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ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
Ire1α Inhibitor, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: Cell Stress & Chaperones

Article Title: Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes

doi: 10.1016/j.cstres.2026.100163

Figure Lengend Snippet: ER stress inducers promote keretinocyte differentiation partially through UPR activation. Primary mouse keretinocyte were treated with UPR pathway inhibitors: 4μ8C or Kira 6 (IRE1/XPB1 inhibitors), GSK2606414 or GSK2656157 (PERK inhibitors) with or without TM (a and b) or BFA (c and d) for 48 h, followed by detection of ER stress and differentiation markers. Data are mean ± SEM. ns: not significant, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The IRE1α inhibitor 4μ8C (Selleck, S7272) and Kira6 (Selleck, S8658), as well as the PERK inhibitors GSK2606414 (Selleck, S7307) or GSK2656157 (Selleck, S7033), were dissolved in DMSO and used at a final concentration of 4μ8C 1 mM, Kira6 5 μM, GSK2606414 140 μM, GSK2656157 3 μM.

Techniques: Activation Assay