Ferroptosis, a major mechanism of non-apoptotic programmed cell death, critically regulates the homeostasis and functionality of peripheral CD4+ and CD8+ T cells. Here we demonstrate that in mouse, resistance of T cells to ferroptosis depends critically on the composition of standard rodent diets, and that dietary effects on ferroptosis have a crucial role in regulation of T cell homeostasis and immune responses.
In the originally published version of this article, Extended Data Fig. 4 contained inadvertent duplications introduced during figure assembly: panel 4c (the bottom of the second column) erroneously reused images from panel 4a (the bottom of the third column); panel 4c (the upper panel of the third column) erroneously reused images from panel 4a (the upper panel of the rightmost column);
"I can't tell you how many times I've had patients who have had so much trouble losing weight complain to me that their friends can eat whatever they want and never put weight on," Perlman, an integrative and functional medicine doctor and former chief medical officer for Mayo Clinic's integrative medicine program, told Business Insider. It's also one of the biggest misconceptions he hears about metabolic health.
Enzymatic inhibitors are indispensable tools for dissecting biological pathways and developing therapeutic interventions1. They are broadly categorized by their binding sites and mechanisms of action. Among these, orthosteric inhibitors, which bind to the catalytic site and directly compete with substrates, have been extensively explored due to their predictable structure-activity relationships. However, such inhibitors are typically substrate-agnostic, as their mechanism relies solely on blocking the active site.
Lipid transfer proteins (LTPs) maintain the specialized lipid compositions of organellar membranes1,2. In humans, many LTPs are implicated in diseases3, but for the majority, the cargo and auxiliary lipids facilitating transfer remain unknown. We have combined biochemical, lipidomic and computational methods to systematically characterize LTP-lipid complexes4 and measure how LTP gains of function affect cellular lipidomes. We identified bound lipids for approximately half of the hundred LTPs analyzed, confirming known ligands, while discovering new ones across most LTP families.