Gene interactions and pathways from curated databases and text-mining

◀ Back to AKT1

AKT1 — RAD50

Text-mined interactions from Literome

Tsygankova et al., Mol Cell Biol 2001 : The ability of TSH to stimulate Akt phosphorylation was markedly enhanced by the expression of activated Rap1A and was repressed in cells expressing a putative dominant negative Rap1A mutant ... Although the expression of activated Rap1A was sufficient to stimulate wortmannin-sensitive Akt phosphorylation, TSH further increased Akt phosphorylation in a phosphatidylinositol 3-kinase- and PKA dependent manner
Wang et al., J Biol Chem 2001 : Moreover, inhibition of Rap1 by a Rap1 GTPase activating protein-1 also resulted in a decrease in ERK and Akt phosphorylation, which was not further decreased by cAMP, suggesting that cAMP inhibits ERK and Akt by inhibiting Rap1 ... The role of Rap1 in ERK and Akt activity was further demonstrated by our observation that an active form of Epac, which activated Rap1 in the absence of cAMP, increased ERK and Akt phosphorylation
Grader-Beck et al., Blood 2003 : Thus, TCR plus CD28 mediated activation of ERK1/2 and PKB , cytokine production, and cell cycle progression, all of which are inhibited by cAMP, require activation of Ras but not Rap1
Albert et al., Mol Cancer Ther 2006 (Breast Neoplasms) : Irradiation induced Akt and mTOR signaling, and this signaling is attenuated by RAD001
Romano et al., Endocrinology 2006 : Under the same conditions, PI3K and Akt inhibition also both increased Raf-1 kinase activity and the levels of GTP bound ( active form ) monomeric G protein Rap1 , which suggests that a down-regulation of the ERK-1/2 cascade is induced by the PI3K/Akt signaling pathway in unstimulated cells
Mabuchi et al., Cancer Res 2007 (Disease Models, Animal...) : In vivo effects of RAD001 on Akt-mTOR signaling, tumor cell proliferation, and blood vessel area were analyzed by immunohistochemistry and Western blot analysis
Tamburini et al., Blood 2008 (Leukemia, Myeloid, Acute) : In 19 AML samples with constitutive PI3K/Akt activation, the rapamycin derivative inhibitor everolimus ( RAD001 ) increased Akt phosphorylation ... This mTOR C1-mediated Akt up-regulation was explained by an insulin-like growth factor-1 (IGF-1)/IGF-1 receptor autocrine loop : ( 1 ) blast cells expressed functional IGF-1 receptors, and IGF-1 induced Akt activation was increased by RAD001 , ( 2 ) a neutralizing anti-IGF-1R alpha-IR3 monoclonal antibody reversed the RAD001 induced Akt phosphorylation, and ( 3 ) autocrine production of IGF-1 was detected in purified blast cells by quantitative reverse transcription-polymerase chain reaction and immunofluorescence ... This RAD001 induced PI3K/Akt up-regulation was due to an up-regulated expression of the IRS2 adaptor
Breuleux et al., Mol Cancer Ther 2009 (Neoplasms) : In contrast, increased AKT S473 phosphorylation induced by RAD001 did not correlate
Edreira et al., J Biol Chem 2009 : cAMP dependent protein kinase (PKA) mediated phosphorylation of Rap1b is required for cAMP dependent mitogenesis, tumorigenesis, and inhibition of AKT activity
Malchinkhuu et al., Mol Biol Cell 2009 (Glioma) : The expression of tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 ( PTEN ) is required for the inhibitory ISO induced and Rap1B mediated actions on the migration, Rac1 activation, and Akt activation in response to LPA
Mancini et al., J Cell Biochem 2010 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Moreover, RAD 001 induced inhibition of Akt causes the de-phosphorylation of tuberous sclerosis tumor suppressor protein TSC2 at 14-3-3 binding sites, TSC2 release from 14-3-3 sigma ( restoring its inhibitory function on mTORC1 ) and nuclear import ( promoting the nuclear translocation of cyclin dependent kinase [ CDK ] inhibitor p27 ( Kip1 ), the stabilization of p27 ( Kip1 ) ligand with CDK2, and the G ( 0 ) /G ( 1 ) arrest )
Tawa et al., Circ Res 2010 (Disease Models, Animal...) : Rap1 regulated the interaction between afadin and phosphatidylinositol 3-kinase (PI3K), recruitment of the afadin-PI3K complex to the leading edge, and the activation of Akt , indicating the involvement of Rap1 and afadin in the PI3K-Akt signaling pathway
Loehberg et al., Biochem Pharmacol 2012 (Breast Neoplasms...) : The anticancer drug RAD001 ( everolimus ) is a known mTOR-inhibitor, but mTOR-inhibition leads to phosphorylation of Akt inducing resistance against RAD001 treatment ... Therefore, our aim was to test, if Chloroquine could inhibit tumor growth and prevent RAD001 induced Akt activation ... The Chloroquine effect of overcoming the RAD001 induced activation of the oncogene Akt , as well as the promising antitumor activity in our mammary tumor animal model present Chloroquine as an interesting combination partner for the mTOR-inhibitor RAD001
Ren et al., Cancer Lett 2012 (Carcinoma, Non-Small-Cell Lung...) : This combination abrogated RAD001 induced Akt phosphorylation and exerted enhanced suppressive effect on 4EBP1 phosphorylation
Chan et al., Cancer Chemother Pharmacol 2013 (Carcinoma, Hepatocellular...) : Although the addition of the TKI258 only slightly suppressed the phosphorylation of AKT induced by RAD001 , the pi-mTOR and its downstream signaling pathways including pi-p70S6K, pi-S6 and pi-4EBP1 were lowered in the combination
Hisamatsu et al., Mol Cancer Ther 2013 : Treatment with RAD001 induced mTORC2 mediated AKT activation in RAD001-sensitive CCC cells