Reciprocal Regulation between Primary Cilia and mTORC1.
AMPK
LKB1
Tsc2
autophagy
ciliogenesis
mTOR
mTORC1
polycystin-1
primary cilia
Journal
Genes
ISSN: 2073-4425
Titre abrégé: Genes (Basel)
Pays: Switzerland
ID NLM: 101551097
Informations de publication
Date de publication:
26 06 2020
26 06 2020
Historique:
received:
30
05
2020
revised:
22
06
2020
accepted:
24
06
2020
entrez:
2
7
2020
pubmed:
2
7
2020
medline:
13
3
2021
Statut:
epublish
Résumé
In quiescent cells, primary cilia function as a mechanosensor that converts mechanic signals into chemical activities. This unique organelle plays a critical role in restricting mechanistic target of rapamycin complex 1 (mTORC1) signaling, which is essential for quiescent cells to maintain their quiescence. Multiple mechanisms have been identified that mediate the inhibitory effect of primary cilia on mTORC1 signaling. These mechanisms depend on several tumor suppressor proteins localized within the ciliary compartment, including liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), polycystin-1, and polycystin-2. Conversely, changes in mTORC1 activity are able to affect ciliogenesis and stability indirectly through autophagy. In this review, we summarize recent advances in our understanding of the reciprocal regulation of mTORC1 and primary cilia.
Identifiants
pubmed: 32604881
pii: genes11060711
doi: 10.3390/genes11060711
pmc: PMC7349257
pii:
doi:
Substances chimiques
TRPP Cation Channels
0
polycystic kidney disease 1 protein
0
polycystic kidney disease 2 protein
0
Protein Kinases
EC 2.7.-
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Protein Serine-Threonine Kinases
EC 2.7.11.1
STK11 protein, human
EC 2.7.11.1
AMP-Activated Protein Kinase Kinases
EC 2.7.11.3
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM132127
Pays : United States
Organisme : NIGMS NIH HHS
ID : GM132127
Pays : United States
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