Gene interactions and pathways from curated databases and text-mining

◀ Back to MAPK3

ESR1 — MAPK3

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: MAPK3 → estradiol/ESR1 complex (ESR1) (increases, ESR1 Activity)
    Duan et al., J Biol Chem 2001*
    Evidence: The results showed that transcriptional activation of the SRE by E2 was due to ERalpha activation of the MAPK pathway...The role of ERalpha expression in mediating increased reporter gene activity was further investigated and shown to be related to enhanced ERK1/2 activation...in cells transfected with pSS and ERalpha or HE11 (DNA binding domain deletion), E2 induced CAT activity; similar results were observed for CHO cells using pSRE (Fig. 3E), suggesting that this kinase-dependent response i...
  • OpenBEL Selventa BEL large corpus: MAPK3 → estradiol/ESR1 complex (ESR1) (increases, ESR1 Activity)
    Acconcia et al., J Cell Physiol 2005*
    Evidence: The E2-ER alpha complex rapidly activated multiple signal transduction pathways (i.e., ERK/MAPK, PI3K/AKT) committed to both cell cycle progression and apoptotic cascade prevention.
  • OpenBEL Selventa BEL large corpus: ESR1 → MAPK3 (directlyIncreases, ESR1 Activity)
    Evidence: 7838153;12093745;9528769;10949034;16076840;15528270;15461668;15059947;12118371;7491495
  • OpenBEL Selventa BEL large corpus: ESR1 → MAPK3 (directlyIncreases, ESR1 Activity)
    Evidence: For instance, activation of epidermal growth factor receptor (EGFR) by EGF leads to phosphorylation of the Ser118 residue in the ERalpha AF-1 domain by p44/42 mitogen-activated protein kinase (MAPK), which in turn recruits the coactivator p68/p72 and activates target gene transcription in a ligand-independent manner [80,81].

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Improta-Brears et al., Proc Natl Acad Sci U S A 1999 (Breast Neoplasms) : In this study, we have used a pharmacological approach to dissect this novel pathway in MCF-7 breast cancer cells and have determined that in the presence of endogenous estrogen receptor , activation of MAPK by E2 is preceded by a rapid increase in cytosolic calcium
Lu et al., Endocrinology 2001 : These results indicate that induction of the TGFbeta3 promoter by the E(2)/ERalpha complex requires the concomitant activation of PKC and MAPK signaling and provide a novel framework for the design of more effective estrogen based therapeutic strategies
de Jager et al., J Biol Chem 2001 : Egr-1 mRNA and protein were rapidly and strongly induced by estrogen in an estrogen receptor dependent manner via the extracellular signal regulated kinase, ERK1/2
Song et al., Mol Endocrinol 2002 (Breast Neoplasms) : Together our results demonstrate that ERalpha can mediate the rapid effects of E2 on Shc, MAPK , Elk-1, and morphological changes in breast cancer cells
Lu et al., FEBS Lett 2002 : Induction of nuclear localization of ERalpha by estrogen independent, but not estrogen dependent stimulation was blocked by both pharmacologic and genetic inhibition of mitogen activated protein ( MAP ) kinase activation
Atanaskova et al., Oncogene 2002 (Breast Neoplasms) : Immunohistochemical staining demonstrates that progesterone receptor (PR) and pS2, two E ( 2 ) -regulated gene products, are significantly increased in MEK/MCF-7 cell tumors compared to those of MCF-7 control tumors, suggesting that activation of ERalpha by MAPK enhances the expression of E ( 2 ) -regulated genes and accelerates tumor growth
Zhang et al., Biochem Biophys Res Commun 2002 : This study further determines the cause and effect relationship between the presence of membrane ERalpha and MAPK activation
Ostrovsky et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Specific activation of MAPK by expression of an active Raf1-estrogen receptor chimera protein reduced significantly the number of myoblasts undergoing programmed cell death in the differentiation medium
Martin et al., J Biol Chem 2003 (Breast Neoplasms...) : However, the complete suppression of MAPK activity in the LTED cells did not inhibit ERalpha Ser118 phosphorylation suggesting that ER activity remained ligand-dependant
Geraldes et al., Circ Res 2003 (MAP Kinase Signaling System) : These results suggest that in PSMCs, 17betaE reduces p42/44 and p38 MAPK activity through ERbeta stimulation, whereas in contrast, in porcine aortic endothelial cells, 17betaE induces p42/44 and p38 MAPK through ERalpha activation
Song et al., Proc Natl Acad Sci U S A 2004 : Down-regulation of Shc, ERalpha , or IGF-1R with specific small inhibitory RNAs all blocked E2-induced mitogen activated protein kinase phosphorylation
Catalano et al., J Biol Chem 2004 (Disease Progression...) : Taking into account that unliganded ERalpha is an effector of mitogen activated protein kinase ( MAPK ) signal and that leptin is able, via Janus kinase, to activate the Ras dependent MAPK pathway, in the present study we investigate the ability of leptin to transactivate ERalpha
Holloway et al., Mol Endocrinol 2004 (Breast Neoplasms...) : Here, we show that down-regulation of ERalpha is not mediated by a specific ERK-1 vs. ERK-2 substrate
Tang et al., Endocrinology 2004 (Breast Neoplasms...) : Thyroid hormone causes mitogen activated protein kinase dependent phosphorylation of the nuclear estrogen receptor ... Because estrogen can activate MAPK and cause MAPK dependent serine phosphorylation of nuclear estrogen receptor (ER)alpha , we studied whether thyroid hormone also promoted MAPK mediated ERalpha phosphorylation
Simoncini et al., Steroids 2004 : For instance, estrogens and glucocorticoids trigger rapid vasodilatation due to rapid induction of nitric oxide synthesis in endothelial cells via the estrogen receptor dependent activation of MAPK and PI3K, leading to relevant pathophysiological consequences, in vitro and in vivo
Yen et al., Mol Pharmacol 2005 : Taken together, such results provide evidence that diosgenin up-regulates VEGF-A and promotes angiogenesis in preosteoblast-like cells by a hypoxia-inducible factor-1alpha dependent mechanism involving the activation of src kinase, p38 MAPK , and Akt signaling pathways via estrogen receptor
Kronblad et al., Oncogene 2005 (Breast Neoplasms) : MAPK signaling as well as ERalpha regulation has earlier been independently linked to hypoxia and we now demonstrate HIF-1alpha and ERK1/2-activation in vivo towards the necrotic zone in DCIS of the breast, parallel with ERalpha downregulation
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
Frigo et al., Mol Endocrinol 2006 : Here, we demonstrate that the p38 MAPK stimulates both ERalpha- and ERbeta mediated transcription in MCF-7 breast carcinoma, Ishikawa endometrial adenocarcinoma, and human embryonic kidney 293 cells
Creighton et al., Cancer Res 2006 (Breast Neoplasms...) : Our results confirm that increased MAPK activation causes loss of ERalpha expression and suggest that hyperactivation of MAPK plays a role in the generation of the ERalpha- phenotype 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
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
Di et al., Hum Reprod 2008 (Leiomyoma...) : ER alpha is involved in the transient activation of ERK/mitogen activated protein kinase ( MAPK ) by genistein via its early association with IGF-IR, leading to hyper-responsiveness of LM cells and confirming that ER signaling is enhanced by activation of ERK/MAPK in LM cells
Sabnis et al., Cancer Res 2008 (Breast Neoplasms...) : The expression of phosphorylated mitogen activated protein kinase ( MAPK ) was reduced and ERalpha and aromatase levels increased compared with LTLT-Ca cells and were similar to levels in MCF-7Ca cells
Liu et al., J Nutr Biochem 2010 (Breast Neoplasms) : Delayed activation of extracellular-signal regulated kinase 1/2 is involved in genistein- and equol induced cell proliferation and estrogen-receptor-alpha mediated transcription in MCF-7 breast cancer cells
Yamnik et al., FEBS Lett 2010 (Breast Neoplasms) : mTOR/S6K1 and MAPK/RSK signaling pathways coordinately regulate estrogen receptor alpha serine 167 phosphorylation
Sabnis et al., Mol Cancer Ther 2010 : In off group tumors, Her-2/p-MAPK activation gradually decreased and ERalpha and aromatase protein ( and activity ) increased
Kang et al., Mol Endocrinol 2010 : G1 induced activities mediated by ER-alpha36, such as transcription activation activity of a VP16-ER-alpha36 fusion protein and activation of the MAPK/ERK1/2 in ER-alpha36 expressing cells
Mendoza et al., J Endocrinol 2011 : The reduction in the p38 MAPK activity caused a significant increase in the expressions of estrogen receptor-a ( ERa ) and the progesterone receptor, but eliminated the expression of ERß
Kato et al., Science 1995 : Activation of the estrogen receptor through phosphorylation by mitogen activated protein kinase
Joel et al., J Biol Chem 1998 : Estradiol induced phosphorylation of serine 118 in the estrogen receptor is independent of p42/p44 mitogen activated protein kinase