The retrograde vesicular trafficking GARP complex, which is mutated in a neurodegenerative disease, is important for sphingolipid homeostasis in yeast and mammalian cells.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.

The ORMDL proteins function to restrain the de novo sphingolipid biosynthetic pathway during myelination, when there is a high demand for sphingolipids to prevent excessive accumulation of metabolic intermediates.

TORC2-Ypk1 signaling upregulates flux through the sphingolipid pathway not only by increasing the supply of long-chain base precursors, but also by increasing their use in synthesizing complex sphingolipids.

SIRT1, a cellular metabolic sensor, transcriptionally promotes sphingomyelin degradation in embryonic stem cells, which in turn modulates their membrane fluidity and neural differentiation.

Sphingolipids govern the compartmentalization of yeast cells through the assembly of lateral diffusion barriers in ER membranes.

The iron/sphingolipid/PDK1/Mef2 pathway is activated in mammals upon loss of Frataxin.

Sphingolipids regulate vacuolar fission via nuclear vacuole junction to adapt to intracellular and extracellular environments in budding yeast.

Endothelial sphingolipid biosynthesis is essential for maintaining vascular development, neovascular proliferation, non-CNS tissue sphingolipid levels, and hepatocyte response to stress.

A lipid acts to promote the development of nematode worm larvae through activation of an enzyme complex called TORC1.