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MTOR — PLD2
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Kam et al., FASEB J 2004
:
Role of
phospholipase D1 in the regulation of
mTOR activity by lysophosphatidic acid ... The reduction in
PLD activity in both situations
impaired the effect of LPA on
mTOR signaling but did not inhibit the effect of PDGF
Hornberger et al., Proc Natl Acad Sci U S A 2006
:
The
role of
phospholipase D and phosphatidic acid in the mechanical activation of
mTOR signaling in skeletal muscle ... Finally, pharmacological inhibition of
PLD blocked the mechanically induced increase in PA and the activation of
mTOR signaling
Ha et al., Cell Signal 2006
:
PLD2 dependent
mTOR activation appears to require PLD2 binding to mTOR/raptor with lipase activity, since lipase-inactive PLD2 can not trigger mTOR activation despite its ability to interact with mTOR/raptor
Foster et al., Cancer Res 2007
:
Although the regulation of mTOR by the PI3K signaling pathway is well established, a
role for
PLD and PA in regulating
mTOR has been controversial ... In this review, the evidence implicating
PLD and PA in the
regulation of
mTOR is summarized, and the implications of this novel and potentially important mechanism for regulating mTOR are discussed
Yoon et al., J Cell Sci 2008
:
Instead,
PLD1 positively
regulates mTOR signaling leading to the production of IGF2, an autocrine factor instrumental for the initiation of satellite cell differentiation
Toschi et al., Mol Cell Biol 2009
:
Phospholipase D ( PLD ) and its metabolite phosphatidic acid ( PA ) have been implicated in the
regulation of
mTOR ; however, their role has been controversial
Hsu et al., Carcinogenesis 2010
(Bone Neoplasms...) :
In contrast, depletion of interleukin-8 (IL-8) from A549-CM and NCI-H460-CM decreased the osteoclastogenesis-inductive properties of A549-CM and NCI-H460-CM. Induction of osteoclast differentiation by lung cancer-derived-CM and rhIL-8 was associated with increased
phospholipase D ( PLD ) activation, and the
activations of protein kinase C (PKC) alpha/betaII, extracellular signal regulated kinase ( ERK ) 1/2 and AKT/the
mammalian target of rapamycin (mTOR) ... PLD inhibitor also completely decreased AKT and mTOR phosphorylation, whereas phosphatidylinositol-3-kinase (PI3K) inhibitor only partially decreased mTOR phosphorylation, suggesting that
mTOR activation by
PLD is through both PI3K/AKT dependent and PI3K/AKT independent manner
Suryawan et al., J Appl Physiol 2010
:
Our results suggest that the enhanced activation of
mTORC1 in muscle of neonatal pigs is in part
due to regulation by PRAS40,
PLD1 , and the Rag GTPases
Arous et al., Diabetologia 2011
:
Oleate mediated
mTORC1 activation
required phospholipase D activation, which produces phosphatidic acid and is known to render mTORC1 rapamycin resistant
Baan et al., Gut 2012
(Colorectal Neoplasms) :
Both proliferation and
mTOR activity
depended on
PLD , an enzyme that generates phosphatidic acid ( PA ) ... 5-ASA interferes with proliferation of colorectal cancer cells via inhibition of
PLD dependent generation of PA and loss of
mTOR signalling
Razmara et al., Cell communication and signaling : CCS 2013
:
In addition, PDGF-BB induced activation of
mTORC1 , as measured by phosphorylation of the downstream S6 protein, was
dependent on
phospholipase D ( PLD ) ...
mTORC1 is activated in a
PLD dependent manner and promotes phosphorylation of the S6 protein, whereas mTORC2, in concert with PLC? signaling, promotes Akt phosphorylation
Jaafar et al., Cell communication and signaling : CCS 2013
(Muscular Atrophy) :
It is established that
Phospholipase D ( PLD ) activates
mTOR signaling , through the binding of its product phosphatidic acid ( PA ) to mTOR protein