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T osmostress signaling to the Spc1 MAPK, and therefore these MAPKKK paralogues do not appear to be redundant. Indeed, a previous study found that overexpression of Wis4 cannot complementMolecular Biology of the Celldetected the Wis4 in1 heteromer complex (Figure 2C). The observed Wis4 in1 interaction showed little change before and after osmostress and oxidative stress, suggesting constitutive int
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Other studies have shown that accumulation of Al in the cerebellum increased the lipid peroxidative products. In one study, oral administration of Al (100 mg/kg/d) for 2 mo increased lipid peroxidation in the cerebellum of adult rats [31]. The cerebellar TBARS levels also increased in rats intraperitoneally injected with aluminum lactate (7 mg Al/kg/d) for 11 wk [32]. Nehru et al further identifie
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With Roc2, Cul5EY mutants develop normally and do not display any overt morphological defects. That Roc2 and Cul5 mutant animals are viable and display no obvious developmental defects is consistent with our analysis of Roc-Cullin interactions indicating that Roc2 and Cul5 bind exclusively to each other. Indeed, Roc2 and Cul5 accumulation in vivo is interdependent: Roc2 was undetectable in Cul5 mu
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With Roc2, Cul5EY mutants develop normally and do not display any overt morphological defects. That Roc2 and Cul5 mutant animals are viable and display no obvious developmental defects is consistent with our analysis of Roc-Cullin interactions indicating that Roc2 and Cul5 bind exclusively to each other. Indeed, Roc2 and Cul5 accumulation in vivo is interdependent: Roc2 was undetectable in Cul5 mu
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Binding pockets [8]. Thus, imatinib is successful as a targeted therapy in GIST through inhibition of KIT or PDGFRA, and in other cancers, including Philadelphia chromosome-positive chronic myelogenous leukemias through inhibition of Bcr-Abl [9]. Clinical studies with imatinib have reported objective response rates of 50-70 and an estimated median survival of 57 months in patients with advanced G
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Binding pockets [8]. Thus, imatinib is successful as a targeted therapy in GIST through inhibition of KIT or PDGFRA, and in other cancers, including Philadelphia chromosome-positive chronic myelogenous leukemias through inhibition of Bcr-Abl [9]. Clinical studies with imatinib have reported objective response rates of 50-70 and an estimated median survival of 57 months in patients with advanced G
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