Highlights • Loss of CRY2 stabilizes c-MYC and enhances cellular transformation • CRY2 can function as a co-factor for the SCF substrate adaptor FBXL3 • c-MYC phosphorylated on threonine 58 (T58) interacts with CRY2 • SCFFBXL3+CRY2 promotes the ubiquitylation and turnover of c-MYC
TSRI researchers find an unexpected role for proteins involved with our daily “circadian” clocks in influencing cancer growth. The new research suggests disruptions in circadian rhythms might leave levels of an important cancer-linked protein, cMYC unchecked. “This appears to have big implications for the connection between circadian rhythms and cancer,” said TSRI biologist Katja Lamia, senior author of the study.
There is growing evidence that shift work and frequent jet lag can raise a person’s risk of ...
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