◀ Back to JUN

GNRH1 — JUN

Text-mined interactions from Literome

Mulvaney et al., J Biol Chem 2000 (Calcium Signaling) : GnRH induced induction and activation of the JNK target c-Jun was inhibited after chelation of intracellular calcium, whereas induction of c-Fos, a known target of ERK, was unaffected
Roelle et al., J Biol Chem 2003 (MAP Kinase Signaling System) : Activation of c-Jun N-terminal kinase and p38 MAPK by GnRH was unaffected by EGFR or gelatinase inhibition that, however, suppressed GnRH induction of c-Jun and c-Fos
Kraus et al., Cancer Res 2004 (MAP Kinase Signaling System...) : Using specific inhibitors, we found that the apoptotic effect of GnRH-a is mediated by c-Jun NH2-terminal kinase (JNK) and inhibited by the phosphatidylinositol 3'-kinase (PI3K)-protein kinase B (PKB) pathway
Salisbury et al., Mol Endocrinol 2009 : GnRH regulated expression of Jun and JUN target genes in gonadotropes requires a functional interaction between TCF/LEF family members and beta-catenin ... GnRH regulates gonadotrope function through a complex transcriptional network that includes three members of the immediate early gene family : Egr1, Jun , and Atf3 ... Reduction of beta-catenin in LbetaT2 cells, through stable expression of short hairpin RNA, also selectively compromises GnRH regulation of Jun expression and levels of JUN protein ... Together, these results indicate that GnRH regulation of Jun transcription requires a functional interaction between TCF/LEF and beta-catenin and that alteration of either impacts expression of JUN downstream targets such as Cga
Binder et al., Mol Endocrinol 2012 (Calcium Signaling) : GnRH regulation of Jun and Atf3 requires calcium, calcineurin, and NFAT ... In this study we tested the hypothesis that GnRH specifically regulates the accumulation of Jun and Atf3 mRNA through a pathway that includes intracellular Ca²?, calcineurin, and nuclear factor of activated T cells ( NFAT ) ... Additionally, although small interfering RNA specific for Nfat4 only marginally reduced GnRH regulation of Jun , Fos, and Atf3 mRNA accumulation, activity of an activator protein-1-responsive reporter construct was reduced by 48 %
Lindaman et al., Mol Cell Endocrinol 2013 (MAP Kinase Signaling System) : Here, we investigate the mechanism of c-Jun induction by GnRH , the sole regulator of c-Jun in the gonadotrope ... We identify that GnRH phosphorylates ATF2 via p38 and JNK, the same pathways responsible for GnRH induction of c-Jun ... Functional ATF2 is necessary for both GnRH induction of c-Jun and FSHß ... Taken together, these studies elucidate the specificity of c-Jun induction by GnRH in the gonadotrope by demonstrating GnRH activation of the p38 and JNK signaling pathways that lead to phosphorylation of ATF2, providing critical insight into GnRH regulation of its target gene, the gonadotropin subunit FSHß
Andrade et al., Mol Endocrinol 2013 : GnRH also stimulated c-Jun N-terminal kinase (JNK) and ERK activation, whereas insulin alone stimulated Akt
Bruder et al., Mol Endocrinol 1996 : Phorbol ester inhibition of rat gonadotropin releasing hormone promoter activity : role of Fos and Jun in the repression of transcription
Levi et al., Mol Endocrinol 1998 : Stimulation of Jun N-terminal kinase (JNK) by gonadotropin releasing hormone in pituitary alpha T3-1 cell line is mediated by protein kinase C, c-Src, and CDC42 ... In this study, GnRH was shown to activate Jun N-Terminal Kinase (JNK)/SAPK in alpha T3-1 cells in a PKC- and tyrosine kinase dependent manner
Jung et al., Brain Res Mol Brain Res 1998 : Since NMDA ( 100 microM ) and SNP ( 1 microM ) markedly induced c-jun expression, but not c-fos expression, we hypothesized that Jun activation is responsible for the transcriptional activation of GnRH gene expression