Gene interactions and pathways from curated databases and text-mining

◀ Back to EGFR

EGFR — PRL

Text-mined interactions from Literome

Huang et al., Oncogene 2006 (Breast Neoplasms) : Notably, PRL also caused phosphorylation of the EGFR and ErbB-2 at sites detected by PTP101, an antibody that recognizes threonine phosphorylation at consensus motifs for ERK induced phosphorylation ... Our data suggest that PRL synergistically augments EGF signaling in T47D breast cancer cells at least in part by lessening EGF induced EGFR downregulation and that this effect requires PRL induced ERK activity and threonine phosphorylation of EGFR
Muraoka-Cook et al., Mol Endocrinol 2008 : We found that full prolactin mediated STAT5A activation and binding to the endogenous beta-casein promoter required ErbB4/HER4 but did not require ErbB1/epidermal growth factor receptor
Vlotides et al., Cancer Res 2008 (Pituitary Neoplasms...) : These results show that EGFR inhibition controls tumor growth and PRL secretion in experimental lacto-somatotroph tumors
Li et al., Cell Signal 2008 (Fibrosarcoma) : GH- or PRL induced EGFR phosphorylation alters subsequent EGF induced EGFR downregulation and signal characteristics in an ERK dependent fashion
Fukuoka et al., Mol Endocrinol 2011 (Prolactinoma) : Because human epidermal growth factor receptor 2 ( HER2 ) /ErbB2 is overexpressed in prolactinomas and ErbB receptor ligands regulate prolactin (PRL) gene expression, we tested the role of HER2/ErbB2 in prolactinoma hormone regulation and adenoma cell proliferation to assess the rationale for targeting this receptor for prolactinoma therapy ... Lapatinib, a dual tyrosine kinase inhibitor ( TKI ) of both epidermal growth factor receptor (EGFR)/ErbB1 and HER2, blocked receptor signaling, and suppressed PRL expression more than gefitinib, a TKI of EGFR/ErbB1
Dahlhoff et al., J Biol Chem 2011 : In vivo evidence for epidermal growth factor receptor (EGFR) mediated release of prolactin from the pituitary gland
Al-Aidaroos et al., J Clin Invest 2013 (Colorectal Neoplasms) : Mechanistically, PRL-3 induced activation of EGFR was attributed primarily to transcriptional downregulation of protein tyrosine phosphatase 1B (PTP1B), an inhibitory phosphatase for EGFR