https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14352 Wed 11 Apr 2018 11:37:50 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:14871 Wed 11 Apr 2018 10:34:19 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:50344 Thu 20 Jul 2023 14:26:55 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18436 Sat 24 Mar 2018 07:59:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18386 Sat 24 Mar 2018 07:52:36 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22856 PTEN and LKB1 - genes encoding phosphatase and tensin homolog and liver kinase B1, respectively - leads to the spontaneous development of cancer in mice. PTEN converts phosphatidylinositol (3,4,5)-trisphosphate (PIP₃) to phosphatidylinositol (4,5)-bisphosphate (PIP₂), whereas LKB1 activates the 5' adenosine monophosphate-activated protein kinase (AMPK). The kinase AKT and the kinase complex mTORC1 may play key roles in carcinogenesis and are components of signaling pathways that also contain PTEN and LKB1. We propose that via activation of AKT and mTORC1, the double knockout of PTEN and LKB1 contributes to distinct cell-specific aspects of tumor development and progression. Whereas mTORC1 promotes cancer initiation and progression through cell growth, survival, and proliferation, independent induction of the immune inhibitory molecule PD-L1 by activated AKT enables the tumors to evade immunosurveillance.]]> Sat 24 Mar 2018 07:16:02 AEDT ]]>