39058 Search Results


tbk1 sirna  (Santa Cruz Biotechnology)
92
Santa Cruz Biotechnology tbk1 sirna
TLR4 Activation Induces G0 Arrest, Dephosphorylates SAMHD1, and Blocks HIV-1 Infection in an Interferon-Independent Manner (A) MDMs were treated with TAK242, BX795, and RUXO 6 h before addition of LPS. Cells were infected by vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 5, mean ± SEM). Cells from a representative donor were used for immunoblotting. (B) A simplified diagram of TLR4 signaling in response to LPS. LPS activates both MyD88-dependent and -independent signaling pathways. BX795, an inhibitor of <t>TBK1;</t> RUXO (ruxolitinib), an inhibitor of JAK1/2 kinase that suppresses IFN signaling; TAK242, an inhibitor of TLR4 signaling. (C) IRF3/NF-κB nuclear translocation assay. Cells were exposed to LPS in the absence or presence of TAK242, BX795, and RUXO, and 2 h later stained for IRF3/NF-κB. The percentage of cells with nuclear staining was determined (n = 3, mean ± SEM). Scale bars, 20 μm. (D) Expression data of TRIF and TBK1 in MDMs, displayed as cycle threshold (Ct) values (n = 3, mean ± SEM). (E–H) MDMs were transfected with control or TRIF, TBK1 <t>siRNA.</t> mRNA expression is shown as fold change relative to control (n = 3, mean ± SEM) (E). Cells from a representative donor were used for immunoblotting (F). Cells were exposed to LPS in control or KD cells, and 2 h later stained for IRF3/NF-κB. % of cells with nuclear staining was determined (n = 3, mean ± SEM) (G). MDMs transfected with control or TRIF, TBK1 siRNA were treated with LPS. Cells were infected by VSV-G-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 3 donors, mean ± SEM). Cells from a representative donor were used for immunoblotting (H). ∗∗∗ p ≤ 0.001; ∗∗ p ≤ 0.01; ∗ p ≤ 0.1; ns p, non-significant, paired t test.
Tbk1 Sirna, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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catalogue sc390585  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology catalogue sc390585
TLR4 Activation Induces G0 Arrest, Dephosphorylates SAMHD1, and Blocks HIV-1 Infection in an Interferon-Independent Manner (A) MDMs were treated with TAK242, BX795, and RUXO 6 h before addition of LPS. Cells were infected by vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 5, mean ± SEM). Cells from a representative donor were used for immunoblotting. (B) A simplified diagram of TLR4 signaling in response to LPS. LPS activates both MyD88-dependent and -independent signaling pathways. BX795, an inhibitor of <t>TBK1;</t> RUXO (ruxolitinib), an inhibitor of JAK1/2 kinase that suppresses IFN signaling; TAK242, an inhibitor of TLR4 signaling. (C) IRF3/NF-κB nuclear translocation assay. Cells were exposed to LPS in the absence or presence of TAK242, BX795, and RUXO, and 2 h later stained for IRF3/NF-κB. The percentage of cells with nuclear staining was determined (n = 3, mean ± SEM). Scale bars, 20 μm. (D) Expression data of TRIF and TBK1 in MDMs, displayed as cycle threshold (Ct) values (n = 3, mean ± SEM). (E–H) MDMs were transfected with control or TRIF, TBK1 <t>siRNA.</t> mRNA expression is shown as fold change relative to control (n = 3, mean ± SEM) (E). Cells from a representative donor were used for immunoblotting (F). Cells were exposed to LPS in control or KD cells, and 2 h later stained for IRF3/NF-κB. % of cells with nuclear staining was determined (n = 3, mean ± SEM) (G). MDMs transfected with control or TRIF, TBK1 siRNA were treated with LPS. Cells were infected by VSV-G-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 3 donors, mean ± SEM). Cells from a representative donor were used for immunoblotting (H). ∗∗∗ p ≤ 0.001; ∗∗ p ≤ 0.01; ∗ p ≤ 0.1; ns p, non-significant, paired t test.
Catalogue Sc390585, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
catalogue sc390585 - by Bioz Stars, 2026-02
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sp1  (Active Motif)
90
Active Motif sp1
TLR4 Activation Induces G0 Arrest, Dephosphorylates SAMHD1, and Blocks HIV-1 Infection in an Interferon-Independent Manner (A) MDMs were treated with TAK242, BX795, and RUXO 6 h before addition of LPS. Cells were infected by vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 5, mean ± SEM). Cells from a representative donor were used for immunoblotting. (B) A simplified diagram of TLR4 signaling in response to LPS. LPS activates both MyD88-dependent and -independent signaling pathways. BX795, an inhibitor of <t>TBK1;</t> RUXO (ruxolitinib), an inhibitor of JAK1/2 kinase that suppresses IFN signaling; TAK242, an inhibitor of TLR4 signaling. (C) IRF3/NF-κB nuclear translocation assay. Cells were exposed to LPS in the absence or presence of TAK242, BX795, and RUXO, and 2 h later stained for IRF3/NF-κB. The percentage of cells with nuclear staining was determined (n = 3, mean ± SEM). Scale bars, 20 μm. (D) Expression data of TRIF and TBK1 in MDMs, displayed as cycle threshold (Ct) values (n = 3, mean ± SEM). (E–H) MDMs were transfected with control or TRIF, TBK1 <t>siRNA.</t> mRNA expression is shown as fold change relative to control (n = 3, mean ± SEM) (E). Cells from a representative donor were used for immunoblotting (F). Cells were exposed to LPS in control or KD cells, and 2 h later stained for IRF3/NF-κB. % of cells with nuclear staining was determined (n = 3, mean ± SEM) (G). MDMs transfected with control or TRIF, TBK1 siRNA were treated with LPS. Cells were infected by VSV-G-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 3 donors, mean ± SEM). Cells from a representative donor were used for immunoblotting (H). ∗∗∗ p ≤ 0.001; ∗∗ p ≤ 0.01; ∗ p ≤ 0.1; ns p, non-significant, paired t test.
Sp1, supplied by Active Motif, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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chromatin immunoprecipitation (chip) grade sp1 antibody #39058  (Active Motif)
90
Active Motif chromatin immunoprecipitation (chip) grade sp1 antibody #39058
(A) Diagram of the OPG proximal promoter. Numbers represent the number of nucleotides relative to the transcriptional start site (+1). Four <t>Sp1</t> sites located in the region from −1486 to −1286 are shown, as are the two Runx2 binding elements located at −994 to −990 and −309 to −303, respectively. (B) Luciferase reporter assay performed in UMR106 osteoblasts co-transfected with −1486/+133 OPG Luc or −1286/+133 OPG Luc plasmid and either an empty vector (EV) control, wild type Cx43 expression vector (Cx43), or mutant Cx43 plasmids bearing the G138R or R76S mutation. ***, p-value < 0.001 relative to empty vector (EV) control sample by ANOVA.
Chromatin Immunoprecipitation (Chip) Grade Sp1 Antibody #39058, supplied by Active Motif, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/chromatin immunoprecipitation (chip) grade sp1 antibody #39058/product/Active Motif
Average 90 stars, based on 1 article reviews
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sp1 active motif 39058  (Active Motif)
90
Active Motif sp1 active motif 39058
(A) Diagram of the OPG proximal promoter. Numbers represent the number of nucleotides relative to the transcriptional start site (+1). Four <t>Sp1</t> sites located in the region from −1486 to −1286 are shown, as are the two Runx2 binding elements located at −994 to −990 and −309 to −303, respectively. (B) Luciferase reporter assay performed in UMR106 osteoblasts co-transfected with −1486/+133 OPG Luc or −1286/+133 OPG Luc plasmid and either an empty vector (EV) control, wild type Cx43 expression vector (Cx43), or mutant Cx43 plasmids bearing the G138R or R76S mutation. ***, p-value < 0.001 relative to empty vector (EV) control sample by ANOVA.
Sp1 Active Motif 39058, supplied by Active Motif, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
sp1 active motif 39058 - by Bioz Stars, 2026-02
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Image Search Results


TLR4 Activation Induces G0 Arrest, Dephosphorylates SAMHD1, and Blocks HIV-1 Infection in an Interferon-Independent Manner (A) MDMs were treated with TAK242, BX795, and RUXO 6 h before addition of LPS. Cells were infected by vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 5, mean ± SEM). Cells from a representative donor were used for immunoblotting. (B) A simplified diagram of TLR4 signaling in response to LPS. LPS activates both MyD88-dependent and -independent signaling pathways. BX795, an inhibitor of TBK1; RUXO (ruxolitinib), an inhibitor of JAK1/2 kinase that suppresses IFN signaling; TAK242, an inhibitor of TLR4 signaling. (C) IRF3/NF-κB nuclear translocation assay. Cells were exposed to LPS in the absence or presence of TAK242, BX795, and RUXO, and 2 h later stained for IRF3/NF-κB. The percentage of cells with nuclear staining was determined (n = 3, mean ± SEM). Scale bars, 20 μm. (D) Expression data of TRIF and TBK1 in MDMs, displayed as cycle threshold (Ct) values (n = 3, mean ± SEM). (E–H) MDMs were transfected with control or TRIF, TBK1 siRNA. mRNA expression is shown as fold change relative to control (n = 3, mean ± SEM) (E). Cells from a representative donor were used for immunoblotting (F). Cells were exposed to LPS in control or KD cells, and 2 h later stained for IRF3/NF-κB. % of cells with nuclear staining was determined (n = 3, mean ± SEM) (G). MDMs transfected with control or TRIF, TBK1 siRNA were treated with LPS. Cells were infected by VSV-G-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 3 donors, mean ± SEM). Cells from a representative donor were used for immunoblotting (H). ∗∗∗ p ≤ 0.001; ∗∗ p ≤ 0.01; ∗ p ≤ 0.1; ns p, non-significant, paired t test.

Journal: Cell Reports

Article Title: TLR4-Mediated Pathway Triggers Interferon-Independent G0 Arrest and Antiviral SAMHD1 Activity in Macrophages

doi: 10.1016/j.celrep.2020.03.008

Figure Lengend Snippet: TLR4 Activation Induces G0 Arrest, Dephosphorylates SAMHD1, and Blocks HIV-1 Infection in an Interferon-Independent Manner (A) MDMs were treated with TAK242, BX795, and RUXO 6 h before addition of LPS. Cells were infected by vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 5, mean ± SEM). Cells from a representative donor were used for immunoblotting. (B) A simplified diagram of TLR4 signaling in response to LPS. LPS activates both MyD88-dependent and -independent signaling pathways. BX795, an inhibitor of TBK1; RUXO (ruxolitinib), an inhibitor of JAK1/2 kinase that suppresses IFN signaling; TAK242, an inhibitor of TLR4 signaling. (C) IRF3/NF-κB nuclear translocation assay. Cells were exposed to LPS in the absence or presence of TAK242, BX795, and RUXO, and 2 h later stained for IRF3/NF-κB. The percentage of cells with nuclear staining was determined (n = 3, mean ± SEM). Scale bars, 20 μm. (D) Expression data of TRIF and TBK1 in MDMs, displayed as cycle threshold (Ct) values (n = 3, mean ± SEM). (E–H) MDMs were transfected with control or TRIF, TBK1 siRNA. mRNA expression is shown as fold change relative to control (n = 3, mean ± SEM) (E). Cells from a representative donor were used for immunoblotting (F). Cells were exposed to LPS in control or KD cells, and 2 h later stained for IRF3/NF-κB. % of cells with nuclear staining was determined (n = 3, mean ± SEM) (G). MDMs transfected with control or TRIF, TBK1 siRNA were treated with LPS. Cells were infected by VSV-G-pseudotyped HIV-1 18 h later. The percentage of infected cells was determined 48 h post-infection (n = 3 donors, mean ± SEM). Cells from a representative donor were used for immunoblotting (H). ∗∗∗ p ≤ 0.001; ∗∗ p ≤ 0.01; ∗ p ≤ 0.1; ns p, non-significant, paired t test.

Article Snippet: TBK1 siRNA , Santa Cruz , #sc-39058.

Techniques: Activation Assay, Infection, Virus, Western Blot, Protein-Protein interactions, Nuclear Translocation Assay, Staining, Expressing, Transfection, Control

Journal: Cell Reports

Article Title: TLR4-Mediated Pathway Triggers Interferon-Independent G0 Arrest and Antiviral SAMHD1 Activity in Macrophages

doi: 10.1016/j.celrep.2020.03.008

Figure Lengend Snippet:

Article Snippet: TBK1 siRNA , Santa Cruz , #sc-39058.

Techniques: Purification, Control, Virus, Recombinant, Transfection, Western Blot, Plasmid Preparation, Software, Membrane

(A) Diagram of the OPG proximal promoter. Numbers represent the number of nucleotides relative to the transcriptional start site (+1). Four Sp1 sites located in the region from −1486 to −1286 are shown, as are the two Runx2 binding elements located at −994 to −990 and −309 to −303, respectively. (B) Luciferase reporter assay performed in UMR106 osteoblasts co-transfected with −1486/+133 OPG Luc or −1286/+133 OPG Luc plasmid and either an empty vector (EV) control, wild type Cx43 expression vector (Cx43), or mutant Cx43 plasmids bearing the G138R or R76S mutation. ***, p-value < 0.001 relative to empty vector (EV) control sample by ANOVA.

Journal: Biochemical and biophysical research communications

Article Title: Connexin43 Regulates Osteoprotegerin Expression via ERK1/2 -dependent Recruitment of Sp1

doi: 10.1016/j.bbrc.2018.12.173

Figure Lengend Snippet: (A) Diagram of the OPG proximal promoter. Numbers represent the number of nucleotides relative to the transcriptional start site (+1). Four Sp1 sites located in the region from −1486 to −1286 are shown, as are the two Runx2 binding elements located at −994 to −990 and −309 to −303, respectively. (B) Luciferase reporter assay performed in UMR106 osteoblasts co-transfected with −1486/+133 OPG Luc or −1286/+133 OPG Luc plasmid and either an empty vector (EV) control, wild type Cx43 expression vector (Cx43), or mutant Cx43 plasmids bearing the G138R or R76S mutation. ***, p-value < 0.001 relative to empty vector (EV) control sample by ANOVA.

Article Snippet: The chromatin immunoprecipitation (ChIP) grade Sp1 antibody (#39058) was from Active Motif, and the anti-Runx2 antibody (#D130–3) from MBL International.

Techniques: Binding Assay, Luciferase, Reporter Assay, Transfection, Plasmid Preparation, Control, Expressing, Mutagenesis

(A) ChIP performed in UMR106 osteoblasts transfected with an empty vector (EV) control, wild type Cx43 expression vector (Cx43), or mutant Cx43 plasmids bearing the hypomorphic G138R or R76S mutation and precipitated using Sp1 antibodies. Data show result of qPCR on bead fractions amplified by the primers to the OPG proximal promoter (n=4/group). Data are normalized to inputs. The empty vector (EV) control is set to a value of 1. ***, p-value < 0.001 relative to empty vector (EV) control sample by ANOVA. (B) (A) ChIP performed in UMR106 using Runx2 antibodies (n=4/group). (C) Model of Cx43-dependent regulation of Tnfrsf11b/OPG gene expression and inhibition of osteoclastogenesis.

Journal: Biochemical and biophysical research communications

Article Title: Connexin43 Regulates Osteoprotegerin Expression via ERK1/2 -dependent Recruitment of Sp1

doi: 10.1016/j.bbrc.2018.12.173

Figure Lengend Snippet: (A) ChIP performed in UMR106 osteoblasts transfected with an empty vector (EV) control, wild type Cx43 expression vector (Cx43), or mutant Cx43 plasmids bearing the hypomorphic G138R or R76S mutation and precipitated using Sp1 antibodies. Data show result of qPCR on bead fractions amplified by the primers to the OPG proximal promoter (n=4/group). Data are normalized to inputs. The empty vector (EV) control is set to a value of 1. ***, p-value < 0.001 relative to empty vector (EV) control sample by ANOVA. (B) (A) ChIP performed in UMR106 using Runx2 antibodies (n=4/group). (C) Model of Cx43-dependent regulation of Tnfrsf11b/OPG gene expression and inhibition of osteoclastogenesis.

Article Snippet: The chromatin immunoprecipitation (ChIP) grade Sp1 antibody (#39058) was from Active Motif, and the anti-Runx2 antibody (#D130–3) from MBL International.

Techniques: Transfection, Plasmid Preparation, Control, Expressing, Mutagenesis, Amplification, Gene Expression, Inhibition