NIH R01 · 2024
The role of FIT2 in VLDL assembly, hepatic triglyceride homeostasis, and lipoprotein atherogenicity
This R01 application focuses on the mechanisms that control the generation of very low density lipoproteins (VLDLs) in liver cells. Prior work from the MPIs, which has resulted in 15 publications, established that a major mechanism controlling the secretion and circulation of VLDL is the regulated degradation of apolipoprotein (apoB) in the endoplasmic reticulum (ER). This metabolically orchestrated event requires the ER-associated degradation (ERAD) pathway, which was named and first elucidated by MPI Brodsky. In contrast, when neutral lipids (primarily triacylglycerols; TGs) are sufficient, apoB is co-translationally lipidated by MTP, and the nascent VLDL particles are expanded by lipids…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.