TSC2 Integrates Wnt and Energy Signals via a Coordinated Phosphorylation by AMPK and GSK3 to Regulate Cell Growth
@article{Inoki2006TSC2IW, title={TSC2 Integrates Wnt and Energy Signals via a Coordinated Phosphorylation by AMPK and GSK3 to Regulate Cell Growth}, author={Ken Inoki and Hongjia Ouyang and Tianqing Zhu and Charlotta Lindvall and Yian Wang and Xiaojie Zhang and Qian Yang and Christina N. Bennett and Yuko Harada and Kryn Stankunas and Cun-Yu Wang and Xi He and Ormond A. MacDougald and Ming You and Bart O. Williams and Kun Liang Guan}, journal={Cell}, year={2006}, volume={126}, pages={955-968} }
1,245 Citations
Consequences of interrupted Rheb-to-AMPK feedback signaling in tuberous sclerosis complex and cancer
- Biology, MedicineSmall GTPases
- 2011
How Rheb-to-AMPK, and p27 signaling may impact on disease progression and treatment of TSC, including sporadic lymphangioleio-myomatosis (S-LAM) and malignancies is discussed.
TSC1/TSC2 inactivation inhibits AKT through mTORC1-dependent up-regulation of STAT3-PTEN cascade.
- BiologyCancer letters
- 2011
PKG-Modified TSC2 Regulates mTORC1 Activity to Counter Adverse Cardiac Stress
- Biology, MedicineNature
- 2019
It is shown that phosphorylation or gain- or loss-of-function mutations at either of two adjacent serine residues in TSC2 can bidirectionally control mTORC1 activity stimulated by growth factors or haemodynamic stress, and consequently modulate cell growth and autophagy.
Maintaining glycogen synthase kinase-3 activity is critical for mTOR kinase inhibitors to inhibit cancer cell growth.
- Biology, ChemistryCancer research
- 2014
A novel mechanism by which mTORC2 promotes cell growth is defined, with potential implications for understanding the clinical action of mTOR kinase inhibitors, which are being evaluated in cancer clinical trials.
IKKβ Suppression of TSC1 Links Inflammation and Tumor Angiogenesis via the mTOR Pathway
- Biology, MedicineCell
- 2007
Growth factor signaling pathways converge on the TSC complex to control mTOR
- Biology
- 2019
The goals of this dissertation were to characterize the mechanisms by which upstream growth factor signaling pathways converge on the TSC complex to activate mTORC1, and to determine the significance of these mechanisms in disease and to gain more mechanistic details surrounding this regulation.
Crosstalk between mTORC1 and cAMP Signaling
- Biology, Medicine
- 2015
It is shown that mTORC1 is potently inhibited by hormones that stimulating cAMP, and the data indicate that cAMP acts through protein kinase A (PKA) to inhibit m TORC1.
IKBKE inhibits TSC1 to activate the mTOR/S6K pathway for oncogenic transformation.
- BiologyTurkish journal of biology = Turk biyoloji dergisi
- 2018
This work proposes a mechanism where IKKε, through regulating TSC1 stability in cancer cells, may create an alternative regulatory loop for the activation of mTOR signaling, and results can potentially be important for the development of novel therapeutic strategies targeting m TOR signaling.
Regulation of the Mammalian Target Of Rapamycin Complex 2 (mTORC2)
- Biology, Chemistry
- 2006
The results suggest that mTORC2 hyperactivation may contribute to the pathophysiology of diseases such as cancer and Tuberous Sclerosis Complex.
Repression of the protein kinase PIM3 by an mTORC1-regulated microRNA
- Biology, Chemistry
- 2017
PIM inhibition in combination with mTOR inhibitors may be a promising therapy in some cancer settings, and it is shown that PIM3 repression is mediated by miR-33, an intronic microRNA encoded within the SREBP loci, the expression of which is decreased with rapamycin.
References
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The data suggest that hamartin and tuberin negatively regulate beta-Catenin stability and activity by participating in the beta-catenin degradation complex.