Activation of MAPK pathways and downstream transcription factors in 2-aminobiphenyl-induced apoptosis

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Title:	Activation of MAPK pathways and downstream transcription factors in 2-aminobiphenyl-induced apoptosis
Authors:	陳師慶;Chen, Lei‐Chin;Chueh, Tsung‐Cheng;Tuan, Yen‐Fan;Chen, Chien‐Cheng;Chien, Chih‐Ching;Lee, Huey‐Yin;Chen, Ssu‐Ching
Contributors:	生醫理工學院生命科學系
Keywords:	2-aminobiphenyl;acetylcysteine;Acetylcysteine - pharmacology;Activating Transcription Factor 2 - antagonists & inhibitors;Activating Transcription Factor 2 - biosynthesis;Aminobiphenyl Compounds - toxicity;apoptosis;Apoptosis - drug effects;ATF-2;c-Jun;Caspase 3 - metabolism;caspase-3;Cells, Cultured;DNA Damage;ERK;Humans;JNK;MAP Kinase Signaling System - drug effects;mitogen-activated protein kinase;N-acetylcysteine;Oxidative stress;Phosphorylation;Proto-Oncogene Proteins c-jun - antagonists & inhibitors;Proto-Oncogene Proteins c-jun - biosynthesis;Reactive Oxygen Species - metabolism;signal transduction;transcription factors;Transcription Factors - drug effects
Date:	2015-01-01
Issue Date:	2026-04-23 11:11:32 (UTC+8)
Publisher:	John Wiley and Sons Inc.;United States: John Wiley & Sons
Abstract:	摘要： 2‐Aminobiphenyls (2‐ABP) induces oxidative DNA damage and leads to apoptosis. The precise signaling pathways of inducing apoptosis in vitro are still unknown. This study provides insight into the relationship between 2‐ABP‐induced apoptosis and the activation of MAPK and downstream transcription factors using pharmacological inhibitors of ERK, p38, and JNK pathways. Results showed that 2‐ABP induced the activation of ERK and JNK but not p38. The ERK/JNK pathways downstream transcription factors, c‐Jun and ATF‐2, were also activated by 2‐ABP. The inhibitory effects of ERK inhibitor, U0126, on 2‐ABP‐induced caspase‐3 activity were not detected. However, JNK inhibitor, SP600125, significantly attenuated the caspase‐3 activity induced by 2‐ABP. The expression of the transcription factors c‐Jun and ATF‐2 were decreased in 2‐ABP treated cells in the presence of ERK/JNK inhibitors, suggesting that the expression of ERK/JNK pathways leads to the downstream activation of c‐Jun and ATF‐2. N‐acetylcysteine, an ROS scavenger, inhibited 2‐ABP‐induced activation of ERK and JNK, the cell death and caspase‐3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase‐3 in a ROS/JNK‐dependent signaling cascade. © 2013 Wiley Periodicals, Inc. Environ Toxicol 30: 205–211, 2015. 其他題名： Environ. Toxicol 出版者： United States: John Wiley & Sons 出版日期： 2015-02 出處： Environmental toxicology, 2015-02, Vol.30 (2), p.205-211 資源來源： Wiley Online Library Journals 版權： 2013 Wiley Periodicals, Inc. 版權： 2015 Wiley Periodicals, Inc. 識別號： ISSN: 1520-4081 識別號： ISSN: 1522-7278 識別號： EISSN: 1522-7278 識別號： DOI: 10.1002/tox.21886 識別號： PMID: 23836369 識別號： CODEN: ETOXFH
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