Protein kinase C iota (PKCι) and pVHL are both needed for lysosomal degradation of α5 integrin in renal carcinoma cells.

ABSTRACT:

Background

von Hippel-Lindau (VHL) hereditary cancer syndrome is caused by mutations in the VHL tumor suppressor gene and is characterized by a predisposition to form various types of tumors, including renal cell carcinomas, hemangioblastomas, and pheochromocytomas. The protein products of the VHL gene, pVHL, are part of an ubiquitin ligase complex that tags hypoxia inducible factor alpha (HIF-α) for proteosomal degradation. pVHL has also been reported to bind to atypical protein kinase C (aPKC).

Methods and results

To better understand the relationship between pVHL and aPKC, the PKC iota (PKCι) isoform of aPKC was knocked out in renal carcinoma cells, both pVHL-negative and those with replaced pVHL. Cellular properties associated with pVHL function were assayed. Knockout of

SUBMITTER: Schurr AF 

PROVIDER: S-EPMC11782342 | biostudies-literature | 2025 Jan

REPOSITORIES: biostudies-literature