◀ Back to AKT1
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