Gene interactions and pathways from curated databases and text-mining

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AKT1 — PRL

Text-mined interactions from Literome

Al-Sakkaf et al., J Endocrinol 2000 (Lymphoma) : The aim of the present study was to examine the effect of PRL on the activation of PKB and to find out whether this has any role on the PRL induced survival of Nb2 cells ... Furthermore, Western blot analysis using phosphospecific PKB antibody on lysates from PRL treated Nb2 cells showed that phosphorylation of PKB in response to PRL was inhibited by STS ( 0.5 microM ), but not by Dex ( 100 nM )
Fresno Vara et al., Mol Biol Cell 2001 : Consistently, transient expression of SrcDM in W53 cells also blocked PRL activation of Akt
Tessier et al., Endocrinology 2001 : We have also shown that protein kinase B phosphorylation on serine 473 as well as its nuclear translocation are stimulated by PRL in decidual cells
Hayakawa et al., Endocrinology 2002 : Regulation of the PRL promoter by Akt through cAMP response element binding protein
Ruffion et al., Eur Urol 2003 (Prostatic Neoplasms) : PRL also enhanced the phosphorylation of Akt/PKB in these cells
Secondo et al., J Neurochem 2003 : In addition, exogenous PRL induced a phosphorylation of protein kinase B (PKB) ( Akt ) that was prevented both by the two MAPK inhibitors PD 098059 and U 0126, and by the PI3'-K inhibitors wortmannin and LY-294002
Bailey et al., Mol Endocrinol 2004 : PI3K activates a downstream serine/threonine kinase, Akt ; therefore, we investigated the role of Akt in the interaction between PRL and TGF-beta signaling
Domínguez-Cáceres et al., Oncogene 2004 : PRL stimulation of W53 cells resulted in Akt translocation to the nucleus, phosphorylation of FKHRL1 transcription factor, and its nuclear exclusion
Bishop et al., J Endocrinol 2006 (Lymphoma) : This study showed that PRL stimulated the phosphorylation of mTOR, p70S6K, Akt , and Jak2 kinases in a dose- and time dependent manner in PRL dependent rat Nb2 lymphoma cells
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
Wang et al., Cancer Res 2007 (Colorectal Neoplasms) : In these cells, PRL-3 activates Akt and inactivates glycogen synthase kinase-3beta as assessed by phosphospecific antibodies
Neilson et al., Mol Endocrinol 2007 (Breast Neoplasms) : Finally, suppression of Jak1 by lentiviral delivery of Jak1 short hairpin RNA blocked PRL activation of ERK and signal transducer and activator of transcription ( Stat ) 3 and suppressed PRL activation of Jak2, Stat5a, Stat5b, and Akt , as well as tyrosine phosphorylation of PRLR
Arendt et al., Am J Pathol 2009 (Breast Neoplasms) : Both in vitro and in vivo, PRL and TGFalpha cooperatively enhanced Akt phosphorylation, which is associated with endocrine resistance in human disease
Di Rosa et al., J Cell Biochem 2009 (MAP Kinase Signaling System) : In addition, PRL induced a phosphorylation of AKT that was prevented both by the two MAPK inhibitors SB203580 and U0126 and by the PI3-K inhibitors wortmannin and LY-294002
Pujianto et al., Endocrinology 2010 : Western blot analyses indicated that the prosurvival effect of PRL on human spermatozoa involved the stimulation of Akt phosphorylation, whereas inhibitors of phosphatidylinositol-3-OH kinase and Akt negated this effect, as did the direct induction of sperm capacitation with cAMP analogues
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