Publication: The mystery of oncogenic KRAS: Lessons from studying its wild-type counter part
Issued Date
2017-10-02
Resource Type
ISSN
21541256
21541248
21541248
Other identifier(s)
2-s2.0-84981205611
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Mahidol University
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SCOPUS
Bibliographic Citation
Small GTPases. Vol.8, No.4 (2017), 233-236
Suggested Citation
Yuan I. Chang, Alisa Damnernsawad, Guangyao Kong, Xiaona You, Demin Wang, Jing Zhang The mystery of oncogenic KRAS: Lessons from studying its wild-type counter part. Small GTPases. Vol.8, No.4 (2017), 233-236. doi:10.1080/21541248.2016.1215656 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/41767
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Title
The mystery of oncogenic KRAS: Lessons from studying its wild-type counter part
Abstract
© 2017 Taylor & Francis. 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.