Structure of the γ–ε complex of cyanobacterial F1-ATPase reveals a suppression mechanism of the γ subunit on ATP hydrolysis in phototrophs
IFN-γ-response mediator GBP-1 represses human cell proliferation by inhibiting the Hippo signaling transcription factor TEAD
Isoform-specific AMPK association with TBC1D1 is reduced by a mutation associated with severe obesity
Differential receptor selectivity of the FGF15/FGF19 orthologues determines distinct metabolic activities in db/db mice
Mitochondrial-derived reactive oxygen species influence ADP sensitivity, but not CPT-I substrate sensitivity
In this issue of the Biochemical Journal, Thomas et al. report on the interaction between AMPK and one of its target proteins TBC1D1. The research shows that the association is AMPK-isoform-specific and that it is disrupted by a mutation linked to obesity. The cover image, taken from the article, shows Western blot analysis of the phosphorylation of transiently expressed GFP-TBC1D1 as well as AMPK and ACC from Flp-In HEK293 cells that stably express FLAG-AMPK-α1 or FLAG-AMPK-α2. For further details, see pages 2969–2983.