◀ Back to PIK3R1
MLST8 — PIK3R1
Text-mined interactions from Literome
Brito et al., Atherosclerosis 2009
(Atherosclerosis) :
The activation of
mTOR signaling by oxLDL,
requires the upstream activation of
PI3K and Akt, as assessed by the inhibitory effect of the PI3K inhibitor Ly294002 on mTOR activation and DNA synthesis
Huang et al., Biochem Soc Trans 2009
:
Through negative-feedback mechanisms,
mTORC1 activity
inhibits growth factor stimulation of
PI3K
Park et al., Haematologica 2010
(Leukemia, Myeloid, Acute) :
However, as
mTORC1 activation is independent of PI3K/AKT in acute myeloid leukemia, dual
PI3K and mTOR inhibitors may
induce apoptosis in blast cells
Kim et al., J Lipid Res 2010
:
The lipogenic effects of GIP in the presence of insulin are therefore at least partially mediated by upregulation of adipocyte LPL gene transcription through a pathway involving
PI3-K/PKB/AMPK dependent
CREB/TORC2 activation
Tan et al., Cancer Cell 2010
(Cell Transformation, Neoplastic...) :
On loss of PPP2R2B,
mTORC1 inhibitor rapamycin
triggers a compensatory Myc phosphorylation in PDK1 dependent, but
PI3K and AKT independent manner, resulting in resistance
Lee et al., PloS one 2010
(Endotoxemia) :
Furthermore, in vitro cellular studies demonstrated that LPS ( lipopolysaccharide ) activation of
mTORC1-S6K still occurs in the
presence of
PI3K-Akt inhibition alone, but can be suppressed by concurrent inhibition of PI3K-Akt and MEK-ERK pathways
Chen et al., J Biol Chem 2011
:
The
PI3K dependent signaling kinase complex
mTORC2 ( mammalian target of rapamycin complex 2 ) has been defined as the regulatory Ser-473 kinase of Akt
Willems et al., Leukemia 2012
(Leukemia, Myeloid, Acute) :
In addition, the
mTORC1 dependent
PI3K/Akt feedback
activation was fully abrogated in AZD8055 treated AML cells
Gulhati et al., Carcinogenesis 2012
(Colorectal Neoplasms...) :
In this study, we show that inhibition of
mTORC1 with rapamycin
leads to feedback activation of
PI3K/Akt and Ras-MAPK signaling, resulting in cell survival and possible contribution to rapamycin resistance
Bridges et al., Mol Biol Cell 2012
:
In this paper, we show that PIKFYVE and
PI3K-C2a are
necessary for activation of
mTORC1 and its translocation to the plasma membrane in 3T3-L1 adipocytes
Shanmugasundaram et al., Oncogene 2013
(Carcinoma, Renal Cell...) :
Here we provide additional genetic evidence that
PI3K signaling
activates mTORC2 kinase activity
Finlay et al., J Exp Med 2012
:
The present study now demonstrates that
mTORC1 activity in CD8 ( + ) T cells is not
dependent on
PI3K or Akt but is critical to sustain glucose uptake and glycolysis in CD8 ( + ) T cells
Razmara et al., Cell communication and signaling : CCS 2013
:
Thus, whereas both mTORC1 and
mTORC2 are activated in a
PI3K dependent manner, different additional signaling pathways are needed ... Thus, whereas both
mTORC1 and mTORC2 are activated in a
PI3K dependent manner, different additional signaling pathways are needed