| First Author | Gu Y | Year | 2017 |
| Journal | Cancer Cell | Volume | 32 |
| Issue | 1 | Pages | 115-128.e7 |
| PubMed ID | 28697340 | Mgi Jnum | J:243263 |
| Mgi Id | MGI:5908032 | Doi | 10.1016/j.ccell.2017.06.001 |
| Citation | Gu Y, et al. (2017) Stabilization of the c-Myc Protein by CAMKIIgamma Promotes T Cell Lymphoma. Cancer Cell 32(1):115-128.e7 |
| abstractText | Although high c-Myc protein expression is observed alongside MYC amplification in some cancers, in most cases protein overexpression occurs in the absence of gene amplification, e.g., T cell lymphoma (TCL). Here, Ca2+/calmodulin-dependent protein kinase II gamma (CAMKIIgamma) was shown to stabilize the c-Myc protein by directly phosphorylating it at serine 62 (S62). Furthermore, CAMKIIgamma was shown to be essential for tumor maintenance. Inhibition of CAMKIIgamma with a specific inhibitor destabilized c-Myc and reduced tumor burden. Importantly, high CAMKIIgamma levels in patient TCL specimens correlate with increased c-Myc and pS62-c-Myc levels. Together, the CAMKIIgamma:c-Myc axis critically influences the development and maintenance of TCL and represents a potential therapeutic target for TCL. |
