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10.1080/21541248.2016.1215656

http://scihub22266oqcxt.onion/10.1080/21541248.2016.1215656
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C5680677!5680677!27449543
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suck abstract from ncbi


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pmid27449543      Small+GTPases 2017 ; 8 (4): 233-6
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  • The mystery of oncogenic KRAS: Lessons from studying its wild-type counter part #MMPMID27449543
  • Chang YI; Damnernsawad A; Kong G; You X; Wang D; Zhang J
  • Small GTPases 2017[]; 8 (4): 233-6 PMID27449543show ga
  • Using conditional knock-in mouse models, we and others have shown that despite the very high sequence identity between Nras and Kras proteins, oncogenic Kras displays a much stronger leukemogenic activity than oncogenic Nras in vivo. In this manuscript, we will summarize our recent work of characterizing wild-type Kras function in adult hematopoiesis and in oncogenic Kras-induced leukemogenesis. We attribute the strong leukemogenic activity of oncogenic Kras to 2 unique aspects of Kras signaling. First, Kras is required in mediating cell type- and cytokine-specific ERK1/2 signaling. Second, oncogenic Kras, but not oncogenic Nras, induces hyperactivation of wild-type Ras, which significantly enhances Ras signaling in vivo. We will also discuss a possible mechanism that mediates oncogenic Kras-evoked hyperactivation of wild-type Ras and a potential approach to down-regulate oncogenic Kras signaling.
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