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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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MTOR — PCNA

Text-mined interactions from Literome

Panwalkar et al., Cancer 2004 (Hematologic Neoplasms) : Inhibitors of mTOR also prevent cyclin dependent kinase (CDK) activation, inhibit retinoblastoma protein phosphorylation, and accelerate the turnover of cyclin D1, leading to a deficiency of active CDK4/cyclin D1 complexes, all of which may help cause G1-phase arrest
Wing et al., J Biol Chem 2005 (MAP Kinase Signaling System) : Activation of mTOR by FGF9 induces p70 ribosomal S6 kinase ( S6K1 ) phosphorylation, cyclin expression, and cell proliferation, which are independent of phosphatidylinositol 3-kinase and Akt
Coiffier et al., Leukemia & lymphoma 2009 (Hematologic Neoplasms...) : Mantle cell lymphoma ( MCL ) was the first hematologic malignancy in which mTOR inhibition was explored as a treatment strategy, owing to its characteristic overexpression of cyclin D1, a G1 cyclin regulated by mTOR signaling
Xu et al., Cancer Res 2006 (Prostatic Neoplasms) : DHT treatment increased mTOR activity as assessed by phosphorylation of the downstream targets p70 S6 kinase and 4E-BP1, and mTOR inhibition with rapamycin blocked the DHT stimulated increase in cyclin D proteins
Giles et al., Curr Mol Med 2005 (Hematologic Neoplasms...) : As a consequence of inhibiting its downstream messengers, mTOR inhibitors prevent cyclin dependent kinase (CDK) activation, inhibit retinoblastoma protein phosphorylation, and accelerate the turnover of cyclin D1, leading to a deficiency of active CDK4/cyclin D1 complexes, all of which may help cause GI phase arrest
Huang et al., Cancer Lett 2009 (Carcinoma...) : Also, we found blockage mTORC1 inhibited Cyclin D1 expression in CNE-2 cells and enhanced cell apoptosis
Velazquez-Garcia et al., Diabetes 2011 (Glucose Intolerance) : Phosphorylation/inactivation of GSK-3ß and phosphorylation/activation of mTOR , critical regulators of D-cyclin expression and ß-cell proliferation, were enhanced in TG mouse islets, without changes in Akt phosphorylation status