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AKT1 — TRAF6
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
Funakoshi-Tago et al., Eur J Biochem 2003
:
Furthermore,
TRAF6 and c-Src induced JNK activation was significantly
inhibited by PI3-kinase inhibitor or a dominant negative mutant of
Akt ( Akt DN ) ... Furthermore,
TRAF6 and c-Src induced JNK activation was significantly
inhibited by PI3-kinase inhibitor or a dominant negative mutant of
Akt ( Akt DN )
Lee et al., Biochem Biophys Res Commun 2003
(MAP Kinase Signaling System) :
The RANK signaling mechanisms involved in these responses include the recruitment of
TNF receptor associated factor proteins, the activation of transcription factors ( NF-kappaB, AP-1, and NFAT2 ), the cascades of mitogen activated protein kinases ( ERK, JNK, and p38 ), and the induction of Src- and phosphatidylinositol 3-kinase dependent
Akt activation
Choi et al., Blood 2009
:
Ligation of IL-33 with ST2 rapidly increased endothelial nitric oxide ( NO ) production through
TRAF6 mediated activation of phosphoinoside-3-kinase,
Akt , and endothelial NO synthase
Yang et al., Science 2009
(Neoplasms, Experimental) :
The E3 ligase
TRAF6 regulates
Akt ubiquitination and activation
Jakus et al., J Nutr Biochem 2013
:
Moreover, Akt was identified previously as a direct target of TRAF6, and we found that, similarly to MAPKs, phosphorylation pattern of
Akt followed the activation of
TRAF6 , and it was inhibited by resveratrol at all time points
Schnetzke et al., J Cancer Res Clin Oncol 2013
(Leukemia, Myeloid, Acute) :
The E3 ubiquitin ligase
TRAF6 inhibits LPS induced
AKT activation in FLT3-ITD positive MV4-11 AML cells ... Based on the observation that TRAF6 might play a role in AKT phosphorylation, we hypothesized that
TRAF6 can
enhance the constitutive FLT3-ITD-driven activation of
AKT after LPS stimulation
Farook et al., Cell death & disease 2013
:
Here we show that upregulation of a pro-apototic protein, GADD34, attenuates
TRAF6 mediated
Akt activation in a controlled cortical impact model of TBI in mice