PMID- 32351714
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230926
IS  - 2058-7716 (Print)
IS  - 2058-7716 (Electronic)
IS  - 2058-7716 (Linking)
VI  - 6
DP  - 2020
TI  - How does mTOR sense glucose starvation? AMPK is the usual suspect.
PG  - 27
LID - 10.1038/s41420-020-0260-9 [doi]
LID - 27
AB  - Glucose is a major requirement for biological life. Its concentration is 
      constantly sensed at the cellular level, allowing for adequate responses to any 
      changes of glucose availability. Such responses are mediated by key sensors and 
      signaling pathway components that adapt cellular metabolism to glucose levels. 
      One of the major hubs of these responses is mechanistic target of rapamycin 
      (mTOR) kinase, which forms the mTORC1 and mTORC2 protein complexes. Under 
      physiological glucose concentrations, mTORC1 is activated and stimulates a number 
      of proteins and enzymes involved in anabolic processes, while restricting the 
      autophagic process. Conversely, when glucose levels are low, mTORC1 is inhibited, 
      in turn leading to the repression of numerous anabolic processes, sparing ATP and 
      antioxidants. Understanding how mTORC1 activity is regulated by glucose is not 
      only important to better delineate the biological function of mTOR, but also to 
      highlight potential therapeutic strategies for treating diseases characterized by 
      deregulated glucose availability, as is the case of cancer. In this perspective, 
      we depict the different sensors and upstream proteins responsible of controlling 
      mTORC1 activity in response to changes in glucose concentration. This includes 
      the major energy sensor AMP-activated protein kinase (AMPK), as well as other 
      independent players. The impact of such modes of regulation of mTORC1 on cellular 
      processes is also discussed.
CI  - (c) The Author(s) 2020.
FAU - Leprivier, Gabriel
AU  - Leprivier G
AD  - 1Institute for Neuropathology, Medical Faculty, Heinrich Heine University, 
      Moorenstr. 5, 40225 Dusseldorf, Germany. ISNI: 0000 0001 2176 9917. GRID: 
      grid.411327.2
FAU - Rotblat, Barak
AU  - Rotblat B
AUID- ORCID: 0000-0003-2985-7115
AD  - 2Department of Life Sciences, Ben-Gurion University of the Negev, Beer-Sheva, 
      84105 Israel. ISNI: 0000 0004 1937 0511. GRID: grid.7489.2
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20200422
PL  - United States
TA  - Cell Death Discov
JT  - Cell death discovery
JID - 101665035
PMC - PMC7176732
OTO - NOTNLM
OT  - Cell biology
OT  - Cell signalling
COIS- Conflict of interestThe authors declare that they have no conflict of interest.
EDAT- 2020/05/01 06:00
MHDA- 2020/05/01 06:01
PMCR- 2020/04/22
CRDT- 2020/05/01 06:00
PHST- 2020/02/09 00:00 [received]
PHST- 2020/03/13 00:00 [revised]
PHST- 2020/03/31 00:00 [accepted]
PHST- 2020/05/01 06:00 [entrez]
PHST- 2020/05/01 06:00 [pubmed]
PHST- 2020/05/01 06:01 [medline]
PHST- 2020/04/22 00:00 [pmc-release]
AID - 260 [pii]
AID - 10.1038/s41420-020-0260-9 [doi]
PST - epublish
SO  - Cell Death Discov. 2020 Apr 22;6:27. doi: 10.1038/s41420-020-0260-9. eCollection 
      2020.