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Servicebio Inc perk
Perk, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/perk/pm42046449-79-26-31?v=Servicebio+Inc
Average 86 stars, based on 1 article reviews
perk - by Bioz Stars, 2026-07
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Differential expression, ERS/UPR-associated <t>pathways,</t> <t>and</t> <t>PERK–ATF4–CHOP</t> axis-gene signals from bulk microarray data. (A) Volcano plot of IRI versus Sham shows widespread transcriptional remodeling, with multiple stress- and injury-related genes among the prominently altered signals. (B) Hallmark GSEA dot plot indicates enrichment of the Hallmark Unfolded Protein Response and Hallmark Apoptosis pathways, accompanied by activation of injury-response pathways such as Hypoxia, TNFα/NF-κB, inflammatory response, and p53 signaling. (C) ssGSEA heatmap at the sample level shows condition-related increases in UPR_total and Apoptosis activity in the IRI group, with branch-specific variation across UPR-related scores. (D) Heatmap of PERK–ATF4–CHOP axis genes shows increased z-score expression of Atf4 and Ddit3/CHOP in IRI samples relative to Sham samples.
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Differential expression, ERS/UPR-associated <t>pathways,</t> <t>and</t> <t>PERK–ATF4–CHOP</t> axis-gene signals from bulk microarray data. (A) Volcano plot of IRI versus Sham shows widespread transcriptional remodeling, with multiple stress- and injury-related genes among the prominently altered signals. (B) Hallmark GSEA dot plot indicates enrichment of the Hallmark Unfolded Protein Response and Hallmark Apoptosis pathways, accompanied by activation of injury-response pathways such as Hypoxia, TNFα/NF-κB, inflammatory response, and p53 signaling. (C) ssGSEA heatmap at the sample level shows condition-related increases in UPR_total and Apoptosis activity in the IRI group, with branch-specific variation across UPR-related scores. (D) Heatmap of PERK–ATF4–CHOP axis genes shows increased z-score expression of Atf4 and Ddit3/CHOP in IRI samples relative to Sham samples.
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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), <t>GSK2606414</t> 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), <t>GSK2606414</t> 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), <t>GSK2606414</t> 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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Image Search Results


Differential expression, ERS/UPR-associated pathways, and PERK–ATF4–CHOP axis-gene signals from bulk microarray data. (A) Volcano plot of IRI versus Sham shows widespread transcriptional remodeling, with multiple stress- and injury-related genes among the prominently altered signals. (B) Hallmark GSEA dot plot indicates enrichment of the Hallmark Unfolded Protein Response and Hallmark Apoptosis pathways, accompanied by activation of injury-response pathways such as Hypoxia, TNFα/NF-κB, inflammatory response, and p53 signaling. (C) ssGSEA heatmap at the sample level shows condition-related increases in UPR_total and Apoptosis activity in the IRI group, with branch-specific variation across UPR-related scores. (D) Heatmap of PERK–ATF4–CHOP axis genes shows increased z-score expression of Atf4 and Ddit3/CHOP in IRI samples relative to Sham samples.

Journal: Frontiers in Pharmacology

Article Title: Integrated transcriptomics identifies ER stress–associated apoptosis in post-resuscitation AKI and supports early Dl-3-n-butylphthalide–associated renoprotection in a porcine TCA model

doi: 10.3389/fphar.2026.1841271

Figure Lengend Snippet: Differential expression, ERS/UPR-associated pathways, and PERK–ATF4–CHOP axis-gene signals from bulk microarray data. (A) Volcano plot of IRI versus Sham shows widespread transcriptional remodeling, with multiple stress- and injury-related genes among the prominently altered signals. (B) Hallmark GSEA dot plot indicates enrichment of the Hallmark Unfolded Protein Response and Hallmark Apoptosis pathways, accompanied by activation of injury-response pathways such as Hypoxia, TNFα/NF-κB, inflammatory response, and p53 signaling. (C) ssGSEA heatmap at the sample level shows condition-related increases in UPR_total and Apoptosis activity in the IRI group, with branch-specific variation across UPR-related scores. (D) Heatmap of PERK–ATF4–CHOP axis genes shows increased z-score expression of Atf4 and Ddit3/CHOP in IRI samples relative to Sham samples.

Article Snippet: Among these branches, PERK–ATF4–CHOP signaling can shift from adaptive proteostasis regulation toward pro-apoptotic signaling under severe or sustained stress.

Techniques: Quantitative Proteomics, Microarray, Activation Assay, Activity Assay, Expressing

PT pseudo-bulk pathway enrichment and PERK–ATF4–CHOP axis-gene signals (A) Hallmark GSEA dot plot from PT pseudo-bulk analysis highlights Unfolded Protein Response and Apoptosis among the significantly altered pathways in the Sham versus IRI_12 h contrast. Because the contrast direction is Sham versus IRI_12h, negative NES values indicate enrichment toward the IRI_12 h condition. (B) PT pseudo-bulk volcano plot shows extensive transcriptional remodeling, with ERS/UPR- and apoptosis-related genes represented among the significantly altered signals. (C) Heatmap of axis-gene logFC across key PT pseudo-bulk contrasts shows coordinated changes in core UPR mediators, including Hspa5, Eif2ak3/PERK, Atf4, Ddit3/CHOP, Ern1/Xbp1, and Atf6, together with apoptosis-related genes including Bax, Bak1, Casp3/8/9, and Bcl2l1. Stars indicate FDR <0.05. (D) Bar plots of representative PT pseudo-bulk axis genes show contrast-level changes in PERK–ATF4–CHOP branch components, UPR-related mediators, and apoptosis-related effectors, including Eif2ak3/PERK, Atf4, Ddit3/CHOP, Hspa5, Ern1, Xbp1, Bax, and Bcl2l1. Stars indicate FDR <0.05.

Journal: Frontiers in Pharmacology

Article Title: Integrated transcriptomics identifies ER stress–associated apoptosis in post-resuscitation AKI and supports early Dl-3-n-butylphthalide–associated renoprotection in a porcine TCA model

doi: 10.3389/fphar.2026.1841271

Figure Lengend Snippet: PT pseudo-bulk pathway enrichment and PERK–ATF4–CHOP axis-gene signals (A) Hallmark GSEA dot plot from PT pseudo-bulk analysis highlights Unfolded Protein Response and Apoptosis among the significantly altered pathways in the Sham versus IRI_12 h contrast. Because the contrast direction is Sham versus IRI_12h, negative NES values indicate enrichment toward the IRI_12 h condition. (B) PT pseudo-bulk volcano plot shows extensive transcriptional remodeling, with ERS/UPR- and apoptosis-related genes represented among the significantly altered signals. (C) Heatmap of axis-gene logFC across key PT pseudo-bulk contrasts shows coordinated changes in core UPR mediators, including Hspa5, Eif2ak3/PERK, Atf4, Ddit3/CHOP, Ern1/Xbp1, and Atf6, together with apoptosis-related genes including Bax, Bak1, Casp3/8/9, and Bcl2l1. Stars indicate FDR <0.05. (D) Bar plots of representative PT pseudo-bulk axis genes show contrast-level changes in PERK–ATF4–CHOP branch components, UPR-related mediators, and apoptosis-related effectors, including Eif2ak3/PERK, Atf4, Ddit3/CHOP, Hspa5, Ern1, Xbp1, Bax, and Bcl2l1. Stars indicate FDR <0.05.

Article Snippet: Among these branches, PERK–ATF4–CHOP signaling can shift from adaptive proteostasis regulation toward pro-apoptotic signaling under severe or sustained stress.

Techniques:

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