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primary atf4 mouse mab  (Proteintech)


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    Structured Review

    Proteintech primary atf4 mouse mab
    IR-induced injury leads to increased S100A9 and related pathway activation in fatty livers HFD fed C57 mice were used to establish liver IR models. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Serum ALT levels. (B) Immunofluorescence staining and quantification of CD11b + macrophages in ischemia fatty livers, scale bars: 50 μm, 20 μm. (C) Volcano Plot displaying 748 genes to be upregulated and 625 genes downregulated. (D) KEGG pathway enrichment analysis of major biological pathways contributing to fatty liver IR stress. (E) Heatmap showing the expression of different genes. (F) Western-assisted analysis and relative density ratio of S100A9, TLR2, and <t>ATF4</t> in liver tissues. (G) Immunochemistry staining and quantification of S100A9 positive cells in ischemia fatty livers, scale bars: 50 μm, 20 μm. (H) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. ALT, alanine aminotransferase; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; IR, ischemia reperfusion.
    Primary Atf4 Mouse Mab, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 619 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+atf4+mouse+mab/ATF4+Antibody/pmc11776876-49-5-10
    Average 96 stars, based on 619 article reviews
    primary atf4 mouse mab - by Bioz Stars, 2026-08
    96/100 stars

    Images

    1) Product Images from "TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY"

    Article Title: TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY

    Journal: Shock (Augusta, Ga.)

    doi: 10.1097/SHK.0000000000002470

    IR-induced injury leads to increased S100A9 and related pathway activation in fatty livers HFD fed C57 mice were used to establish liver IR models. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Serum ALT levels. (B) Immunofluorescence staining and quantification of CD11b + macrophages in ischemia fatty livers, scale bars: 50 μm, 20 μm. (C) Volcano Plot displaying 748 genes to be upregulated and 625 genes downregulated. (D) KEGG pathway enrichment analysis of major biological pathways contributing to fatty liver IR stress. (E) Heatmap showing the expression of different genes. (F) Western-assisted analysis and relative density ratio of S100A9, TLR2, and ATF4 in liver tissues. (G) Immunochemistry staining and quantification of S100A9 positive cells in ischemia fatty livers, scale bars: 50 μm, 20 μm. (H) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. ALT, alanine aminotransferase; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; IR, ischemia reperfusion.
    Figure Legend Snippet: IR-induced injury leads to increased S100A9 and related pathway activation in fatty livers HFD fed C57 mice were used to establish liver IR models. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Serum ALT levels. (B) Immunofluorescence staining and quantification of CD11b + macrophages in ischemia fatty livers, scale bars: 50 μm, 20 μm. (C) Volcano Plot displaying 748 genes to be upregulated and 625 genes downregulated. (D) KEGG pathway enrichment analysis of major biological pathways contributing to fatty liver IR stress. (E) Heatmap showing the expression of different genes. (F) Western-assisted analysis and relative density ratio of S100A9, TLR2, and ATF4 in liver tissues. (G) Immunochemistry staining and quantification of S100A9 positive cells in ischemia fatty livers, scale bars: 50 μm, 20 μm. (H) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. ALT, alanine aminotransferase; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; IR, ischemia reperfusion.

    Techniques Used: Activation Assay, Immunofluorescence, Staining, Expressing, Western Blot, Quantitative RT-PCR

    S100A9 induces inflammatory injury via macrophage TLR2 activation BMMs were isolated from WT mice and incubated with rS100A9 or rS100A8 respectively for 24 h. (A) Western-assisted analysis of TLR2 and ATF4 in rS100A9-stressed macrophages. (B) Western-assisted analysis of TLR2 and ATF4 in rS100A8-stressed macrophages; BMMs were transfected with the TLR2-siRNA or control vector followed by incubation with rS100A9. (C) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (D) Western-assisted analysis of ATF4 in nuclear extracts. (E) Immunofluorescence staining for ATF4 distribution in macrophages. DAPI was used to visualize nuclei. Scale bars: 50 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage. WT, wild type; qRT-PCR, quantitative real-time PCR.
    Figure Legend Snippet: S100A9 induces inflammatory injury via macrophage TLR2 activation BMMs were isolated from WT mice and incubated with rS100A9 or rS100A8 respectively for 24 h. (A) Western-assisted analysis of TLR2 and ATF4 in rS100A9-stressed macrophages. (B) Western-assisted analysis of TLR2 and ATF4 in rS100A8-stressed macrophages; BMMs were transfected with the TLR2-siRNA or control vector followed by incubation with rS100A9. (C) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (D) Western-assisted analysis of ATF4 in nuclear extracts. (E) Immunofluorescence staining for ATF4 distribution in macrophages. DAPI was used to visualize nuclei. Scale bars: 50 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage. WT, wild type; qRT-PCR, quantitative real-time PCR.

    Techniques Used: Activation Assay, Isolation, Incubation, Western Blot, Transfection, Control, Plasmid Preparation, Quantitative RT-PCR, Immunofluorescence, Staining, Derivative Assay, Real-time Polymerase Chain Reaction

    S100A9 knockdown attenuates liver dysfunction and inflammatory damage following IR of fatty livers C57 mice were injected with AAV9-S100A9-shRNA 48 h before establishing liver IR models using HFD-fed mice. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Western-assisted analysis and relative density ratio of S100A9 in liver tissues. (B) H&E staining of ischemic fatty livers, scale bar: 200 μm, 100 μm. (C) Serum ALT levels. (D) Immunofluorescence staining and quantification of CD11b positive macrophages and immunochemistry staining and quantification of Ly6G positive cells in ischemia fatty livers, scale bar: 40 μm. (E) Western-assisted analysis of TLR2 and ATF4 in liver tissues. (F) Dual immunofluoresence staining for CD68 (red) and TLR2 (green) co-localization in injured fatty livers after IR stimulation, scale bars: 50 μm, 20 μm. (G) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. HFD, high-fat diet; IR, ischemia reperfusion. qRT-PCR, quantitative real-time PCR.
    Figure Legend Snippet: S100A9 knockdown attenuates liver dysfunction and inflammatory damage following IR of fatty livers C57 mice were injected with AAV9-S100A9-shRNA 48 h before establishing liver IR models using HFD-fed mice. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Western-assisted analysis and relative density ratio of S100A9 in liver tissues. (B) H&E staining of ischemic fatty livers, scale bar: 200 μm, 100 μm. (C) Serum ALT levels. (D) Immunofluorescence staining and quantification of CD11b positive macrophages and immunochemistry staining and quantification of Ly6G positive cells in ischemia fatty livers, scale bar: 40 μm. (E) Western-assisted analysis of TLR2 and ATF4 in liver tissues. (F) Dual immunofluoresence staining for CD68 (red) and TLR2 (green) co-localization in injured fatty livers after IR stimulation, scale bars: 50 μm, 20 μm. (G) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. HFD, high-fat diet; IR, ischemia reperfusion. qRT-PCR, quantitative real-time PCR.

    Techniques Used: Knockdown, Injection, shRNA, Western Blot, Staining, Immunofluorescence, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

    ATF4 is responsible for regulating S100A9-triggered NEK7/NLRP3 inflammasome activation in macrophages BMMs were transfected with the ATF4-siRNA or control vector followed by incubation with rS100A9 . (A) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (B) IL-1β release from BMMs. (C) Western-assisted analysis of NEK7 and NLRP3 in BMMs. (D) Dual immunofluoresence staining for NEK7 (red) and NLRP3 (green) co-localization in BMMs, scale bars: 40 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage.
    Figure Legend Snippet: ATF4 is responsible for regulating S100A9-triggered NEK7/NLRP3 inflammasome activation in macrophages BMMs were transfected with the ATF4-siRNA or control vector followed by incubation with rS100A9 . (A) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (B) IL-1β release from BMMs. (C) Western-assisted analysis of NEK7 and NLRP3 in BMMs. (D) Dual immunofluoresence staining for NEK7 (red) and NLRP3 (green) co-localization in BMMs, scale bars: 40 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage.

    Techniques Used: Activation Assay, Transfection, Control, Plasmid Preparation, Incubation, Quantitative RT-PCR, Western Blot, Staining, Derivative Assay

    The schematic diagram of S100A9 regulating IR-induced macrophage NLRP3 inflammasome activation in fatty livers. During fatty liver IR stress, S100A9 is released and accumulated in injured livers. S100A9 interacts with macrophage TLR2, promoting ATF4 activation and the formation of NEK7/NLRP3 inflammasome. It leads to subsequent inflammatory response and liver damage. IR, ischemia reperfusion.
    Figure Legend Snippet: The schematic diagram of S100A9 regulating IR-induced macrophage NLRP3 inflammasome activation in fatty livers. During fatty liver IR stress, S100A9 is released and accumulated in injured livers. S100A9 interacts with macrophage TLR2, promoting ATF4 activation and the formation of NEK7/NLRP3 inflammasome. It leads to subsequent inflammatory response and liver damage. IR, ischemia reperfusion.

    Techniques Used: Activation Assay



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    IR-induced injury leads to increased S100A9 and related pathway activation in fatty livers HFD fed C57 mice were used to establish liver IR models. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Serum ALT levels. (B) Immunofluorescence staining and quantification of CD11b + macrophages in ischemia fatty livers, scale bars: 50 μm, 20 μm. (C) Volcano Plot displaying 748 genes to be upregulated and 625 genes downregulated. (D) KEGG pathway enrichment analysis of major biological pathways contributing to fatty liver IR stress. (E) Heatmap showing the expression of different genes. (F) Western-assisted analysis and relative density ratio of S100A9, TLR2, and <t>ATF4</t> in liver tissues. (G) Immunochemistry staining and quantification of S100A9 positive cells in ischemia fatty livers, scale bars: 50 μm, 20 μm. (H) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. ALT, alanine aminotransferase; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; IR, ischemia reperfusion.
    Primary Atf4 Mouse Mab, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    IR-induced injury leads to increased S100A9 and related pathway activation in fatty livers HFD fed C57 mice were used to establish liver IR models. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Serum ALT levels. (B) Immunofluorescence staining and quantification of CD11b + macrophages in ischemia fatty livers, scale bars: 50 μm, 20 μm. (C) Volcano Plot displaying 748 genes to be upregulated and 625 genes downregulated. (D) KEGG pathway enrichment analysis of major biological pathways contributing to fatty liver IR stress. (E) Heatmap showing the expression of different genes. (F) Western-assisted analysis and relative density ratio of S100A9, TLR2, and ATF4 in liver tissues. (G) Immunochemistry staining and quantification of S100A9 positive cells in ischemia fatty livers, scale bars: 50 μm, 20 μm. (H) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. ALT, alanine aminotransferase; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; IR, ischemia reperfusion.

    Journal: Shock (Augusta, Ga.)

    Article Title: TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY

    doi: 10.1097/SHK.0000000000002470

    Figure Lengend Snippet: IR-induced injury leads to increased S100A9 and related pathway activation in fatty livers HFD fed C57 mice were used to establish liver IR models. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Serum ALT levels. (B) Immunofluorescence staining and quantification of CD11b + macrophages in ischemia fatty livers, scale bars: 50 μm, 20 μm. (C) Volcano Plot displaying 748 genes to be upregulated and 625 genes downregulated. (D) KEGG pathway enrichment analysis of major biological pathways contributing to fatty liver IR stress. (E) Heatmap showing the expression of different genes. (F) Western-assisted analysis and relative density ratio of S100A9, TLR2, and ATF4 in liver tissues. (G) Immunochemistry staining and quantification of S100A9 positive cells in ischemia fatty livers, scale bars: 50 μm, 20 μm. (H) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. ALT, alanine aminotransferase; HFD, high-fat diet; KEGG, Kyoto Encyclopedia of Genes and Genomes; IR, ischemia reperfusion.

    Article Snippet: Macophage ATF4 was detected using primary ATF4 mouse mAb (60035-1-Ig, Proteintech).

    Techniques: Activation Assay, Immunofluorescence, Staining, Expressing, Western Blot, Quantitative RT-PCR

    S100A9 induces inflammatory injury via macrophage TLR2 activation BMMs were isolated from WT mice and incubated with rS100A9 or rS100A8 respectively for 24 h. (A) Western-assisted analysis of TLR2 and ATF4 in rS100A9-stressed macrophages. (B) Western-assisted analysis of TLR2 and ATF4 in rS100A8-stressed macrophages; BMMs were transfected with the TLR2-siRNA or control vector followed by incubation with rS100A9. (C) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (D) Western-assisted analysis of ATF4 in nuclear extracts. (E) Immunofluorescence staining for ATF4 distribution in macrophages. DAPI was used to visualize nuclei. Scale bars: 50 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage. WT, wild type; qRT-PCR, quantitative real-time PCR.

    Journal: Shock (Augusta, Ga.)

    Article Title: TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY

    doi: 10.1097/SHK.0000000000002470

    Figure Lengend Snippet: S100A9 induces inflammatory injury via macrophage TLR2 activation BMMs were isolated from WT mice and incubated with rS100A9 or rS100A8 respectively for 24 h. (A) Western-assisted analysis of TLR2 and ATF4 in rS100A9-stressed macrophages. (B) Western-assisted analysis of TLR2 and ATF4 in rS100A8-stressed macrophages; BMMs were transfected with the TLR2-siRNA or control vector followed by incubation with rS100A9. (C) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (D) Western-assisted analysis of ATF4 in nuclear extracts. (E) Immunofluorescence staining for ATF4 distribution in macrophages. DAPI was used to visualize nuclei. Scale bars: 50 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage. WT, wild type; qRT-PCR, quantitative real-time PCR.

    Article Snippet: Macophage ATF4 was detected using primary ATF4 mouse mAb (60035-1-Ig, Proteintech).

    Techniques: Activation Assay, Isolation, Incubation, Western Blot, Transfection, Control, Plasmid Preparation, Quantitative RT-PCR, Immunofluorescence, Staining, Derivative Assay, Real-time Polymerase Chain Reaction

    S100A9 knockdown attenuates liver dysfunction and inflammatory damage following IR of fatty livers C57 mice were injected with AAV9-S100A9-shRNA 48 h before establishing liver IR models using HFD-fed mice. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Western-assisted analysis and relative density ratio of S100A9 in liver tissues. (B) H&E staining of ischemic fatty livers, scale bar: 200 μm, 100 μm. (C) Serum ALT levels. (D) Immunofluorescence staining and quantification of CD11b positive macrophages and immunochemistry staining and quantification of Ly6G positive cells in ischemia fatty livers, scale bar: 40 μm. (E) Western-assisted analysis of TLR2 and ATF4 in liver tissues. (F) Dual immunofluoresence staining for CD68 (red) and TLR2 (green) co-localization in injured fatty livers after IR stimulation, scale bars: 50 μm, 20 μm. (G) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. HFD, high-fat diet; IR, ischemia reperfusion. qRT-PCR, quantitative real-time PCR.

    Journal: Shock (Augusta, Ga.)

    Article Title: TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY

    doi: 10.1097/SHK.0000000000002470

    Figure Lengend Snippet: S100A9 knockdown attenuates liver dysfunction and inflammatory damage following IR of fatty livers C57 mice were injected with AAV9-S100A9-shRNA 48 h before establishing liver IR models using HFD-fed mice. Samples were harvested after 90-min ischemia and 6 h of reperfusion. (A) Western-assisted analysis and relative density ratio of S100A9 in liver tissues. (B) H&E staining of ischemic fatty livers, scale bar: 200 μm, 100 μm. (C) Serum ALT levels. (D) Immunofluorescence staining and quantification of CD11b positive macrophages and immunochemistry staining and quantification of Ly6G positive cells in ischemia fatty livers, scale bar: 40 μm. (E) Western-assisted analysis of TLR2 and ATF4 in liver tissues. (F) Dual immunofluoresence staining for CD68 (red) and TLR2 (green) co-localization in injured fatty livers after IR stimulation, scale bars: 50 μm, 20 μm. (G) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in the livers. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. HFD, high-fat diet; IR, ischemia reperfusion. qRT-PCR, quantitative real-time PCR.

    Article Snippet: Macophage ATF4 was detected using primary ATF4 mouse mAb (60035-1-Ig, Proteintech).

    Techniques: Knockdown, Injection, shRNA, Western Blot, Staining, Immunofluorescence, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

    ATF4 is responsible for regulating S100A9-triggered NEK7/NLRP3 inflammasome activation in macrophages BMMs were transfected with the ATF4-siRNA or control vector followed by incubation with rS100A9 . (A) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (B) IL-1β release from BMMs. (C) Western-assisted analysis of NEK7 and NLRP3 in BMMs. (D) Dual immunofluoresence staining for NEK7 (red) and NLRP3 (green) co-localization in BMMs, scale bars: 40 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage.

    Journal: Shock (Augusta, Ga.)

    Article Title: TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY

    doi: 10.1097/SHK.0000000000002470

    Figure Lengend Snippet: ATF4 is responsible for regulating S100A9-triggered NEK7/NLRP3 inflammasome activation in macrophages BMMs were transfected with the ATF4-siRNA or control vector followed by incubation with rS100A9 . (A) Detection of cytokines IL-1β, CXCL1, CXCL-2, and IL-6 by qRT-PCR in BMMs. (B) IL-1β release from BMMs. (C) Western-assisted analysis of NEK7 and NLRP3 in BMMs. (D) Dual immunofluoresence staining for NEK7 (red) and NLRP3 (green) co-localization in BMMs, scale bars: 40 μm, 20 μm. N = 3–6/group. All data represent the mean ± SD, * P < 0.05, ** P < 0.01, *** P < 0.001. BBM, bone-derived macrophage.

    Article Snippet: Macophage ATF4 was detected using primary ATF4 mouse mAb (60035-1-Ig, Proteintech).

    Techniques: Activation Assay, Transfection, Control, Plasmid Preparation, Incubation, Quantitative RT-PCR, Western Blot, Staining, Derivative Assay

    The schematic diagram of S100A9 regulating IR-induced macrophage NLRP3 inflammasome activation in fatty livers. During fatty liver IR stress, S100A9 is released and accumulated in injured livers. S100A9 interacts with macrophage TLR2, promoting ATF4 activation and the formation of NEK7/NLRP3 inflammasome. It leads to subsequent inflammatory response and liver damage. IR, ischemia reperfusion.

    Journal: Shock (Augusta, Ga.)

    Article Title: TARGETING S100A9-TLR2 AXIS CONTROLS MACROPHAGE NLRP3 INFLAMMASOME ACTIVATION IN FATTY LIVER ISCHEMIA REPERFUSION INJURY

    doi: 10.1097/SHK.0000000000002470

    Figure Lengend Snippet: The schematic diagram of S100A9 regulating IR-induced macrophage NLRP3 inflammasome activation in fatty livers. During fatty liver IR stress, S100A9 is released and accumulated in injured livers. S100A9 interacts with macrophage TLR2, promoting ATF4 activation and the formation of NEK7/NLRP3 inflammasome. It leads to subsequent inflammatory response and liver damage. IR, ischemia reperfusion.

    Article Snippet: Macophage ATF4 was detected using primary ATF4 mouse mAb (60035-1-Ig, Proteintech).

    Techniques: Activation Assay

    A. qPCR analysis of mRNA levels of Atf4 in mouse CD8+ T cells treated or not with a stress inducer thapsigargin (TG, 100nM, 24 hr) in the presence or absence of CD3/CD28 agonists.

    Journal: Cancer immunology, immunotherapy : CII

    Article Title: Induction of the activating transcription factor-4 in the intratumoral CD8+ T cells sustains their viability and anti-tumor activities

    doi: 10.1007/s00262-022-03286-2

    Figure Lengend Snippet: A. qPCR analysis of mRNA levels of Atf4 in mouse CD8+ T cells treated or not with a stress inducer thapsigargin (TG, 100nM, 24 hr) in the presence or absence of CD3/CD28 agonists.

    Article Snippet: The following antibodies were used to stain the resulting single cell suspensions: anti-mouse CD8-APC antibody (BioLegend, cat#126614) and anti-human CD8-PE/CY7 antibody (BioLegend, cat#344750), anti-mouse ATF4 primary antibody (Cell signaling Technology, cat#11815s, 1:150), anti-human ATF4 primary antibody (Cell signaling technology, cat#11815s, 1:150), goat anti-rabbit secondary antibody (Invitrogen, cat#A32732, 1:500), anti-CD45-APC/Cy7 (BioLegend, cat#157204), anti-CD3-PE (BioLegend, cat#100206), anti-CD8-AF700 (BioLegend, cat#100730), anti- CD69-BV421 (BioLgend, cat#104545, anti-PD-1-PE/Cy7 (BioLegend, cat#109110) and Annexin V-APC (BioLegend, cat#640941), anti-LAG3-PE (BioLegend, cat#125207), anti-TIGIT-Alexa Fluor 700 (R&D system, cat#FAB72671N), anti-TIM3-BV421 (BioLegend, cat#134019).

    Techniques:

    A. mRNA levels of Atf4 in mouse CD8+ T cells treated or not with the media conditioned by MC38 tumor cells (TCM) for 48 hr (n=5).

    Journal: Cancer immunology, immunotherapy : CII

    Article Title: Induction of the activating transcription factor-4 in the intratumoral CD8+ T cells sustains their viability and anti-tumor activities

    doi: 10.1007/s00262-022-03286-2

    Figure Lengend Snippet: A. mRNA levels of Atf4 in mouse CD8+ T cells treated or not with the media conditioned by MC38 tumor cells (TCM) for 48 hr (n=5).

    Article Snippet: The following antibodies were used to stain the resulting single cell suspensions: anti-mouse CD8-APC antibody (BioLegend, cat#126614) and anti-human CD8-PE/CY7 antibody (BioLegend, cat#344750), anti-mouse ATF4 primary antibody (Cell signaling Technology, cat#11815s, 1:150), anti-human ATF4 primary antibody (Cell signaling technology, cat#11815s, 1:150), goat anti-rabbit secondary antibody (Invitrogen, cat#A32732, 1:500), anti-CD45-APC/Cy7 (BioLegend, cat#157204), anti-CD3-PE (BioLegend, cat#100206), anti-CD8-AF700 (BioLegend, cat#100730), anti- CD69-BV421 (BioLgend, cat#104545, anti-PD-1-PE/Cy7 (BioLegend, cat#109110) and Annexin V-APC (BioLegend, cat#640941), anti-LAG3-PE (BioLegend, cat#125207), anti-TIGIT-Alexa Fluor 700 (R&D system, cat#FAB72671N), anti-TIM3-BV421 (BioLegend, cat#134019).

    Techniques:

    A. Frequency of CD3+CD8+ infiltrating T cells in MC38 colon adenocarcinoma tumors from Atf4+/+ or Atf4ΔCD8 mice (n=7).

    Journal: Cancer immunology, immunotherapy : CII

    Article Title: Induction of the activating transcription factor-4 in the intratumoral CD8+ T cells sustains their viability and anti-tumor activities

    doi: 10.1007/s00262-022-03286-2

    Figure Lengend Snippet: A. Frequency of CD3+CD8+ infiltrating T cells in MC38 colon adenocarcinoma tumors from Atf4+/+ or Atf4ΔCD8 mice (n=7).

    Article Snippet: The following antibodies were used to stain the resulting single cell suspensions: anti-mouse CD8-APC antibody (BioLegend, cat#126614) and anti-human CD8-PE/CY7 antibody (BioLegend, cat#344750), anti-mouse ATF4 primary antibody (Cell signaling Technology, cat#11815s, 1:150), anti-human ATF4 primary antibody (Cell signaling technology, cat#11815s, 1:150), goat anti-rabbit secondary antibody (Invitrogen, cat#A32732, 1:500), anti-CD45-APC/Cy7 (BioLegend, cat#157204), anti-CD3-PE (BioLegend, cat#100206), anti-CD8-AF700 (BioLegend, cat#100730), anti- CD69-BV421 (BioLgend, cat#104545, anti-PD-1-PE/Cy7 (BioLegend, cat#109110) and Annexin V-APC (BioLegend, cat#640941), anti-LAG3-PE (BioLegend, cat#125207), anti-TIGIT-Alexa Fluor 700 (R&D system, cat#FAB72671N), anti-TIM3-BV421 (BioLegend, cat#134019).

    Techniques:

    A. Relative ATF4 expression in three CD8+ T cells subtypes isolated from colorectal cancer samples including naïve T cells, effector memory T cells (Tem) and CD103+CD39+ highly active T cells using data from Ref (30). (n=7 for each group).

    Journal: Cancer immunology, immunotherapy : CII

    Article Title: Induction of the activating transcription factor-4 in the intratumoral CD8+ T cells sustains their viability and anti-tumor activities

    doi: 10.1007/s00262-022-03286-2

    Figure Lengend Snippet: A. Relative ATF4 expression in three CD8+ T cells subtypes isolated from colorectal cancer samples including naïve T cells, effector memory T cells (Tem) and CD103+CD39+ highly active T cells using data from Ref (30). (n=7 for each group).

    Article Snippet: The following antibodies were used to stain the resulting single cell suspensions: anti-mouse CD8-APC antibody (BioLegend, cat#126614) and anti-human CD8-PE/CY7 antibody (BioLegend, cat#344750), anti-mouse ATF4 primary antibody (Cell signaling Technology, cat#11815s, 1:150), anti-human ATF4 primary antibody (Cell signaling technology, cat#11815s, 1:150), goat anti-rabbit secondary antibody (Invitrogen, cat#A32732, 1:500), anti-CD45-APC/Cy7 (BioLegend, cat#157204), anti-CD3-PE (BioLegend, cat#100206), anti-CD8-AF700 (BioLegend, cat#100730), anti- CD69-BV421 (BioLgend, cat#104545, anti-PD-1-PE/Cy7 (BioLegend, cat#109110) and Annexin V-APC (BioLegend, cat#640941), anti-LAG3-PE (BioLegend, cat#125207), anti-TIGIT-Alexa Fluor 700 (R&D system, cat#FAB72671N), anti-TIM3-BV421 (BioLegend, cat#134019).

    Techniques: Expressing, Isolation

    OT-I mice were used in crossings to generate OT-I; Atf4+/+ or OT-I; Atf4ΔCD8 mice.

    Journal: Cancer immunology, immunotherapy : CII

    Article Title: Induction of the activating transcription factor-4 in the intratumoral CD8+ T cells sustains their viability and anti-tumor activities

    doi: 10.1007/s00262-022-03286-2

    Figure Lengend Snippet: OT-I mice were used in crossings to generate OT-I; Atf4+/+ or OT-I; Atf4ΔCD8 mice.

    Article Snippet: The following antibodies were used to stain the resulting single cell suspensions: anti-mouse CD8-APC antibody (BioLegend, cat#126614) and anti-human CD8-PE/CY7 antibody (BioLegend, cat#344750), anti-mouse ATF4 primary antibody (Cell signaling Technology, cat#11815s, 1:150), anti-human ATF4 primary antibody (Cell signaling technology, cat#11815s, 1:150), goat anti-rabbit secondary antibody (Invitrogen, cat#A32732, 1:500), anti-CD45-APC/Cy7 (BioLegend, cat#157204), anti-CD3-PE (BioLegend, cat#100206), anti-CD8-AF700 (BioLegend, cat#100730), anti- CD69-BV421 (BioLgend, cat#104545, anti-PD-1-PE/Cy7 (BioLegend, cat#109110) and Annexin V-APC (BioLegend, cat#640941), anti-LAG3-PE (BioLegend, cat#125207), anti-TIGIT-Alexa Fluor 700 (R&D system, cat#FAB72671N), anti-TIM3-BV421 (BioLegend, cat#134019).

    Techniques: