Ral GTPases and cancer: linchpin support of the tumorigenic platform.
A confluence of recent observations has indicted the Ras-family G-proteins RALA and RALB as key offenders in the subversion of core biological systems driving oncogenic transformation. Here, we will focus on current developments highlighting the pivotal contribution of Ral proteins to the regulatory framework supporting tumorigenesis, and evaluate mechanistic connections between Ral effector activation and generation of this framework.
Bodemann
Brian O
BO
Department of Cell Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA.
White
Michael A
MA
D000818:Animals; D018450:Disease Progression; D019204:GTP-Binding Proteins / Q000378:metabolism; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008954:Models, Biological; D009154:Mutation; D009369:Neoplasms / Q000201:enzymology* / Q000235:genetics; D020725:ral GTP-Binding Proteins / Q000378:metabolism*
C483163:Ralb protein, human; D019204:GTP-Binding Proteins; C492198:RALA protein, human; D020725:ral GTP-Binding Proteins