Annika G Sonntag

TL;DR: It is proposed that ZEB1 links EMT-activation and stemness-maintenance by suppressingstemness-inhibiting microRNAs (miRNAs) and thereby is a promoter of mobile, migrating cancer stem cells.

TL;DR: It is found that aa acutely activate AMPK concurrently with mTOR, and it is shown that AMPK under aa sufficiency acts to sustain autophagy, which may be required to maintain protein homoeostasis and deliver metabolite intermediates for biosynthetic processes.

TL;DR: In this paper, the authors identify astrin as an essential negative mTORC1 regulator in the cellular stress response and show that in cancer cells, apoptosis suppression during stress depends on the presence of the raptor to stress granules (SGs).

TL;DR: A data-driven dynamic insulin-mTOR network model is presented that integrates the entire core network and used to investigate the less well understood mechanisms by which insulin regulates mTORC2, and suggests that a previously unknown network structure connects m TORC2 to its upstream cues and clarifies which molecular connectors contribute to mTORc2 activation.

TL;DR: It is shown that in cancer cells, apoptosis suppression during stress depends on astrin, and this work establishes a unifying model of mTORC1 inhibition and activation upon stress.