◀ Back to AKT2

AKT2 — IGF1R

Text-mined interactions from Literome

Nagasawa et al., Biochem J 2005 : EP2 stimulation failed to inhibit tyrosine phosphorylation either of IGF-I receptor or IRS-1 ( insulin receptor substrate-1 ), or activation of phosphoinositide 3-kinase or Akt in response to IGF-I, but potently and dose-dependently inhibited IGF-I induced activation of cellular Rac activity and membrane ruffling
Li et al., Am J Physiol Heart Circ Physiol 2006 : IGF-1R activation increased Akt phosphorylation and soluble FasL expression, and these effects were completely blocked by coincubating hVSMC with ANG II
O'Reilly et al., Cancer Res 2006 : IGF-I receptor inhibition prevents rapamycin induced Akt activation and sensitizes tumor cells to inhibition of mTOR
Patel et al., Int J Cancer 2008 (Colorectal Neoplasms) : These changes were associated with decreased expression and activation ( tyrosine phosphorylation ) of EGFR, HER-2, HER-3 ( 72-100 % ) and IGF-1R ( 67 % ) as well as their downstream effectors such as Akt and cycloxygenase-2 ( 51-97 % )
Duarte et al., Biochim Biophys Acta 2008 : Thus, insulin mediated activation of IR/IGF-1R stimulates PI-3K/Akt and inhibits GSK-3beta signaling pathways, modifying neuronal antioxidant defense-, glucose metabolism- and anti-apoptotic associated protein synthesis
Papageorgiou et al., Mol Med 2008 (Prostatic Neoplasms) : Because the IGF-1R signaling is probably the most important host tissue ( bone ) metastasis microenvironment related survival signaling for prostate cancer cells, we conclude that rosiglitazone effects on IGF-1R mediated activation of ERK1/2 and AKT could have clinical implications for the management of androgen ablation-refractory and chemotherapy-resistant advanced prostate cancer with bone metastasis
Hu et al., Cancer Res 2008 (Carcinoma...) : IGF1R activation by ligand exposure in growth factor deprived cells induces Akt activation in the FET, CBS, and GEO colon cancer cell lines ... On the other hand, a small-molecule IGF1R inhibitor, PQIP, blocked Akt phosphorylation
Engberding et al., Arterioscler Thromb Vasc Biol 2009 (Diabetes Mellitus, Type 2...) : IGF1R overexpression in VSMCs impaired insulin induced Akt phosphorylation
Chu et al., Chin J Physiol 2009 (Heart Diseases) : Western blots and TUNEL assay revealed that in the presence of IGF1R , exogenous IGF-II acts, like IGF-I, would increase phospho-Akt through IGF1R, but does not affect the caspase 3 activation and apoptotic induction in H9c2 cardiomyoblast cells
Ester et al., J Clin Endocrinol Metab 2009 (Chromosome Deletion) : Functional studies in skin fibroblast cultures demonstrated similar levels of IGF1R autophosphorylation and a reduced activation of protein kinase B/Akt upon a challenge with IGF-I in comparison with controls
Chapuis et al., Haematologica 2010 (Blast Crisis...) : Autocrine IGF-1/IGF-1R signaling is responsible for constitutive PI3K/Akt activation in acute myeloid leukemia : therapeutic value of neutralizing anti-IGF-1R antibody ... Specific inhibition of IGF-1R signaling with neutralizing anti-IGF-1R strongly inhibited the constitutive phosphorylation of both IGF-1R and Akt in 70 % of the PI3K activated samples
Huang et al., Clin Cancer Res 2010 (Ovarian Neoplasms) : Taxol induced AKT phosphorylation required IGF1R tyrosine kinase activity and was associated with upregulation of IGF2
Leclerc et al., Journal of molecular signaling 2010 : We determined that activation of P-Akt ( Thr308 ) was mediated by AMPK induced IGF-1R activation via phosphorylation of the insulin receptor substrate-1 (IRS-1) at Ser794 ... Inhibition of IGF-1R signaling using the tyrosine kinase inhibitor HNMPA ( AM ) 3 resulted in significant decrease in P-IRS-1 ( Ser794 ) and P-Akt ( Thr308 )
Tsai et al., J Nutr Biochem 2011 (Neovascularization, Pathologic) : Western blotting and immunoprecipitation demonstrated that denbinobin causes more efficient inhibition of IGF-1 induced activation of IGF-1R and its downstream signaling targets, including, extracellular signal regulated kinase, Akt , mTOR, p70S6K, 4EBP and cyclin D1
Qin et al., J Biochem 2011 : Our data here show that hyperactive AKT leads to the decrease of IGF1R at the transcriptional level, which could be partly restored by phosphatidylinositol-3 kinase (PI3K) inhibitors including wortmannin and LY294002 ... mTOR as a main downstream target of AKT is not involved in the AKT mediated down-regulation of IGF1R
Brevet et al., J Thorac Oncol 2011 (Mesothelioma...) : MET, EGFR, and insulin-like growth factor 1 receptor were the main RTKs activated after mTOR inhibition and contributed to AKT feedback activation
Jameson et al., Mol Cancer Ther 2011 (Carcinoma, Squamous Cell...) : In both the cell lines, IGF1R induced Erk, but not Akt , activation was eliminated by gefitinib
He et al., Ann Oncol 2012 (Breast Neoplasms...) : Human epidermal growth factor receptor ( HER2 ), insulin receptor and IGF-I receptor involve the same PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer
Lin et al., EMBO Mol Med 2012 (Adenocarcinoma...) : Trop-2 could attenuate IGF-1R signalling mediated AKT/ß-catenin and ERK activation through a direct binding of IGF1
Fagan et al., Cancer Res 2012 (Breast Neoplasms) : An IGF1R tyrosine kinase inhibitor, AEW541, with equal potency for the IGF1R and IR, inhibited IGF-I-, IGF-II-, and insulin stimulated Akt phosphorylation, proliferation, and anchorage independent growth in parental cells
Estañ et al., Biochem Pharmacol 2012 (Leukemia) : In summary 2-DG elicits IGF-1R mediated AMPK inactivation and Akt and ERK activation, which facilitates or restrain apoptosis, respectively
Fujita et al., J Biol Chem 2013 : Inhibitors of IGF1R, Src, AKT , and ERK1/2 did not suppress avß3-IGF-IGF1R ternary complex formation, suggesting that activation of these kinases are not required for ternary complex formation
Shu et al., Cellular oncology (Dordrecht) 2013 (Carcinoma, Hepatocellular...) : Klotho is a tumor suppressor that, through the regulation of IGF-1R phosphorylation and subsequent activation of downstream Akt-p70S6K and ERK signaling, regulates HCC tumor cell proliferation, apoptosis, autophagy and invasion
Xie et al., Cancer cell international 2013 : Klotho is a tumor suppressor in gastric cancer, which regulates IGF-1R phosphorylation and the subsequent activation of IRS-1/PI3K/Akt/mTOR signaling, tumor cell proliferation, apoptosis, and autophagy
Chen et al., Cancer Discov 2013 (Carcinoma, Non-Small-Cell Lung...) : The mechanistic basis for this effect seems to be an increased baseline activation of IGF1R mediated activation of AKT in cells that express oncogenic KRAS