Galnt11 regulates kidney function by glycosylating the endocytosis receptor megalin to modulate ligand binding.

ABSTRACT: Chronic kidney disease (CKD) affects more than 20 million Americans and ∼10% of the population worldwide. Genome-wide association studies (GWAS) of kidney functional decline have identified genes associated with CKD, but the precise mechanisms by which they influence kidney function remained largely unexplored. Here, we examine the role of 1 GWAS-identified gene by creating mice deficient for Galnt11, which encodes a member of the enzyme family that initiates protein O-glycosylation, an essential posttranslational modification known to influence protein function and stability. We find that Galnt11-deficient mice display low-molecular-weight proteinuria and have specific defects in proximal tubule-mediated resorption of vitamin D binding protein, α₁-microglobulin, a

SUBMITTER: Tian E 

PROVIDER: S-EPMC6911204 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature