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  • 97
    Millipore ezh2
    <t>EZH2</t> directly silences IRF8 expression
    Ezh2, supplied by Millipore, used in various techniques. Bioz Stars score: 97/100, based on 911 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Durect Corporation 1002 osmotic minipump
    <t>EZH2</t> directly silences IRF8 expression
    1002 Osmotic Minipump, supplied by Durect Corporation, used in various techniques. Bioz Stars score: 86/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Santa Cruz Biotechnology bcl6
    IRF8 contributes to coordinate regulation of p53 and p21 by <t>BCL6</t> and MDM2 in GC B cells. Green arrows and red solid lines indicate transcriptional activation and repression, respectively. Red dashed lines indicate inhibition by induction of protein degradation.
    Bcl6, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 772 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    OriGene irf8
    LPS- and GC-mediated repression of HIV-1 in MDMs is associated with changes in IRF recruitment to the ISRE. (A) MDMs (2×10 6 cells/well) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with PAM3CSK4 (100 ng/ml) or LPS (100 ng/ml). At various time points after TLR stimulation, cells were harvested, lysed, and total cytoplasmic RNA was extracted. Viral RNA accumulation was assessed by semi-quantitative RT-PCR. The data are the average of two donors. (B) MDMs (1.2 × 10 7 cells/plate) were infected with a single-round replication competent HIV-GFP reporter virus at an MOI = 2. Forty-eight hours after infection, cells were treated with LPS (100 ng/ml). At either 1 or 24 hours after LPS treatment, cells were fixed with formaldehyde, lysed, sonicated, and subjected to immunoprecipitation with antibodies against IRF1, IRF2, IRF4, <t>IRF8,</t> or rabbit IgG (isotype control). Association with the HIV-1 ISRE was assessed by semi-quantitative PCR using HIV-1 specific primers. One representative donor (B) and composite data from three donors (C) are shown. (D) MDMs (2×10 6 cells/well) transfected with a controlled scrambled shRNA (white bars) or with shRNA targeting IRF8 (black bars) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with 100 ng/ml PAM3CSK4, 100 ng/ml LPS, a combination of 100 ng/ml PAM3CSK4 and 100 ng/ml LPS, or GC (MOI = 10) for 18 h. The cells were then lysed and assayed for luciferase activity. The experiment was performed three times, each in triplicate, using cells from three different donors. (E) MDMs transfected with an empty vector (white bars) or a vector encoding IRF8 (black bars) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with 100 ng/ml PAM3CSK4, 100 ng/ml LPS, a combination of 100 ng/ml PAM3CSK4 and 100 ng/ml LPS, or GC (MOI = 10) for 18 h. The cells were then lysed and assayed for luciferase activity. The experiment was performed three times, each in triplicate, using cells from three different donors.
    Irf8, supplied by OriGene, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Santa Cruz Biotechnology stat1
    CXCL10 amplified by IFNγ and LPS in VSMCs is <t>STAT1</t> dependent. A, WT and STAT1 −/− VSMCs were treated with 10 ng/ml IFNγ for 8 h or with 1 ug/ml of LPS for 4 h or with IFNγ for 4 h followed by LPS for additional 4 h. RNA was isolated and qRT-PCR for Cxcl10 using Gapdh as internal control was performed. B, Cells were treated as in A. On the medium remained after treatment ELISA for CXCL10 was performed. Data represent means of at least 3 independent biological experiments ±SEM and p
    Stat1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 2779 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    EZH2 directly silences IRF8 expression

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Cutting Edge: EZH2 promotes osteoclastogenesis by epigenetic silencing of the negative regulator IRF8 1

    doi: 10.4049/jimmunol.1501466

    Figure Lengend Snippet: EZH2 directly silences IRF8 expression

    Article Snippet: This study adds to this body of work by identifying a key role for EZH2 and associated H3K27me3 in promoting RANKL-induced osteoclast differentiation.

    Techniques: Expressing

    EZH2 is required for osteoclast differentiation and NFATc1 expression

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: Cutting Edge: EZH2 promotes osteoclastogenesis by epigenetic silencing of the negative regulator IRF8 1

    doi: 10.4049/jimmunol.1501466

    Figure Lengend Snippet: EZH2 is required for osteoclast differentiation and NFATc1 expression

    Article Snippet: This study adds to this body of work by identifying a key role for EZH2 and associated H3K27me3 in promoting RANKL-induced osteoclast differentiation.

    Techniques: Expressing

    IRF8 contributes to coordinate regulation of p53 and p21 by BCL6 and MDM2 in GC B cells. Green arrows and red solid lines indicate transcriptional activation and repression, respectively. Red dashed lines indicate inhibition by induction of protein degradation.

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: IFN Regulatory Factor 8 Regulates MDM2 in Germinal Center B Cells 1

    doi: 10.4049/jimmunol.0803693

    Figure Lengend Snippet: IRF8 contributes to coordinate regulation of p53 and p21 by BCL6 and MDM2 in GC B cells. Green arrows and red solid lines indicate transcriptional activation and repression, respectively. Red dashed lines indicate inhibition by induction of protein degradation.

    Article Snippet: IRF8 also directly regulates the transcriptional activity of Bcl6 ( ).

    Techniques: Activation Assay, Inhibition

    LPS- and GC-mediated repression of HIV-1 in MDMs is associated with changes in IRF recruitment to the ISRE. (A) MDMs (2×10 6 cells/well) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with PAM3CSK4 (100 ng/ml) or LPS (100 ng/ml). At various time points after TLR stimulation, cells were harvested, lysed, and total cytoplasmic RNA was extracted. Viral RNA accumulation was assessed by semi-quantitative RT-PCR. The data are the average of two donors. (B) MDMs (1.2 × 10 7 cells/plate) were infected with a single-round replication competent HIV-GFP reporter virus at an MOI = 2. Forty-eight hours after infection, cells were treated with LPS (100 ng/ml). At either 1 or 24 hours after LPS treatment, cells were fixed with formaldehyde, lysed, sonicated, and subjected to immunoprecipitation with antibodies against IRF1, IRF2, IRF4, IRF8, or rabbit IgG (isotype control). Association with the HIV-1 ISRE was assessed by semi-quantitative PCR using HIV-1 specific primers. One representative donor (B) and composite data from three donors (C) are shown. (D) MDMs (2×10 6 cells/well) transfected with a controlled scrambled shRNA (white bars) or with shRNA targeting IRF8 (black bars) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with 100 ng/ml PAM3CSK4, 100 ng/ml LPS, a combination of 100 ng/ml PAM3CSK4 and 100 ng/ml LPS, or GC (MOI = 10) for 18 h. The cells were then lysed and assayed for luciferase activity. The experiment was performed three times, each in triplicate, using cells from three different donors. (E) MDMs transfected with an empty vector (white bars) or a vector encoding IRF8 (black bars) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with 100 ng/ml PAM3CSK4, 100 ng/ml LPS, a combination of 100 ng/ml PAM3CSK4 and 100 ng/ml LPS, or GC (MOI = 10) for 18 h. The cells were then lysed and assayed for luciferase activity. The experiment was performed three times, each in triplicate, using cells from three different donors.

    Journal: bioRxiv

    Article Title: Interactions with Commensal and Pathogenic Bacteria Induce HIV-1 Latency in Macrophages through Altered Transcription Factor Recruitment to the LTR

    doi: 10.1101/2020.05.18.103333

    Figure Lengend Snippet: LPS- and GC-mediated repression of HIV-1 in MDMs is associated with changes in IRF recruitment to the ISRE. (A) MDMs (2×10 6 cells/well) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with PAM3CSK4 (100 ng/ml) or LPS (100 ng/ml). At various time points after TLR stimulation, cells were harvested, lysed, and total cytoplasmic RNA was extracted. Viral RNA accumulation was assessed by semi-quantitative RT-PCR. The data are the average of two donors. (B) MDMs (1.2 × 10 7 cells/plate) were infected with a single-round replication competent HIV-GFP reporter virus at an MOI = 2. Forty-eight hours after infection, cells were treated with LPS (100 ng/ml). At either 1 or 24 hours after LPS treatment, cells were fixed with formaldehyde, lysed, sonicated, and subjected to immunoprecipitation with antibodies against IRF1, IRF2, IRF4, IRF8, or rabbit IgG (isotype control). Association with the HIV-1 ISRE was assessed by semi-quantitative PCR using HIV-1 specific primers. One representative donor (B) and composite data from three donors (C) are shown. (D) MDMs (2×10 6 cells/well) transfected with a controlled scrambled shRNA (white bars) or with shRNA targeting IRF8 (black bars) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with 100 ng/ml PAM3CSK4, 100 ng/ml LPS, a combination of 100 ng/ml PAM3CSK4 and 100 ng/ml LPS, or GC (MOI = 10) for 18 h. The cells were then lysed and assayed for luciferase activity. The experiment was performed three times, each in triplicate, using cells from three different donors. (E) MDMs transfected with an empty vector (white bars) or a vector encoding IRF8 (black bars) were infected with a single-round, replication-competent HIV-luciferase reporter virus at an MOI = 0.1. Forty-eight hours after infection, cells were treated with 100 ng/ml PAM3CSK4, 100 ng/ml LPS, a combination of 100 ng/ml PAM3CSK4 and 100 ng/ml LPS, or GC (MOI = 10) for 18 h. The cells were then lysed and assayed for luciferase activity. The experiment was performed three times, each in triplicate, using cells from three different donors.

    Article Snippet: In fact, the interaction between IRF8 and IRF1 has been shown to repress HIV-1 transcription in Jurkat cells ( ).

    Techniques: Infection, Luciferase, Quantitative RT-PCR, Sonication, Immunoprecipitation, Real-time Polymerase Chain Reaction, Transfection, shRNA, Activity Assay, Plasmid Preparation

    CXCL10 amplified by IFNγ and LPS in VSMCs is STAT1 dependent. A, WT and STAT1 −/− VSMCs were treated with 10 ng/ml IFNγ for 8 h or with 1 ug/ml of LPS for 4 h or with IFNγ for 4 h followed by LPS for additional 4 h. RNA was isolated and qRT-PCR for Cxcl10 using Gapdh as internal control was performed. B, Cells were treated as in A. On the medium remained after treatment ELISA for CXCL10 was performed. Data represent means of at least 3 independent biological experiments ±SEM and p

    Journal: PLoS ONE

    Article Title: STAT1-Dependent Signal Integration between IFNγ and TLR4 in Vascular Cells Reflect Pro-Atherogenic Responses in Human Atherosclerosis

    doi: 10.1371/journal.pone.0113318

    Figure Lengend Snippet: CXCL10 amplified by IFNγ and LPS in VSMCs is STAT1 dependent. A, WT and STAT1 −/− VSMCs were treated with 10 ng/ml IFNγ for 8 h or with 1 ug/ml of LPS for 4 h or with IFNγ for 4 h followed by LPS for additional 4 h. RNA was isolated and qRT-PCR for Cxcl10 using Gapdh as internal control was performed. B, Cells were treated as in A. On the medium remained after treatment ELISA for CXCL10 was performed. Data represent means of at least 3 independent biological experiments ±SEM and p

    Article Snippet: Indeed, gene ( left panel) and protein expression ( left panel) of IRF8 in WT and STAT1−/− VSMCs in response to IFNγ, LPS or IFNγ+LPS, confirmed the microarray data.

    Techniques: Amplification, Isolation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    Identification of genes prone to synergistic amplification upon treatment with IFNγ and LPS. WT and STAT1 −/− VSMCs were treated as described in Fig. 1 . On RNA isolated from untreated or IFNγ, LPS or IFNγ+LPS treated VSMCs genome-wide expression profiling was performed. A, Venn diagrams revealing number of differentially expressed genes upon stimulation. B, Heat map of the expression of synergistically amplified genes in WT and STAT1 −/− VSMCs . C, Clustering of the synergistically upregulated genes according to their expression profile. AVG, average expression in the group. For details see text.

    Journal: PLoS ONE

    Article Title: STAT1-Dependent Signal Integration between IFNγ and TLR4 in Vascular Cells Reflect Pro-Atherogenic Responses in Human Atherosclerosis

    doi: 10.1371/journal.pone.0113318

    Figure Lengend Snippet: Identification of genes prone to synergistic amplification upon treatment with IFNγ and LPS. WT and STAT1 −/− VSMCs were treated as described in Fig. 1 . On RNA isolated from untreated or IFNγ, LPS or IFNγ+LPS treated VSMCs genome-wide expression profiling was performed. A, Venn diagrams revealing number of differentially expressed genes upon stimulation. B, Heat map of the expression of synergistically amplified genes in WT and STAT1 −/− VSMCs . C, Clustering of the synergistically upregulated genes according to their expression profile. AVG, average expression in the group. For details see text.

    Article Snippet: Indeed, gene ( left panel) and protein expression ( left panel) of IRF8 in WT and STAT1−/− VSMCs in response to IFNγ, LPS or IFNγ+LPS, confirmed the microarray data.

    Techniques: Amplification, Isolation, Genome Wide, Expressing

    IRF8 mediated cross-talk and functional activity of synergistically amplified chemokines. WT, STAT1 −/− and IRF8 −/− VSMCs and HMECs were treated as described in Fig. 1 . A, RNA was isolated and qRT-PCR for IRF8 using GAPDH as internal control was performed in VSMCs (left panel) and ECs (right panel). B, Protein extracts were analyzed for IRF8, tyrosine-phosphorylated STAT1, total STAT1 and GAPDH. C, CCL5 mRNA expression (left panel) and protein presence in the medium (right panel) was measured. D, Expression profiles of Cxcl9 (left panel) and Cxcl10 (right panel) between VSMCs WT , and IRF8 −/− were compared. E, Migration assay of CD45 + /CD3 + performed on conditioned medium remained after treatment of VSMCs WT and STAT1 −/ − . Data represent means of at least 3 independent biological experiments ±SEM and p

    Journal: PLoS ONE

    Article Title: STAT1-Dependent Signal Integration between IFNγ and TLR4 in Vascular Cells Reflect Pro-Atherogenic Responses in Human Atherosclerosis

    doi: 10.1371/journal.pone.0113318

    Figure Lengend Snippet: IRF8 mediated cross-talk and functional activity of synergistically amplified chemokines. WT, STAT1 −/− and IRF8 −/− VSMCs and HMECs were treated as described in Fig. 1 . A, RNA was isolated and qRT-PCR for IRF8 using GAPDH as internal control was performed in VSMCs (left panel) and ECs (right panel). B, Protein extracts were analyzed for IRF8, tyrosine-phosphorylated STAT1, total STAT1 and GAPDH. C, CCL5 mRNA expression (left panel) and protein presence in the medium (right panel) was measured. D, Expression profiles of Cxcl9 (left panel) and Cxcl10 (right panel) between VSMCs WT , and IRF8 −/− were compared. E, Migration assay of CD45 + /CD3 + performed on conditioned medium remained after treatment of VSMCs WT and STAT1 −/ − . Data represent means of at least 3 independent biological experiments ±SEM and p

    Article Snippet: Indeed, gene ( left panel) and protein expression ( left panel) of IRF8 in WT and STAT1−/− VSMCs in response to IFNγ, LPS or IFNγ+LPS, confirmed the microarray data.

    Techniques: Functional Assay, Activity Assay, Amplification, Isolation, Quantitative RT-PCR, Expressing, Migration

    Effect of STAT1 dependent signal integration on chemokine expression. WT and STAT1 −/− VSMCs , HMECs or WT aortic ring segments were treated as described in Fig. 1 . A, RNA from VSMCs was isolated and qRT-PCR for Ccl5 , Cxcl9 using Gapdh as internal control was performed. B, On the medium remained after treatment of VSMCs ELISA for Ccl5 and Cxcl9 was performed. C, Expression of CXCL10, CXCL9 and CCL5 upon stimulation in ECs. D, RNA from incubated aortic rings was isolated and qRT-PCR for Cxcl10 , Cxcl9 using Gapdh as internal control was performed. Data represent means of at least 3 independent biological experiments ±SEM and p

    Journal: PLoS ONE

    Article Title: STAT1-Dependent Signal Integration between IFNγ and TLR4 in Vascular Cells Reflect Pro-Atherogenic Responses in Human Atherosclerosis

    doi: 10.1371/journal.pone.0113318

    Figure Lengend Snippet: Effect of STAT1 dependent signal integration on chemokine expression. WT and STAT1 −/− VSMCs , HMECs or WT aortic ring segments were treated as described in Fig. 1 . A, RNA from VSMCs was isolated and qRT-PCR for Ccl5 , Cxcl9 using Gapdh as internal control was performed. B, On the medium remained after treatment of VSMCs ELISA for Ccl5 and Cxcl9 was performed. C, Expression of CXCL10, CXCL9 and CCL5 upon stimulation in ECs. D, RNA from incubated aortic rings was isolated and qRT-PCR for Cxcl10 , Cxcl9 using Gapdh as internal control was performed. Data represent means of at least 3 independent biological experiments ±SEM and p

    Article Snippet: Indeed, gene ( left panel) and protein expression ( left panel) of IRF8 in WT and STAT1−/− VSMCs in response to IFNγ, LPS or IFNγ+LPS, confirmed the microarray data.

    Techniques: Expressing, Isolation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Incubation

    STAT1-mediated abolished response to norepinephrine and sodium nitroprusside is associated with disturbed NO production. A, WT and STAT1 −/− VSMCs were treated as described in Fig. 1 . RNA was isolated and qRT-PCR for Nos2 using Gapdh as internal control was performed (upper panel) B, After stimulation as described in Fig. 1 , medium was refreshed and left for 24 h. Next, 100 µl of the medium was taken and the product of Nos2- nitrite was measured. Data represent means of at least 3 independent biological experiments ±SEM and p

    Journal: PLoS ONE

    Article Title: STAT1-Dependent Signal Integration between IFNγ and TLR4 in Vascular Cells Reflect Pro-Atherogenic Responses in Human Atherosclerosis

    doi: 10.1371/journal.pone.0113318

    Figure Lengend Snippet: STAT1-mediated abolished response to norepinephrine and sodium nitroprusside is associated with disturbed NO production. A, WT and STAT1 −/− VSMCs were treated as described in Fig. 1 . RNA was isolated and qRT-PCR for Nos2 using Gapdh as internal control was performed (upper panel) B, After stimulation as described in Fig. 1 , medium was refreshed and left for 24 h. Next, 100 µl of the medium was taken and the product of Nos2- nitrite was measured. Data represent means of at least 3 independent biological experiments ±SEM and p

    Article Snippet: Indeed, gene ( left panel) and protein expression ( left panel) of IRF8 in WT and STAT1−/− VSMCs in response to IFNγ, LPS or IFNγ+LPS, confirmed the microarray data.

    Techniques: Isolation, Quantitative RT-PCR