Contents
Vol 13, Issue 633
Focus
- The tale of a tail: The secret behind IGF-1R’s oncogenic power
The C-terminal tail of IGF-1R promotes cancer cell migration by mediating adhesion-dependent translocation to the Golgi (Rieger et al., in 26 May 2020 issue).
Research Articles
- IGF-1 receptor activity in the Golgi of migratory cancer cells depends on adhesion-dependent phosphorylation of Tyr1250 and Tyr1251
Translocation of the IGF-1 receptor to the Golgi promotes cancer cell migration.
- Myeloma cells shift osteoblastogenesis to adipogenesis by inhibiting the ubiquitin ligase MURF1 in mesenchymal stem cells
Myeloma cells repress osteoblastogenesis by inhibiting the degradation of PPARγ2 in mesenchymal stem cells.
Editors' Choice
- Protection between tissues and across species
Lactobacilli in the gut stimulate Nrf2-dependent antioxidant responses in the liver.
About The Cover

Online Cover This week features a Research Article that shows that translocation of the IGF-1 receptor to the Golgi promotes cancer cell migration. The image shows IGF-1R (green), the cis-Golgi marker GM130 (red), and nuclei (blue) in mouse embryonic fibroblasts in the absence of IGF-1 (upper left) and after stimulation with IGF-1 (lower right). Yellow indicates colocalization of IGF-1R and GM130. [Image: Rieger et al./Science Signaling]