If you’re at #HUPO2025, be sure to stop by my poster and learn about the latest developments in the BioPlex project!
LRRC58 does so by serving as an E3 substrate adaptor that targets CDO1 for ubiquitylation and proteasomal degradation. We found that cysteine itself serves as a molecular signal to turn on and off LRRC58-mediated CDO1 degradation, and LRRC58 depletion stabilizes CDO1 to drive cysteine consumption.
We developed a MS and machine learning approach to globally identify protein regulators of metabolism. We found protein LRRC58 controls cellular cysteine catabolism by mediating degradation of CDO1, the rate-limiting enzyme of the catabolic cysteine shunt to taurine. www.nature.com/articles/s41...
lab at Dana-Farber, Nils @nilsburger.bsky.social at UTSW, Sumeet Khetarpal at UVA, Hilina, Katherine, Eric in the Fischer lab at Dana-Farber, and Ed Huttlin @edhuttlin.bsky.social and the Gygi lab @harvardcellbio.bsky.social.