Learn more about the research of Mayo Clinic's Gene Editing and Cellular Engineering Laboratory led by David (Chun-Wei) D.

MYC was down after treatment in experimental models and clinical samples, and rescuing MYC effectively reversed all of the AR inhibition-induced phenotypes, including the switch from glycolysis to ...

MYC production and phosphorylation were unaffected by treatment, thus resulting in reduced metabolic activities and propagation in U87 cell lines.

MYC phosphorylation by known or unknown kinases at specific site sets the stage for MYC degradation. Phosphorylation of indicated sites recruit FBW7 dimer and forms the SCF complex consisting of Skp1, ...

Hypoxia does not increase glycolysis in proliferating primary cells and antagonizes the increase in glycolysis caused by activation of hypoxia-inducible factor in normoxia, in part, through activation ...

Dr. Welcker wrestled with accepting this long-standing model for years until he decided to thoroughly and meticulously dissect this model to see for himself whether the different phosphorylation sites ...

Taken together, the present study demonstrated for the first time that PKM2-dependent c-Myc-Ser-62 phosphorylation stabilized c-Myc, thereby increasing survivin expression, which is required for ...

They further learned that an mTOR inhibitor capable of blocking 4EBP1 phosphorylation has remarkable therapeutic efficacy in Myc-driven hematologic cancers: The experimental drug, called MLN0128 ...

In vivo xenograft studies revealed that c-Myc phosphorylation by PKCζ is a critical event in the control of metastasis. Collectively, these results establish PKCζ as an important tumor suppressor and ...

The PI3‐kinase pathway involves Akt‐mediated phosphorylation of FoxO transcription factors. In a nonphosphorylated state, FoxO factors inhibit induction of multiple Myc target genes, Myc‐induced cell ...