Natalie von der Lehr

TL;DR: The results suggest that Skp2 is a transcriptional cofactor for c-Myc and indicates a close relationship between transcription activation and transcription factor ubiquitination.

TL;DR: It is shown that Myc represses differentiation-induced expression of the cyclin-dependent kinase (CDK) inhibitor p21CIP1 (CDKN1A, p21), known to play an important role in cell fate decisions during growth and differentiation, in hematopoietic cells.

TL;DR: The results show that proteasome-mediated turnover of c-Myc is substantially impaired in Burkitt's lymphoma cells with mutated Thr58 or other mutations that abolish Thr58 phosphorylation, whereas endogenous or ectopically expressed wild type c- myc proteins turn over at normal rates in these cells.

TL;DR: It is found that although Ras interfered with Myc-induced apoptosis, Myc repressed Ras-induced senescence, together abrogating two main barriers of tumorigenesis, highlighting that pharmacological inhibition of Cdk2 activity is a potential therapeutical principle for cancer therapy, in particular for tumors with activated Myc or Ras.

TL;DR: It is shown here that c-Myc interacts with Skp2 as part of the SCFSkp2 E3 ubiquitin ligase complex, suggesting a role of the ubiquit in/proteasome system in c- myc-regulated transcription.