| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.63493876 |
| Moreover , we found that ERalpha binds to the p85alpha regulatory subunit of PI3K in the absence or presence of estradiol in epithelial cells and subsequently activates PI3K / AKT2 , suggesting ERalpha regulation of PI3K / AKT2 through a nontranscriptional and ligand independent mechanism . 0.63493876^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Therefore , nascent apoB is subject to ER associated degradation , re uptake , and a third distinct degradative pathway that appears to target lipoproteins after considerable assembly and involves a post ER compartment and PI3K signaling . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| These findings indicate that PRL stimulation of ERalpha expression requires Jak 2 and also that PRL can induce Stat5b phosphorylation through two tyrosine kinases , Jak 2 and one downstream of PI3K . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Activation of eNOS by raloxifene was blocked by the PI3K inhibitor wortmannin and by the ER antagonist ICI 182 , 780 but not by transcriptional or translational inhibitors . ^^^ The ability of raloxifene to facilitate ERalpha PI3K interaction may provide additional insight into the structure function relationship of specific SERMs , which promote the nontranscriptional effects of ER . . ^^^ The selective estrogen receptor modulator ( SERM ) raloxifene is effective for the treatment of postmenopausal osteoporosis , but its ability to activate eNOS via PI3K is unknown . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| We have recently described a novel , non transcriptional mechanism for ER signaling in human as well as in animal endothelial cells , showing that ER alpha can physically and functionally couple to the lipid kinase phosphatidylinositol 3 OH kinase ( PI3K ) . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| To evaluate the role of the phosphatidylinositol 3 kinase ( PI3K ) / Akt pathway in breast cancer cell survival and therapeutic resistance , we analyzed a panel of six breast cancer cell lines that varied in erbB 2 and estrogen receptor status . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| VEGF A expression in rat pituitary tumor cells is mediated through ER independent but PI3K Akt dependent signaling pathway . 17alpha E ( 2 ) , a weak estrogen exhibited both agonistic and antagonistic effects , and caused a time and dose dependent induction of VEGF A mRNA expression in GH 3 rat pituitary tumor cells . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Third , constitutively active PI3K or Akt induced ER activity but reduced PR levels and activity . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| 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 . ^^^ Because PI3K is mainly a cytoplasmic complex , we studied the cellular site of interaction between this enzyme and ERalpha , and we dissected the molecular mechanisms that mediate this interaction . ^^^ METHODS AND RESULTS : By using cultured human saphenous vain endothelial cells , we found that cell membrane bound ERalpha colocalizes with PI3K and may be responsible for PI3K activation . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Activation of ERK1 / 2 by deltaRaf 1 : ER * represses Bim expression independently of the JNK or PI3K pathways . ^^^ The ability of deltaRaf 1 : ER * to repress Bim ( EL ) expression required the ERK pathway but was independent of the PI3K > PDK > PKB pathway . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Here we demonstrate the ability of DeltaMEK 1 : ER to activate the phosphatidylinositol 3 kinase ( PI3K ) / Akt / p70 ribosomal S 6 kinase ( p 70 ( S6K ) ) pathway and the importance of this pathway in MEK 1 mediated prevention of apoptosis . ^^^ Stimulation of DeltaMEK 1 : ER by 4HT resulted in ERK , PI3K , Akt and p 70 ( S6K ) activation . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| The results showed that the PI3K pathway , as well as ER , were strongly involved in both G 1 S progression and cyclin D 1 promoter activity by acting on its proximal region ( 254 base pairs ) . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| In breast cancer cells , PI3K / Akt and mTOR pathways seem to be critical for the proliferative responses mediated by the epidermal growth factor receptor , the insulin growth factor receptor , and the estrogen receptor . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| In contrast , treatment of cells with LY 294002 , to inhibit phosphoinositide 3 kinase ( PI3K ) , caused downregulation of Bcl 2 and Mcl 1 and allowed deltaMEKK 1 : ER * to elicit a robust apoptotic response characterized by activation of Bax and caspases . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Simultaneous incubation of the vessels with 17beta E 2 plus ICI , 182 , 780 , an estrogen receptor antagonist , or wortmannin , an inhibitor of phosphatidylinositol 3 kinase ( PI3K ) phosphorylation or the transcriptional inhibitor DRB , prevented the reduced arteriolar tone and the enhanced CYP mediated FID caused by incubation of vessels with 17beta E 2 . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Addition of the estrogen receptor antagonist tamoxifen did not reverse the protective effect of betaE 2 , whereas the PI3K inhibitor LY 294002 inhibited the protective effect of betaE 2 , suggesting that betaE 2 mediates its effect through some PI3K dependent pathway , independent of the estrogen receptor . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Recent data have indicated that the estrogen receptor alpha ( ERalpha ) , through interaction with p 85 , regulates phosphoinositide 3 kinase ( PI3K ) activity , revealing a physiologic , nonnuclear function of the ERalpha potentially relevant in cell proliferation and apoptosis . ^^^ In our study , using MCF 7 , we have analyzed the ability of RES to modulate the ERalpha dependent PI3K pathway . ^^^ Immunoprecipitation and kinase activity assays showed that RES increased the ERalpha associated PI3K activity with a maximum stimulatory effect at concentrations close to 10 microM ; concentrations > 50 microM decreased PI3K activity . ^^^ Stimulation of PI3K activity by RES was ERalpha dependent since it could be blocked by the antiestrogen ICI 182 , 780 . ^^^ Nevertheless , the amount of PI3K immunoprecipitated by the ERalpha remained unchanged in presence of RES , indicating that ERalpha availability was not limiting PI3K activity . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| For instance we have provided , for the first time , a different interaction of the two ERs with the PI3K / Akt pathway , because ER alpha interacts with the p 55 regulatory subunit of PI3K , whereas ER beta interacts with Akt 1 . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Cytokine independent cells were obtained from DeltaMEK 1 : ER infected cells at a frequency of 5 10 10 ( 5 ) indicating that low frequency of cells expressing beta estradiol regulated DeltaMEK 1 : ER became factor independent , while activated PI3K or Akt by themselves did not relieve cytokine dependence . ^^^ In contrast , cytokine independent cells were recovered approximately 25 to 250 fold more frequently from DeltaMEK 1 : ER infected cells also infected with either activated PI3K or Akt . ^^^ MEK / PI3K and MEK / Akt responsive cells could be maintained long term as long as either beta estradiol or the estrogen receptor antagonist 4 hydroxy tamoxifen ( 4HT ) were provided . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| We also describe the rapid assembly of a membrane associated molecular complex , comprised of ER , c Src and the regulatory unit of phosphatidylinositol 3 kinase ( PI3K ) , p 85 , in response to estrogen . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| A possible direct interaction between ERalpha and PPARgamma was ascertained by co immunoprecipitation assay , whereas their modulatory role in the phosphatidylinositol 3 kinase ( PI3K ) / AKT pathway was evaluated by determining PI3K activity and AKT phosphorylation . ^^^ Moreover , we have documented the physical and functional interactions of ERalpha and PPARgamma , which also involve the p 85 regulatory subunit of PI3K . ^^^ Interestingly , ERalpha and PPARgamma pathways have an opposite effect on the regulation of the PI3K / AKT transduction cascade , explaining , at least in part , the divergent response exerted by the cognate ligands 17beta estradiol and BRL 49653 on MCF 7 cell proliferation . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Akt phosphorylation by estradiol was inhibited by the PI3K inhibitor , wortmannin , but not by the ER antagonist , ICI 182 780 . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| This benzo [ a ] pyrene induced osteoblast proliferation could be inhibited by the estrogen receptor antagonist ICI 182780 and tamoxifen , PD 98059 [ extracellular signal regulated kinase ( ERK ) / mitogen activated protein kinase ( MAPK ) inhibitor ] , and LY 294002 [ phosphatidylinositol 3 kinase ( PI3K ) inhibitor ] but not alpha naphthoflavone ( aryl hydrocarbon receptor antagonist ) and SB 203580 ( p 38 MAPK inhibitor ) . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Stimulation of 5 ErbB : ER activity resulted in the activation of the phosphatidylinositol 3 kinase ( PI3K ) / Akt and Raf / MEK / ERK kinase cascades . ^^^ MEK or PI3K inhibitors suppressed ERK or Akt activation , respectively , and induced apoptosis in the 5 ErbB : ER responsive cells . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| In this report we have explored the mechanism linking the loss of expression of ERalpha in breast cancer cells with overexpression of Her 2 / neu , which signals constitutively via a phosphatidylinositol 3 kinase ( PI3K ) / Akt kinase pathway . ^^^ 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 . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| We previously showed that RES alters the cell cycle and induces apoptosis in MCF 7 breast tumor cells by interfering with the estrogen receptor ( ERaalpha ) dependent phosphoinositide 3 kinase ( PI3K ) pathway . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| As a whole , these studies suggest that E 2 induction of TGF beta release from cortical astrocytes could provide a mechanism of neuroprotection , and that E 2 stimulation of TGF beta expression and release from astrocytes occurs via an ER dependent mechanism involving mediation by the PI3K / Akt signaling pathway . . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Recently , it has been known that ER activates phosphatidylinositol 3 OH kinase ( PI3K ) through binding with the p 85 regulatory subunit of PI3K . ^^^ Therefore , possible mechanisms may include ER mediated phosphoinositide metabolism with subsequent formation of phosphatidylinositol 3 , 4 , 5 trisphosphate ( PIP ( 3 ) ) , which is generated from phosphatidylinositol 4 , 5 bisphosphate via PI3K activation . ^^^ The present study demonstrates that 17beta estradiol ( E 2 ) up regulates PI3K in an ERalpha dependent manner , but not ERbeta , and stimulates cell growth in breast cancer cells . ^^^ However , these effects of E 2 on breast cancer cells were not observed in the MDA MB 231 cell line , indicating that the E 2 mediated up regulation of PI3K / Akt pathway is ERalpha dependent . ^^^ These results suggest that estrogen activates PI3K / Akt signaling through ERalpha dependent mechanism in MCF 7 cells . . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Transfection of PI3K siRNA in breast cancer cells resulted in a significant decrease in cell viability and induction of apoptosis irrespective of their estrogen receptor alpha ( ERalpha ) or ErbB 2 status . ^^^ PI3K depletion also resulted in a significant G ( 1 ) phase cell cycle arrest in ERalpha positive breast cancer cells . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| We have shown that growth factor signaling pathways can directly down regulate PR levels via the phosphatidylinositol 3 ' kinase ( PI3K ) / Akt / mTOR pathway , and that this can occur independent of ER . ^^^ Furthermore , loss of PTEN , a negative regulator of the PI3K / Akt signaling pathway , has been shown to be associated with specific loss of PR and no change in ER levels . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| In addition , we investigated the regulation of ER protein levels as a potential mechanism for its regulation by the PI3K / GSK3 pathway ; GSK 3 blockade increased ERalpha protein stability , whereas PI3K inhibition decreased it . ^^^ In summary , our findings suggest that ER dependent gene expression in N2a cells is controlled by the PI3K / Akt / GSK3 signaling pathway . . ^^^ In this report we present evidence suggesting that glycogen synthase kinase 3 ( GSK 3 ) , an effector kinase of the phosphatidylinositol 3 kinase ( PI3K ) pathway , may affect ERalpha activity in N2a neuroblastoma cells . ^^^ Pharmacological or genetic inhibition of the PI3K / Akt pathway , whose activity is inversely correlated with that of GSK 3 , increased ERalpha mediated transcription , and this effect was blocked by GSK 3 inhibitors . ^^^ As in other cell types , IGF 1 increased ERalpha activity in absence of estradiol by a mechanism independent of PI3K . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| Here we show that the ER isoform , ER alpha , binds in a ligand dependent manner to the p85alpha regulatory subunit of phosphatidylinositol 3 OH kinase ( PI ( 3 ) K ) . ^^^ Recruitment and activation of PI ( 3 ) K by ligand bound ER alpha are independent of gene transcription , do not involve phosphotyrosine adapter molecules or src homology domains of p85alpha , and extend to other steroid hormone receptors . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| In turn , stimulation of Src activity is abolished in ERalpha expressing NIH 3T3 fibroblasts by co transfection of the dominant negative p85alpha and in MCF 7 cells by the PI 3 kinase inhibitor , LY 294002 . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| ERalpha protein ( 66 and 50 kDa ) coimmunoprecipitated with eNOS as well as with the p85alpha regulatory subunit of PI 3 kinase , further implicating ERalpha in kinase activation of eNOS . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| PI3K / Akt signaling pathway by estrogen receptor ( ER ) dependent and ER independent mechanisms in endometrial cancer cells . ^^^ The main aims are to study if PI3K / Akt signaling pathway can be activated by 17beta estradiol ( E 2 ) via non nuclear action and to investigate the relationship of the action of E 2 and ER in endometrial cancer cells expressing with different status of ER . ^^^ ICI 182780 could block the activation of PI3K / Akt in ER positive Ishikawa cells but not in HEC 1A cells with poor expressed ER . ^^^ This study demonstrated that E 2 is able to promptly activate PI3K / Akt signal pathway in Ishikawa cells in an ER dependent manner and ER independent in HEC 1A cells . ^^^ Blockage of PI3K / Akt cascade may become a potential and effective way to control endometrial carcinoma , especially in ER negative cancers , which show no response to endocrinal therapy . . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| These findings suggested that 5GG might be a useful chemopreventive or therapeutic agent for hormone dependent breast cancer through suppressing the functions of ERalpha by lysosome dependent depletion and modulating the ErbB / PI3K / Akt pathway . . ^^^ Pentagalloylglucose inhibits estrogen receptor alpha by lysosome dependent depletion and modulates ErbB / PI3K / Akt pathway in human breast cancer MCF 7 cells . ^^^ |
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| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| We sought to determine whether E 2 neuroprotective mechanisms are mediated by a unified signaling cascade activated by estrogen receptor ( ER ) PI3K interaction within the same population of neurons or whether E 2 activation of extracellular signal regulated kinase 1 / 2 ( ERK1 / 2 ) and Akt are independent signaling events in different neuronal populations . ^^^ Immunoprecipitation of E 2 treated cortical neurons was conducted to determine a protein protein interaction between ER and the PI3K regulatory subunit p 85 . ^^^ 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 . 17Beta estradiol ( E 2 ) induced neuroprotection is dependent on mitogen activated protein kinase ( MAPK ) and phosphatidylinositol 3 kinase ( PI3K ) signaling cascades . ^^^ |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: P27986 and P03372 |
Pubmed |
SVM Score :0.0 |
| NA |
|