The Ras branch of small Gtpases: Ras family members don’t fall far from the tree

Reuther, Gary W.; Der, Channing J.

doi:10.1016/s0955-0674(99)00071-x

Cited by 374 publications

(249 citation statements)

References 77 publications

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“…A viable hypothesis for the delay of AJ formation in the early mouse embryo is that an inhibitor or repressor of Ecadherin/catenin interactions represses the establishment of stable adhesion complexes. Recent studies have revealed a potential role for IQGAPs, targets of the Rho GTPases (Cdc42 and Rac1) in inhibition of E -cadherin/catenin interactions (107)(108)(109)(110)(111). IQGAP1 binds to the amino terminus of beta-catenin complexed with E-cadherin in vivo and in vitro, promoting dissociation of alpha-catenin, thereby disrupting cadherin-mediated cell adhesion (108)(109)(110)(111).…”

Section: Cell-to Cell Adhesionmentioning

confidence: 99%

Regulation of blastocyst formation

Watson¹

2001

Front Biosci

115

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Section: Cell-to Cell Adhesionmentioning

confidence: 99%

Regulation of blastocyst formation

Watson¹

2001

Front Biosci

115

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“…The level of the active GTP-bound form results from the balance of the competing activity of GTPase-activating proteins (GAP) and guanine nucleotide exchange factors (GEF) (Feig, 1994;Reuther and Der, 2000). Each Ras protein can work as an oncoprotein upon mutational activation (Rodenhuis, 1992;de Vries et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Ras-dependent carbon metabolism and transformation in mouse fibroblasts

et al. 2006

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Mutational activation of ras genes is required for the onset and maintenance of different malignancies. Here we show, using a combination of molecular physiology, nutritional perturbations and transcriptional profiling, that full penetrance of phenotypes related to oncogenic Ras activation, including the shift of carbon metabolism towards fermentation and upregulation of key cell cycle regulators, is dependent upon glucose availability. These responses are induced by Ras activation, being specifically reverted by downregulation of the Ras pathway obtained through the expression of a dominant-negative Rasspecific guanine nucleotide exchange protein. Our data allow to link directly to ras activation the alteration in energy metabolism of cancer cells, their fragility towards glucose shortage and ensuing apoptotic death.

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“…Ral proteins are small GTPases that have been implicated in the control of cell proliferation and Ras-mediated oncogenic transformation (14,48). The two known Ral isoforms, RalA and RalB, are 85% identical and comprise a distinct family within the Ras superfamily of GTPases (10).…”

mentioning

confidence: 99%