NIH R01 · 2024
PROJECT SUMMARY The loss of endogenous tumor suppressors is an obligatory step in tumor onset and progression, but the underlying mechanisms are elusive and the breadth of their targets mostly unknown. We have now discovered that Parkin, a mitochondria-associated E3 ubiquitin ligase biallelically altered in early-onset Parkinson’s Disease, functions as a novel, dual mode tumor suppressor. This involves inhibition of intrinsic tumor traits of cell motility and metabolism but also reprogramming of an antitumor immune microenvironment. In this pathway, Parkin recruitment to mitochondria “primes” immunogenic cell death, controls the release of Damage- Associated Molecular Pattern (DAMP), and…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.