism defects, leading to neurological disorders and suggests dietary intervention as a potential treatment.