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Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

CHAC1 exacerbates arsenite cytotoxicity by lowering intracellular glutathione levels
J Toxicol Sci. 2023;48(9):487-494. doi: 10.2131/jts.48.487.ABSTRACTWe here examined whether CHAC1 is implicated in arsenite (As(III))-induced cytotoxicity in HaCaT cells. We found that HaCaT cells in which the intracellular GSH levels were elevated by transfection with CHAC1 siRNA showed decreased sensitivity to As(III) compared to the control cells. Treatment with BSO (an inhibitor of GSH biosynthesis) abolished the decrease in sensitivity to As(III), suggesting that an increase in intracellular GSH levels was involved in the decrease in sensitivity to As(III) due to the decrease in the levels of CHAC1 expression. When we...
Source: Journal of Toxicological Sciences - September 4, 2023 Category: Toxicology Authors: Daigo Sumi Hiroki Taguchi Kumiko Takeuchi Hitomi Fujishiro Source Type: research

Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

CHAC1 exacerbates arsenite cytotoxicity by lowering intracellular glutathione levels
J Toxicol Sci. 2023;48(9):487-494. doi: 10.2131/jts.48.487.ABSTRACTWe here examined whether CHAC1 is implicated in arsenite (As(III))-induced cytotoxicity in HaCaT cells. We found that HaCaT cells in which the intracellular GSH levels were elevated by transfection with CHAC1 siRNA showed decreased sensitivity to As(III) compared to the control cells. Treatment with BSO (an inhibitor of GSH biosynthesis) abolished the decrease in sensitivity to As(III), suggesting that an increase in intracellular GSH levels was involved in the decrease in sensitivity to As(III) due to the decrease in the levels of CHAC1 expression. When we...
Source: Journal of Toxicological Sciences - September 4, 2023 Category: Toxicology Authors: Daigo Sumi Hiroki Taguchi Kumiko Takeuchi Hitomi Fujishiro Source Type: research

Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

CHAC1 exacerbates arsenite cytotoxicity by lowering intracellular glutathione levels
J Toxicol Sci. 2023;48(9):487-494. doi: 10.2131/jts.48.487.ABSTRACTWe here examined whether CHAC1 is implicated in arsenite (As(III))-induced cytotoxicity in HaCaT cells. We found that HaCaT cells in which the intracellular GSH levels were elevated by transfection with CHAC1 siRNA showed decreased sensitivity to As(III) compared to the control cells. Treatment with BSO (an inhibitor of GSH biosynthesis) abolished the decrease in sensitivity to As(III), suggesting that an increase in intracellular GSH levels was involved in the decrease in sensitivity to As(III) due to the decrease in the levels of CHAC1 expression. When we...
Source: Journal of Toxicological Sciences - September 4, 2023 Category: Toxicology Authors: Daigo Sumi Hiroki Taguchi Kumiko Takeuchi Hitomi Fujishiro Source Type: research

Transcription Factor JunB Suppresses Hepatitis C Virus Replication
Kobe J Med Sci. 2023 Aug 31;69(3):E86-E95.ABSTRACTWe previously reported that hepatitis C virus (HCV) infection activates the reactive oxygen species (ROS)/c-Jun N-terminal kinase (JNK) signaling pathway. Activation of JNK contributes to the development of liver diseases, including metabolic disorders, steatosis, liver cirrhosis and hepatocellular carcinoma. JNK is known to have numerous target genes, including JunB, a member of activator protein-1 transcription factor family. However, the roles of JunB in the HCV life cycle and HCV-associated pathogenesis remain unclear. To clarify a physiological role of JunB in HCV infe...
Source: Kobe J Med Sci - September 4, 2023 Category: General Medicine Authors: Adi Ariffianto Lin Deng Saki Harada Yujiao Liang Chieko Matsui Takayuki Abe Ikuo Shoji Source Type: research

CHAC1 exacerbates arsenite cytotoxicity by lowering intracellular glutathione levels
J Toxicol Sci. 2023;48(9):487-494. doi: 10.2131/jts.48.487.ABSTRACTWe here examined whether CHAC1 is implicated in arsenite (As(III))-induced cytotoxicity in HaCaT cells. We found that HaCaT cells in which the intracellular GSH levels were elevated by transfection with CHAC1 siRNA showed decreased sensitivity to As(III) compared to the control cells. Treatment with BSO (an inhibitor of GSH biosynthesis) abolished the decrease in sensitivity to As(III), suggesting that an increase in intracellular GSH levels was involved in the decrease in sensitivity to As(III) due to the decrease in the levels of CHAC1 expression. When we...
Source: Journal of Toxicological Sciences - September 4, 2023 Category: Toxicology Authors: Daigo Sumi Hiroki Taguchi Kumiko Takeuchi Hitomi Fujishiro Source Type: research