Title : ROS-mediated PERK-eIF2α-ATF4 pathway plays an important role in arsenite-induced L-02 cells apoptosis via regulating CHOP-DR5 signaling.

Pub. Date : 2020 Oct

PMID : 32506763






4 Functional Relationships(s)
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1 Further results showed that NaAsO2 increased expression in biomarker of endoplasmic reticulum (ER) stress and activated the protein kinase R-like ER kinase (PERK)-eukaryotic translation initiation 2alpha (eIF2alpha)-activating transcription factor 4 (ATF4) pathway. sodium arsenite activating transcription factor 4 Homo sapiens
2 Further results showed that NaAsO2 increased expression in biomarker of endoplasmic reticulum (ER) stress and activated the protein kinase R-like ER kinase (PERK)-eukaryotic translation initiation 2alpha (eIF2alpha)-activating transcription factor 4 (ATF4) pathway. sodium arsenite activating transcription factor 4 Homo sapiens
3 PERK inhibitor and ATF4 siRNA significantly attenuated NaAsO2 -induced CHOP and DR5 expressions. sodium arsenite activating transcription factor 4 Homo sapiens
4 Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity. sodium arsenite activating transcription factor 4 Homo sapiens