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AKT3 — TSC2
Pathways - manually collected, often from reviews:
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Potter et al., Nat Cell Biol 2002
:
Akt regulates growth by directly phosphorylating
Tsc2 ... Stimulating
Akt/PKB signalling in vivo markedly
increases cell growth/size, disrupts the Tsc1-Tsc2 complex and disturbs the distinct subcellular localization of Tsc1 and
Tsc2
Potter et al., Biochem Soc Trans 2003
:
We have shown that
Akt regulates the
Tsc1-Tsc2 complex by directly phosphorylating Tsc2 ... We have shown that
Akt regulates the Tsc1-Tsc2 complex by directly phosphorylating
Tsc2
Hahn-Windgassen et al., J Biol Chem 2005
:
Here we establish an additional pathway by which
Akt inhibits
TSC2 and activates mTOR ... Currently, the
Akt mediated phosphorylation of TSC2 and the inhibition of AMPK mediated phosphorylation of
TSC2 are viewed as two separate pathways, which activate mTOR ... Our results demonstrate that
Akt lies upstream of these two pathways and
induces full inhibition of
TSC2 and activation of mTOR both through direct phosphorylation and by inhibition of AMPK mediated phosphorylation of TSC2
Kayampilly et al., Endocrinology 2007
(MAP Kinase Signaling System) :
Because
Akt is the upstream
activator of
TSC2 phosphorylation, the effect of Akt inhibition was examined to test whether FSH mediated TSC2 phosphorylation proceeds through an Akt dependent pathway ... These results demonstrate the
involvement of ERK rather than
Akt in FSH mediated
TSC2 phosphorylation in granulosa cells
Dan et al., J Immunol 2008
:
mTOR is negatively controlled by the tuberous sclerosis complex 1/2 (TSC1/2), and activation of
Akt induces phosphorylation of
TSC2 , which blocks the repressive TSC1/2 activity
Huang et al., Biochem Soc Trans 2009
:
Akt/PKB ( protein kinase B ) both regulates and is
regulated by the TSC ( tuberous sclerosis complex )
1-TSC2 complex
Codeluppi et al., J Neurosci 2009
(Disease Models, Animal...) :
This occurs through
Akt mediated phosphorylation of the GTPase activating protein
Tuberin , which inhibits Tuberin 's ability to inactivate the small GTPase Rheb
Pollizzi et al., Molecular cancer 2009
(Disease Models, Animal...) :
Loss of either TSC1 or
TSC2 in TSC hamartomas
leads to activation of mTORC1 and suppression of
AKT
Zhang et al., PloS one 2009
:
Loss of function of the
TSC1-TSC2 complex results in constitutive mTORC1 signaling and, through mTORC1 dependent feedback mechanisms and loss of mTORC2 activity,
leads to a concomitant block of
Akt signaling to its other downstream targets
Hwang et al., BMB Rep 2011
(Ischemia) :
The loss of
TSC2 , which is upstream of mTOR, activates S6K1, promotes cell growth and survival, activates mTOR kinase activities, inhibits mTORC1 and mTORC2 via mTOR inhibitors, and
suppresses S6K1 and
Akt
Das et al., J Biol Chem 2012
(Tuberous Sclerosis) :
TSC2 deficiency
induces constitutive activation of mTOR, leading to a state of insulin resistance due to a negative feedback regulation, resulting in reduced
Akt phosphorylation