| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8727396 | Gastroenterology | 2017 | 68 Pages |
Abstract
Cigarette smoke promotes cell death and features of pancreatitis in EtOH-sensitized acinar cells by suppressing the adaptive unfolded protein response signaling pathway. It also activates ER stress pathways that promote acinar cell death.
Keywords
BIAMAHRLPSprotein kinase RNA (PKR)-like ER kinaseXBP1SCSEeIF2αUPRTCDDEtOHC/EBP homologous proteinMTTROSTetrachlorodibenzo-p-dioxinAcroleinEthanolER stressAlcoholALSCHOPcontrol dietSmokingendoplasmic reticulumeukaryotic translation initiation factor 2αcigarette smoke extractlipopolysaccharideElectron microscopyUnfolded protein responsePancreasPropidium iodidePERKReactive oxygen speciesaryl hydrocarbon receptor
Related Topics
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Authors
Aurelia Lugea, Andreas Gerloff, Hsin-Yuan Su, Zhihong Xu, Ariel Go, Cheng Hu, Samuel W. French, Jeremy S. Wilson, Minoti V. Apte, Richard T. Waldron, Stephen J. Pandol,