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Abstract
Signal transduction through Ras translates extracellular signals into biological responses, including cell proliferation, cell survival, growth, and differentiation. For these reasons, dysregulating Ras can have dramatic effects at the cellular and organismal levels. Germline mutations that increase Ras signaling disrupt development, whereas mutational activation of Ras in somatic cells can cause cancer. Thus, identifying additional mechanisms that positively or negatively regulate Ras could have profound implications for treating human diseases. New evidence identifies K-Ras monoubiquitination as a previously unknown means to potentiate Ras signaling.