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PIK3R1 — PRL
Text-mined interactions from Literome
Domínguez-Cáceres et al., Oncogene 2004
:
Activation of the
PI3K by
PRL was necessary for the expression of c-MycmRNA and W53 cell proliferation, as the PI3K inhibitor LY294002 abolished them
Romano et al., Endocrinology 2006
:
Although the PRL promoter was not affected by either PI3K/Akt inhibition or activation,
PRL release increased in
response to the pharmacological
PI3K/Akt inhibitors in unstimulated GH4C1 and rat pituitary primary cells
Hügl et al., JOP : Journal of the pancreas 2007
(Insulinoma) :
PI3'K activation was
essential for
prolactin and glucose stimulated INS-1 cell proliferation
Di Rosa et al., J Cell Biochem 2009
(MAP Kinase Signaling System) :
Prolactin induces chitotriosidase expression in human macrophages through PTK,
PI3-K , and MAPK pathways
Chen et al., Genes Dev 2012
:
Surprisingly, we found that mammary differentiation was due to the
PI3K-Akt dependent synthesis and secretion of autocrine
prolactin and downstream activation of the prolactin receptor (Prlr)-Jak-Stat5 pathway ... Our findings reveal that
PI3K-Akt pathway activation is necessary and
sufficient to induce autocrine
prolactin production in the mammary gland, Stat5 activation, and terminal mammary epithelial differentiation, even in the absence of the normal developmental program that prepares the mammary gland for lactation