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FOS — PRL

Text-mined interactions from Literome

Olazabal et al., Mol Endocrinol 2000 : Using PRLR mutants and the PRLR short form, we have found that both homodimerization of PRLR wild type and the integrity of box-1 and C-distal tyrosine of PRLR intracellular domain are needed in PRL induced proliferation and AP-1 activation ... We found that Dex negatively regulates PRL induced proliferation and AP-1 site activation
Cave et al., Neuroendocrinology 2001 : Within the TH-ir neurones, PRL induced a significant increase in c-Fos in the dorsomedial portion of the mid-arcuate nucleus ( p < 0.05 ) ... PRL also induced c-Fos expression in the supraoptic nucleus (SON) ( 11.7 +/- 3.2 vs. 3.0 +/- 1.4 cells/section for PRL and control rats, respectively ; p < 0.05 ), but not in the medial preoptic nucleus, ventromedial nucleus or the dorsomedial nucleus, areas reported to either contain gonadotropin releasing hormone neurones or express PRL receptors
Domínguez-Cáceres et al., Oncogene 2004 : Since IEG are essential for cell cycle progression, we have studied how PRL controls expression of c-Myc mRNA and c-Fos
Gutzman et al., Mol Endocrinol 2005 (Breast Neoplasms...) : Here we demonstrate that PRL and E2 cooperatively enhance the activity of AP-1 in MCF-7 derived cells
Romero-Prado et al., J Cell Biochem 2006 : In the absence of FBS and in the presence of insulin or prolactin , cells show cytoskeletal organization and an AP-1 transcription site activity resembling proliferative osteochondrocytes while cells in the presence of dexamethasone and added prolactin or TGF-beta resembled differentiated osteoblasts
Andria et al., Biochem Biophys Res Commun 2007 : Prolactin expression is induced in Jurkat T-cells by beta-catenin LEF-1, AP-1 and cAMP
Gutzman et al., Oncogene 2007 (Neoplasms) : Stat5 activation inhibits prolactin induced AP-1 activity : distinct prolactin initiated signals in tumorigenesis dependent on cell context ... Further, reduction of Stat5 protein with siRNA in T47D cells, which contain elevated Stat5, increased PRL induced AP-1 signals, transcripts for the AP-1 target, matrix metalloproteinase-2 and associated invasive behavior