Gene interactions and pathways from curated databases and text-mining

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AKT1 — ESR1

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

Martin et al., Endocrinology 2000 : Studies using mutants of ER-alpha demonstrated that Akt increased estrogen receptor activity through the amino-terminal activation function-1 (AF-1) ... Serines S104 S106, S118, and S167 appear to play a role in the activation of ER-alpha by Akt
Campbell et al., J Biol Chem 2001 (Breast Neoplasms) : Here we show that phosphatidylinositol (PI) 3-kinase and AKT activate ERalpha in the absence of estrogen
Zhang et al., Neuroreport 2001 (Alzheimer Disease) : These results indicate that the neuroprotective effects of E2 may be mediated at least in part via estrogen receptor mediated protein kinase B activation
Sun et al., Cancer Res 2001 (Breast Neoplasms) : However, AKT2 induced ERalpha activity was not inhibited by tamoxifen but was completely abolished by ICI 164,384, implicating that AKT2 activated ERalpha contributes to tamoxifen resistance
Stoica et al., Mol Endocrinol 2003 (Breast Neoplasms) : Transient transfection of ERalpha into these cells restored Akt activation by estradiol, suggesting that estradiol activation of Akt requires the ERalpha
Simoncini et al., Arterioscler Thromb Vasc Biol 2003 : By interacting with phosphatidylinositol 3-kinase (PI3K), estrogen receptor (ER) alpha leads to activation of protein kinase Akt and to subsequent increase in endothelial nitric oxide synthase activity
Stoica et al., Oncogene 2003 : Transient transfection of ER-alpha into these cells restored Akt phosphorylation by HRG-beta1, suggesting the requirement of ER-alpha ... Akt leads to nuclear ER-alpha phosphorylation, thereby altering its expression and transcriptional activity
Stoica et al., Oncogene 2003 (Breast Neoplasms) : The recent study examines whether Akt is involved in the ER-alpha regulation by estradiol ( genomic effect )
Guo et al., Mol Cell Biol 2004 : The constitutively activated myristylated Akt reduced ERalpha expression, whereas agents that negatively affect the PI3K/Akt pathway, i.e., wortmannin, celecoxib, and the green tea polyphenol epigallocatechin-3 gallate, induced ERalpha
Anter et al., Circ Res 2005 : Conversely, constitutively active MKK6 induced p38 MAPK activation that recapitulated the effects of polyphenols by inducing ERalpha phosphorylation and downstream activation of Akt , and eNOS
Zhang et al., J Mol Endocrinol 2005 (Breast Neoplasms...) : The results showed that IGF-I dependent phosphorylation of Akt and mitogen activated protein kinase, induction of G ( 1 ) -S-phase progression and enhanced expression of cyclin D1 and cyclin E were dependent on ERalpha
Duong et al., Cancer Res 2006 (Breast Neoplasms) : AKT regulation of estrogen receptor beta transcriptional activity in breast cancer
Mannella et al., J Neurosci 2006 (Alzheimer Disease...) : Estrogen receptor protein interaction with phosphatidylinositol 3-kinase leads to activation of phosphorylated Akt and extracellular signal regulated kinase 1/2 in the same population of cortical neurons : a unified mechanism of estrogen action
Lehnes et al., Endocrinology 2007 (Cell Transformation, Neoplastic) : Cumulatively, our results suggest that Akt1 and ErbB2 are involved in in vivo tumorigenesis and modulation of estrogen receptor-alpha expression and activity
Tissier et al., J Mol Cell Cardiol 2007 (Myocardial Infarction...) : In conclusion, genistein exerts pharmacological postconditioning with a similar potency as 17beta-estradiol through a pathway involving activation of the estrogen receptor , of PI3K/Akt and mitochondrial preservation
Ma et al., Mol Endocrinol 2007 : BRCA1 underexpression also enhanced estrogen-inducible ER-alpha activity in a PI3K/Akt dependent manner
Boland et al., Steroids 2008 : ERbeta plays a major role in the inhibition of apoptosis by 17beta-estradiol at the level of mitochondria, whereas ERalpha and ERbeta mediate the activation of Akt to the same extent, suggesting differential involvement of ER isoforms depending on the step of the apoptotic/survival pathway involved
Wang et al., Biochim Biophys Acta 2008 (Breast Neoplasms) : The estrogen receptor interacting protein HPIP increases estrogen-responsive gene expression through activation of MAPK and AKT ... Here, we report that hematopoietic PBX interacting protein ( HPIP ) interacts both with ERalpha and with ERbeta, and increases ERalpha target gene expression through activation of MAPK and AKT and enhanced ERalpha phosphorylation
Park et al., Cell Signal 2008 : We have investigated the effect of Akt on estrogen receptor (ER) alpha protein level and its transcriptional activity ... Transient transfection studies revealed that constitutively active Akt1 up-regulated ERalpha at the post-transcriptional level ... Studies using Akt inhibitor and dominant negative Akt1 showed that Akt1 kinase activity is required for the up-regulation of ERalpha ... Cycloheximide decay assays and studies with proteasome inhibitor indicated that Akt1 mediated up-regulation of ERalpha was maintained by inhibiting proteasome mediated degradation of ERalpha ... The inhibitory effect of Akt1 on ERalpha transcriptional activity was not attributable to changes in subcellular distribution of ERalpha ... Taken together, these data suggest that Akt1 could increase ERalpha protein level with simultaneous reduction in its transcriptional activity, possibly by modulating association of ERalpha to the target gene promoters
Lee et al., Mol Cells 2008 (Breast Neoplasms) : In contrast, the effect of the PI3K/Akt inhibitor on ER alpha was blocked in cells that were treated with LY294002 in the presence of the proteasome inhibitors
Bhat-Nakshatri et al., Mol Cell Biol 2008 (Breast Neoplasms) : In this study, we analyzed the effect of AKT on genome-wide ERalpha binding in MCF-7 breast cancer cells ... Combining the ERalpha DNA binding pattern with gene expression data from primary tumors revealed specific effects of AKT on ERalpha binding and estrogen regulated expression of genes that define prognostic subgroups and tamoxifen sensitivity of ERalpha positive breast cancer
Hwang et al., Toxicol Appl Pharmacol 2008 : Mechanism of phytoestrogen puerarin mediated cytoprotection following oxidative injury : estrogen receptor dependent up-regulation of PI3K/Akt and HO-1
Yang et al., Zhonghua Yi Xue Za Zhi 2008 : Estrogen receptor may play a role in estrogen induced Akt activation
Van Themsche et al., Endocr Relat Cancer 2009 (Breast Neoplasms...) : In these cells, only the hybrid induced apoptosis in an ERalpha dependent manner, inactivated both X-linked inhibitor of apoptosis protein and Akt , and induced selective nuclear accumulation of ERalpha and the expression of ER-regulated genes c-myc and tff1, which was blocked by ERalpha-specific antagonist ICI 282 780
Chang et al., Anticancer Res 2009 (Breast Neoplasms) : Our results showed that in MCF-7 cells KGF increased Akt phosphorylation and induced ER-alpha mRNA expression which could be blocked by a PI3K/Akt pathway inhibitor, LY
Galluzzo et al., Am J Physiol Cell Physiol 2009 : In particular, ER-alpha dependent Akt activation participates in regulating the first step of myogenic differentiation
Sunters et al., J Biol Chem 2010 : Strain related IGF-IR activation of AKT requires estrogen receptor alpha (ERalpha) with which IGF-1R physically associates
Papa et al., J Cell Sci 2011 : Upon IMS stress, overproduction of reactive oxygen species ( ROS ) and phosphorylation of AKT triggers estrogen receptor ( ER ) activity, which further upregulates the transcription of the mitochondrial regulator NRF1 and the IMS protease OMI ( officially known as HTRA2 )
Hwang et al., Toxicol Appl Pharmacol 2011 : These results indicate that puerarin stimulates eNOS phosphorylation and NO production via activation of an estrogen receptor mediated PI3K/Akt- and CaMKII/AMPK dependent pathway
Jain et al., Nanomedicine (Lond) 2012 (MAP Kinase Signaling System) : Our findings demonstrate that in vitro cadmium containing QDs induce cellular proliferation, estrogen receptor a activation , and biphasic phosphorylation of AKT and ERK1/2, comparable with 17ß-estradiol
Hashimoto et al., Evidence-based complementary and alternative medicine : eCAM 2012 : These results suggest that ginsenoside Rb1 protects PC12 cells from caspase-3 dependent apoptosis through stimulation of estrogen receptor with consequent activation of ERK1/2 and Akt and inhibition of SAPK/JNK and p38