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- W2053668936 abstract "The transformation of cells generally involves multiple genetic lesions that undermine control of both cell death and proliferation. We now report that κB-Ras proteins act as regulators of NF-κB and Ral pathways, which control inflammation/cell death and proliferation, respectively. Cells lacking κB-Ras therefore not only show increased NF-κB activity, which results in increased expression of inflammatory mediators, but also exhibit elevated Ral activity, which leads to enhanced anchorage-independent proliferation (AIP). κB-Ras deficiency consequently leads to significantly increased tumor growth that can be dampened by inhibiting either Ral or NF-κB pathways, revealing the unique tumor-suppressive potential of κB-Ras proteins. Remarkably, numerous human tumors show reduced levels of κB-Ras, and increasing the level of κB-Ras in these tumor cells impairs their ability to undergo AIP, thereby implicating κB-Ras proteins in human disease." @default.
- W2053668936 created "2016-06-24" @default.
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- W2053668936 date "2014-09-01" @default.
- W2053668936 modified "2023-10-16" @default.
- W2053668936 title "κB-Ras Proteins Regulate Both NF-κB-Dependent Inflammation and Ral-Dependent Proliferation" @default.
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- W2053668936 doi "https://doi.org/10.1016/j.celrep.2014.08.015" @default.
- W2053668936 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4177457" @default.
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