Gene interactions and pathways from curated databases and text-mining

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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
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...) : 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 ... 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)
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