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ATF3 — EPHB2

Text-mined interactions from Literome

Inoue et al., Genes Cells 2004 : Furthermore, the ERK pathway inhibits the TNFalpha mediated induction of ATF3 mRNA, but not its stability, suggesting the involvement of ERK activity in the transcriptional regulation of the ATF3 gene
Keeton et al., Endocrinology 2005 (Carcinoma, Hepatocellular...) : We report that : 1 ) insulin induced transcription of ATF-3 , Pip92, and Insig-1 required MEK-ERK activation ; 2 ) insulin induced transcription of ATF-3 and Pip92 reached maximum levels within 15 min and was blocked by wortmannin but not LY294002 ; 3 ) in contrast, the maximum level of insulin induced transcription of Insig-1 was delayed and was not blocked by either wortmannin or LY294002 ; 4 ) insulin activated ERK1/2 in two distinct phases, a rapid peak and a later plateau ; 5 ) the delayed plateau phase of insulin induced ERK1/2 activation was partially phosphatidylinositol 3-OH-kinase dependent ; and 6 ) however, the rapid, insulin induced peak of ERK1/2 activation was blocked by wortmannin but not LY294002
Hamdi et al., DNA repair 2008 (Brain Neoplasms...) : Furthermore, JNK but not ERK is required for ATF3 induction, and both ERK and JNK are necessary for post-transcriptional induction of Fra1 in response to cisplatin or UV
Sandnes et al., Cell Physiol Biochem 2010 : Combined inhibition of JNK and p38, and of ERK1/2 and either JNK or p38 suppressed vasopressin induced expression of LRF-1/ATF3
Prickaerts et al., Epigenetics & chromatin 2012 : H3S28 phosphorylation by itself appears not sufficient to induce PRC1/chromatin dissociation, nor ATF3 transcription, as inhibition of MEK/ERK signaling blocks BMI1/chromatin dissociation and ATF3 expression, despite induced H3S28 phosphorylation
Wu et al., Mol Cell Neurosci 2013 : This effect is independent of tPA 's proteolytic properties and leads to a rapid and transient phosphorylation of the extracellular signal regulated kinases1/2 ( ERK1/2 ), with ERK1/2 mediated activation of the cAMP response element binding protein ( CREB ) and induction of the neuroprotective CREB regulated activating transcription factor 3 (Atf3)