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EPHB2 — GNRH1

Text-mined interactions from Literome

White et al., Mol Endocrinol 1999 : We suggest that GnRH regulation of the GnRHR gene is partially mediated by an ERK dependent activation of a canonical AP-1 site located in the proximal promoter of the GnRHR gene
Mulvaney et al., J Biol Chem 1999 : These observations suggest that calcium influx through L-type channels is required for GnRH induced activation of ERK and c-Fos and that the influence of calcium lies downstream of protein kinase C
Mulvaney et al., J Biol Chem 2000 (Calcium Signaling) : Therefore, although activation of ERK by GnRH requires a specific influx of calcium through L-type calcium channels, JNK activation is independent of extracellular calcium but sensitive to chelation of intracellular calcium
Zhang et al., Mol Cell Endocrinol 2001 : One mechanism requires GnRH induced ERK and JNK activation, while a second MAPK independent pathway requires a thapsigargin-sensitive calcium signal
Gur et al., Comp Biochem Physiol B Biochem Mol Biol 2001 (MAP Kinase Signaling System) : This inhibitor completely blocked GnRH induced increases in ERK activity
Zhang et al., J Biol Chem 2001 (Calcium Signaling) : Egr-1/MGRE binding was induced by GnRH in an ERK dependent manner
Everest et al., Endocrinology 2001 (Breast Neoplasms) : GnRH stimulated ERK2 phosphorylation in Ad GnRH-R infected cells, and this effect, like stimulation of [ ( 3 ) H ] IP accumulation, was blocked by GnRH-R antagonists
Kraus et al., Arch Med Res 2001 (Breast Neoplasms...) : Activation of ERK -- one of the MAPK cascades -- by GnRH in these cells depends mainly on the phosphorylation of Raf1 by PKC, supported by a pathway involving c-Src, dynamin, and Ras
Liu et al., Mol Endocrinol 2002 : GnRH activates ERK1/2 leading to the induction of c-fos and LHbeta protein expression in LbetaT2 cells ... In this paper, we demonstrate that GnRH activates ERK , c-Jun N-terminal kinase, and p38MAPK in the LbetaT2 gonadotrope cell line ... Phosphorylation of both ERK and p38MAPK are stimulated rapidly, 30- to 50-fold in 5 min, but activation of c-Jun N-terminal kinase has slower kinetics, reaching only 10-fold after 30 min. Activation of ERK by GnRH is blocked by inhibition of MAPK kinase ( MEK ) and partially blocked by inhibition of PKC and calcium, but not PI3K or p38MAPK signaling
Liu et al., J Biol Chem 2002 : We have shown previously that GnRH activates ERK and induces the c-fos and LH beta genes in these cells
Allen et al., J Biol Chem 2002 (MAP Kinase Signaling System) : Like Ark, a constitutively active mutant of Rac suppressed GnRH transcription in an ERK dependent manner
Kanasaki et al., Biol Reprod 2002 : GnRH activated ERK , but PACAP did not, and the activation was not inhibited by quinpirol
Shah et al., J Biol Chem 2003 (MAP Kinase Signaling System) : In immortalized hypothalamic GnRH neurons ( GT1-7 cells ), which also express GnRH receptors, GnRH , epidermal growth factor (EGF), and phorbol 12-myristate 13-acetate ( PMA ) caused marked phosphorylation of ERK1/2 ... These findings indicate that Src and Pyk2 act upstream of the EGF receptor to mediate its transactivation, which is essential for GnRH induced ERK1/2 phosphorylation in hypothalamic GnRH neurons
Harris et al., Endocrinology 2003 : Surprisingly, although c-Src is involved in GnRH-A stimulated ERK , its involvement is mapped to another region ( -280/-180 ) containing the glycoprotein-specific element ... Thus, ERK and c-Src but not JNK are involved in basal and GnRH-A-stimulated-alphaCAT , whereas c-Src contribution is independent of ERK activation
Ellsworth et al., Endocrinology 2003 : Neither overexpression of a constitutively active Raf-kinase nor pharmacological blockade of GnRH induced ERK activation eliminated the GnRH response of the GnRHR promoter
Shah et al., J Biol Chem 2003 : Activation of ERK1/2 by the hypothalamic neuropeptide gonadotropin releasing hormone (GnRH) is relatively sustained in alpha T3-1 pituitary gonadotropes and HEK293 cells but is transient in immortalized GT1-7 neurons ... However, GnRH induced ERK1/2 phosphorylation caused by EGFR transactivation was confined to GT1-7 cells and was attenuated by EGFR kinase inhibition ... In contrast, agonist stimulation of GnRH receptors expressed in HEK293 cells caused sustained phosphorylation and nuclear translocation of ERK1/2 by a protein kinase C-dependent but EGFR independent pathway ... GnRH induced activation of ERK1/2 was attenuated by the selective Src kinase inhibitor PP2 and the negative regulatory C-terminal Src kinase in GT1-7 cells but not in HEK293 cells
Chamson-Reig et al., Endocrinology 2003 (Luteoma...) : In the present work, alternate GnRH induced second messengers such as phospholipase A ( 2 ) and phospholipase D activation, cAMP production, ERK1/2 phosphorylation, and the presence of G proteins were evaluated to determine GnRH mechanism of action in tumor cells
Farshori et al., J Steroid Biochem Mol Biol 2003 : GnRH stimulation caused rapid and sustained phosphorylation of ERK1/2 and Pyk2 that was accompanied by their nuclear translocation ... Dominant negative Pyk2 ( PKM ) had no effect on GnRH induced ERK1/2 phosphorylation and c-fos expression ... However, GnRH induced ERK1/2 activation was independent of EGF-R activation ... These results indicate that activation of PKC is responsible for GnRH induced phosphorylation of both ERK1/2 and Pyk2, and that Pyk2 activation does not contribute to GnRH signaling ... Moreover, GnRH induced phosphorylation of ERK1/2 and expression of c-fos in HEK293 cells is independent of Src and EGF-R transactivation, and is mediated through the PKC/Raf/MEK cascade
Liu et al., Endocrinology 2003 (Calcium Signaling) : Activation of individual signaling pathways was able to partially mimic the desensitizing effect of GnRH on ERK , p38 MAPK, c-fos, and LHbeta but not on Gq/11
Roelle et al., J Biol Chem 2003 (MAP Kinase Signaling System) : We found that GnRH induced Src, Ras, and ERK activation were also gelatinase dependent
Bonfil et al., Endocrinology 2004 : ERK activation by GnRH is dependent on protein kinase C ( PKC ), as evident by activation, inhibition, and depletion of 12-O-tetradecanoylphorbol-13-acetate-sensitive PKC subspecies ... ERK activation by GnRH in LbetaT-2 cells does not involve transactivation of epidermal growth factor receptor or mediation via Gbetagamma or beta-arrestin ... Thus, PKC, ERK , JNK, p38, and c-Src, but not Ca ( 2+ ), are involved in GnRH induction of the ovine FSHbeta gene
Nguyen et al., Mol Endocrinol 2004 (MAP Kinase Signaling System) : Based on these findings, we conclude that acute GnRH stimulation of LbetaT2 cells increases translation initiation through ERK signaling
Haisenleder et al., Biol Reprod 2005 : In contrast, both GnRH and T stimulated threefold increases in ERK activity, with additive effects seen following the combination of GnRH+T. E2 had no effect on ERK activity ... In alpha T3 clonal gonadotrope cells, dihydrotestosterone did not activate ERK alone but enhanced and prolonged the ERK responses to GnRH , demonstrating direct effects on the gonadotrope ... Thus, the ERK response to GnRH plus androgen was enhanced in both rat pituitary and alpha T3 cells
Liu et al., Mol Endocrinol 2005 : Adenoviral expression of a kinase-inactive, dominant negative version of PKCdelta impaired GnRH activation of ERK , but not induction of c-Fos and LHbeta proteins, indicating that the novel PKCs signal to the ERK cascade
Roberson et al., Mol Endocrinol 2005 : Our previous studies demonstrate that GnRH induced ERK activation required influx of extracellular Ca2+ in alphaT3-1 and rat pituitary cells ... Inhibition of Cam ( using a dominant negative ) was sufficient to block GnRH induced ERK but not c-Jun N-terminal kinase activity activation
Xie et al., Mol Endocrinol 2005 (MAP Kinase Signaling System) : GnRH induced the alpha-subunit promoter-luciferase reporter approximately 16-fold, and this induction was completely abolished with mutations in the dual cAMP response elements ( CREs ) or the combined inhibition of GnRH induced ERK and c-Jun N-terminal kinase
Klausen et al., Am J Physiol Regul Integr Comp Physiol 2005 (MAP Kinase Signaling System) : PKC and ERK are differentially involved in gonadotropin releasing hormone induced growth hormone gene expression in the goldfish pituitary
Kanasaki et al., Endocrinology 2005 : In contrast, stimulation with continuous GnRH ( 10 nM ) in perifused cells resulted in a more sustained activation of ERK
Caunt et al., J Biol Chem 2006 : Arrestin mediated ERK activation by gonadotropin releasing hormone receptors : receptor-specific activation mechanisms and compartmentalization
Zhang et al., J Mol Endocrinol 2006 : Elevated activity of MKP-2 in alphaT3-1 cells, through either overexpression or activation of the endogenous MKP-2 gene, was correlated with inhibition of GnRH induced activation of ERK and JNK, as well as the expression of ERK- and JNK dependent proto-oncogenes
Kim et al., Endocr Relat Cancer 2006 (Adenocarcinoma...) : In addition, the activation of ERK1/2 by GnRH-I or II was mimicked by phorbol-12-myristate 13-acetate, a PKC activator ... Pretreatment with GF109203X, an inhibitor of PKC, blocked GnRH induced ERK1/2 activation and anti-proliferation ... These results suggest that the activation of PKC is responsible for GnRH induced ERK1/2 activation and anti-proliferation in ovarian cancer cells ... Taken together, these results indicate that binding of GnRH-I and II to the GnRH-I receptor activates ERK1/2 through a PKC dependent pathway and is essential for GnRH induced anti-proliferation of ovarian cancer cells
Navratil et al., Endocrinology 2007 : In the current study, GnRH caused acute and dramatic changes in cellular morphology in the gonadotrope derived alphaT3-1 cell line, which appeared to be mediated by engagement of the actin cytoskeleton ; disruption of actin with jasplakinolide abrogated cell movement and GnRH induced activation of ERK
Nicol et al., J Endocrinol 2008 : We hypothesized that activin and/or GnRH pathways may be modulated by BMP-4, but neither the activin stimulated phosphorylation of Smad2/3 nor the GnRH induced ERK1/2 or cAMP response element binding phosphorylation were modified
Xie et al., Mol Endocrinol 2008 : Calcium influx through L-type voltage gated calcium channels ( VGCC ) is required for ERK activation induced by GnRH in pituitary gonadotropes ... Knockdown of Pyk2 using specific small interfering RNAs revealed that Pyk2 contributed to modulation of GnRH induced ERK but not c-Jun N-terminal kinase activation
White et al., Mol Endocrinol 2008 (MAP Kinase Signaling System) : We show that in Galpha ( q/11 ) -negative cells stably expressing the GnRH receptor, GnRH did not induce activation of ERK , jun-N-terminal kinase, or P38 MAPK ... In contrast to Galpha ( i ) or chimeric Galpha ( qi5 ), transfection of Galpha ( q ) cDNA enabled GnRH to induce phosphorylation of ERK , jun-N-terminal kinase, and P38
Armstrong et al., Mol Endocrinol 2009 : In HeLa cells, GnRH causes transient and protein kinase C ( PKC ) -dependent ERK activation, but termination mechanisms are unknown ... GnRH caused rapid and transient increases in dual phosphorylated ERK2 ( ppERK2 ) and nuclear to cytoplasmic ERK2-green fluorescent protein ( GFP ) ratio, whereas responses to a PKC activating phorbol ester were more sustained ... GnRH also increased expression of nuclear-inducible DUSP1 and -4, but their knockdown did not alter GnRH mediated ERK signaling ... Thus, GnRH mediated ERK responses ( like PKC mediated ERK responses ) are dependent on protein neosynthesis and docking-domain dependent binding, but for GnRH activation ( unlike PKC activation ), this does not reflect dependence on nuclear-inducible DUSPs
Dobkin-Bekman et al., Mol Endocrinol 2009 : A preformed signaling complex mediates GnRH activated ERK phosphorylation of paxillin and FAK at focal adhesions in L beta T2 gonadotrope cells
Park et al., Reproductive biology and endocrinology : RB&E 2009 (Endometrial Neoplasms) : Thus, in the present study, we further examined the possibility that GnRH induces integrin beta3 and activation of focal adhesion kinase ( FAK ) through mitogen activated protein kinases ( MAPKs ), ERK1/2 and p38, to inhibit the growth of HEC1A endometrial cancer cell line
Sari et al., Endocrinology 2009 : Western blotting showed that GnRH stimulated phosphorylation of ERK ( phospho-ERK-1/2 ), and this effect was abolished by RFRP-3
Liu et al., Reproductive biology and endocrinology : RB&E 2010 : In addition, we demonstrated that the activation of JNK, but not ERK1/2 , was required for GnRH I and II-stimulated MMP-26 production in B6Tert-1 cells and primary cytotrophoblasts
Naidich et al., Endocrinology 2010 : PGF ( 2alpha ), PGI ( 2 ), or PGE ( 2 ) had no effect on GnRH stimulated ERK , c-Jun N-terminal kinase, and p38MAPK activation or on GnRH- and high K ( + ) -stimulated intracellular Ca ( 2+ ) elevation in LbetaT2 and gonadotropes in primary culture
Armstrong et al., J Biol Chem 2010 (MAP Kinase Signaling System) : GnRH caused dose dependent ERK2-GFP translocation to the nucleus, providing a live-cell readout for activation ... Pulsatile GnRH caused dose- and frequency dependent ERK2-GFP translocation
Purwana et al., Peptides 2010 : The combination treatment with GnRH and PACAP did not augment the ERK phosphorylation induced by GnRH alone
Takeda et al., Mol Cell Endocrinol 2012 (MAP Kinase Signaling System) : Thus, the difference between BMP-6 and BMP-7 in enhancing GnRH induced FSHß transcription may be due to the differential effects of BMP ligands on GnRH induced ERK signaling
Higa-Nakamine et al., J Cell Physiol 2012 : AG1478, a relatively specific inhibitor of the ErbB family, and small interfering RNA ( siRNA ) for ErbB4 inhibited the GnRH induced activation of ERK in GT1-7 cells, suggesting that EGFR and ErbB4 were necessary for the activation
Sviridonov et al., Mol Cell Endocrinol 2013 (MAP Kinase Signaling System...) : Activation of ERK1/2 by GnRH and PMA was robust in the gonadotrope cell lines, with a smaller effect observed in the prostate cancer cell lines
Andrade et al., Mol Endocrinol 2013 : GnRH also stimulated c-Jun N-terminal kinase (JNK) and ERK activation, whereas insulin alone stimulated Akt