Contents
11 June 2019
Vol 12, Issue 585
Vol 12, Issue 585
Focus
- Amplifying mTORC2 signals through AMPK during energetic stress
mTORC2 is phosphorylated by AMPK during energetic stress to promote cell survival (Kazyken et al. in 11 June 2019 issue).
Research Articles
- AMPK directly activates mTORC2 to promote cell survival during acute energetic stress
AMPK ensures cell survival during energetic stress by stimulating the kinase Akt through mTORC2.
- CDK5 inhibits the clathrin-dependent internalization of TRPV1 by phosphorylating the clathrin adaptor protein AP2μ2
CDK5 inhibits constitutive internalization of the nociceptor TRPV1 and contributes to inflammatory hyperalgesia.
Editors' Choice
- Mitochondrial respiration not required
Chondrocytes survive constitutive hypoxia by suppressing mitochondrial respiration.
About The Cover
Online Cover This week features a Research Article that shows that AMPK ensures cell survival during energetic stress by stimulating the kinase Akt through the multiprotein complex mTORC2 (see also the associated Focus). The image shows a color-enhanced transmission electron micrograph of a hepatocyte. The mitochondria, which are the powerhouses of the cell, have been colored orange. [Image: Don W. Fawcett/Science Source]