Y
Yi-Rong Chen
Researcher at National Health Research Institutes
Publications - 47
Citations - 4232
Yi-Rong Chen is an academic researcher from National Health Research Institutes. The author has contributed to research in topics: Epidermal growth factor receptor & Phosphorylation. The author has an hindex of 25, co-authored 43 publications receiving 4042 citations. Previous affiliations of Yi-Rong Chen include Baylor College of Medicine & Taipei Veterans General Hospital.
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The role of c-Jun N-terminal kinase (JNK) in apoptosis induced by ultraviolet C and gamma radiation. Duration of JNK activation may determine cell death and proliferation.
TL;DR: The data revealed the requirement of the JNK pathway in radiation-induced apoptosis and implicated the importance of the duration of JNK activation in determining the cell fates.
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High Frequency of Epidermal Growth Factor Receptor Mutations with Complex Patterns in Non–Small Cell Lung Cancers Related to Gefitinib Responsiveness in Taiwan
Shiu Feng Huang,Hui Ping Liu,Ling-Hui Li,Yuan Chieh Ku,Yu Ning Fu,Hsien-Yu Tsai,Ya Ting Chen,Yung Feng Lin,Wen Cheng Chang,Han Pin Kuo,Yi Cheng Wu,Yi-Rong Chen,Shih-Feng Tsai,Shih-Feng Tsai +13 more
TL;DR: Data from this study would predict a higher gefitinib response rate in lung adenocarcinoma patients in Chinese and, possibly, other East Asian populations because of the possibility that EGFR mutations play an important role in the tumorigenesis of adenOCarc in lung, especially in East Asians.
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Persistent Activation of c-Jun N-terminal Kinase 1 (JNK1) in γ Radiation-induced Apoptosis
TL;DR: It is shown that lethal doses of γ radiation (GR) induced JNK activities at the early phase of apoptosis in Jurkat T-cells, which implies a distinct regulatory mechanism and specific function of JNK1 in irradiated cells.
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Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin
Yi-Rong Chen,Tse-Hua Tan +1 more
TL;DR: The inhibition of the MEKK1-JNK pathway reveals a possible mechanism of suppression of AP-1 and NF-κB signaling by curcumin, and may explain the potent anti-inflammatory and anti-carcinogenic effects of this chemical.
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Molecular Mechanisms of c-Jun N-terminal Kinase-mediated Apoptosis Induced by Anticarcinogenic Isothiocyanates *
TL;DR: It is reported that phenylmethyl isocyacyanate and phenylethyl isothiocyanates induced sustained c-Jun N-terminal kinase (JNK) activation in a dose-dependent manner and that PMITC and PEITC may have chemotherapeutic functions besides their chemopreventive functions.