Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.

ABSTRACT: Accumulating evidence has implicated impaired extracellular matrix (ECM) clearance as a key factor in fibrotic disease. Despite decades of research elucidating the effectors of ECM clearance, relatively little is understood regarding the upstream regulation of this process. Collagen is the most abundant constituent of normal and fibrotic ECM in mammalian tissues. Its catabolism occurs through extracellular proteolysis and cell-mediated uptake of collagen fragments for intracellular degradation. Given the paucity of information regarding the regulation of this latter process, here we execute unbiased genome-wide screens to understand the molecular underpinnings of cell-mediated collagen clearance. Using this approach, we discover a mechanism through which collagen biosynthesis is sensed by

SUBMITTER: Podolsky MJ 

PROVIDER: S-EPMC10879544 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature