Data on the transcriptional regulation of DNA damage induced apoptosis suppressor (DDIAS) by ERK5/MEF2B pathway in lung cancer cells = 폐암에서 DDIAS의 ERK5/MEF2B 경로에 의한 DNA 손상의 전사제어
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- Data on the transcriptional regulation of DNA damage induced apoptosis suppressor (DDIAS) by ERK5/MEF2B pathway in lung cancer cells = 폐암에서 DDIAS의 ERK5/MEF2B 경로에 의한 DNA 손상의 전사제어
- Joo-Young Im; Sung Hoon Yoon; Bo Kyung Kim; Hyun Seung Ban; Kyung Jae Won; Kyung-Sook Chung; K E Jung; Mi Sun Won
- Bibliographic Citation
- Data in Brief, vol. 9, pp. 257-261
- Publication Year
- The data included in this article are associated with the article entitled “DNA-damage-induced apoptosis suppressor (DDIAS) is upregulated via ERK5/MEF2B signaling and promotes β-catenin-mediated invasion” (J.Y. Im, S.H. Yoon, B.K. Kim, H.S. Ban, K.J. Won, K.S. Chung, K.E. Jung, M. Won) . Quantitative RT-PCR data revealed that genetic or pharmacological inhibition of extracellular signal-regulated kinase 5 (ERK5) suppresses DDIAS transcription in response to epidermal growth factor (EGF) in Hela cells. p300 did not interact with myocyte enhancer factor 2B (MEF2B), a downstream target of ERK5 and affect transcription of DDIAS. Moreover, DDIAS transcription is activated by ERK5/MEF2B signaling on EGF exposure in the non-small cell lung cancer cells (NSCLC) NCI-H1703 and NCI-H1299. DDIAS knockdown suppresses lung cancer cell invasion by decreasing β-catenin protein level on EGF exposure.
- DDIASERK5MEF2BLung cancer
- Appears in Collections:
- Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Biomedical Research > Biotherapeutics Translational Research Center > 1. Journal Articles
Division of Research on National Challenges > 1. Journal Articles
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