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ERBB2 — PRL
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
ERBB2
→
PRL
(increases)
Evidence: Our results indicate that autocrine secretion of PRL stimulates tyrosine phosphorylation of ErbB-2 by Jak2, provides docking sites for Grb2 and stimulates Ras-MAP kinase cascade, thereby causing unrestricted cellular proliferation.
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OpenBEL Selventa BEL large corpus:
ERBB2
→
PRL
(increases)
Evidence: Prolactin (Prl), which also activates Jak2 after binding its cognate receptor, has been shown to cause an increase in ErbB2 phosphorylation. Moreover, blocking autocrine production of Prl in breast tumor cells led to a reduction in ErbB2's phosphotyrosine content and a decrease in MAPK activity [44].
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
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