bay11 7082 Search Results


96
MedChemExpress bay11 7082
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InvivoGen bay117082
Bay117082, supplied by InvivoGen, 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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Selleck Chemicals bay 11 7082
Bay 11 7082, supplied by Selleck Chemicals, 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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Cell Signaling Technology Inc bay11 7082
Bay11 7082, supplied by Cell Signaling Technology Inc, 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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Santa Cruz Biotechnology bay11 7082 bay
Bay11 7082 Bay, 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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BPS Bioscience nsc 95397
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96
TargetMol nf κb inhibitor
<t>JAK-STAT,</t> NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor <t>BAY11-7082</t> ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.
Nf κb Inhibitor, supplied by TargetMol, 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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InvivoGen bay 11 7082
<t>JAK-STAT,</t> NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor <t>BAY11-7082</t> ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.
Bay 11 7082, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/bay 11 7082/product/InvivoGen
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BOC Sciences bay11 7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay11 7082, supplied by BOC Sciences, 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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Sino Biological bay
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay, supplied by Sino Biological, 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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Sino Biological bay11 7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay11 7082, supplied by Sino Biological, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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96
Chem Impex International bay11 7082
PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or <t>BAY11-7082</t> (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6
Bay11 7082, supplied by Chem Impex International, 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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Image Search Results


JAK-STAT, NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor BAY11-7082 ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.

Journal: Microorganisms

Article Title: Spring Viremia of Carp Virus Infection Induces Carp IL-10 Expression, Both In Vitro and In Vivo

doi: 10.3390/microorganisms11112812

Figure Lengend Snippet: JAK-STAT, NF-κB and p38 signaling pathways played important roles in SVCV-induced carp IL-10 production. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with JAK inhibitor CP-690550 ( A , B ), STAT3 inhibitor STA-21 ( C , D ), NF-κB inhibitor BAY11-7082 ( E , F ), p38 inhibitor SB202190 ( G , H ), JNK inhibitor SP600125 ( I , J ) or DMSO for 6 h, 12 h, 24 h and 48 h post-infection. The expression of carp IL-10 mRNA and protein were analyzed using RT-PCR and ELISA, respectively. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and, ns indicates no significant difference p > 0.05 compared with DMSO-treated plus SVCV-infected cells.

Article Snippet: JAK inhibitor (CP-690550), STAT3 inhibitor (STA-21), NF-κB inhibitor (BAY11-7082) and MAPK inhibitors (SP600125 and SB202190) were purchased from TargetMol (Shanghai, China).

Techniques: Infection, Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

( A – F ): Gene expressions of JAK1, JAK2, JAK3, TYK2, STAT5 and STAT6 were analyzed using RT-PCR in EPC cells. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with CP-690550, STA-21, BAY11-7082, SB202190, SP600125 and DMSO, respectively, at 6 h, 12 h, 24 h and 48 h post-infection. The gene expressions were analyzed using RT-PCR. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 compared with DMSO-treated plus SVCV-infected cells.

Journal: Microorganisms

Article Title: Spring Viremia of Carp Virus Infection Induces Carp IL-10 Expression, Both In Vitro and In Vivo

doi: 10.3390/microorganisms11112812

Figure Lengend Snippet: ( A – F ): Gene expressions of JAK1, JAK2, JAK3, TYK2, STAT5 and STAT6 were analyzed using RT-PCR in EPC cells. EPC cells were infected or uninfected with SVCV at MOI of 0.5, followed by treatment with CP-690550, STA-21, BAY11-7082, SB202190, SP600125 and DMSO, respectively, at 6 h, 12 h, 24 h and 48 h post-infection. The gene expressions were analyzed using RT-PCR. Data are presented as the mean ± SD of three independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 compared with DMSO-treated plus SVCV-infected cells.

Article Snippet: JAK inhibitor (CP-690550), STAT3 inhibitor (STA-21), NF-κB inhibitor (BAY11-7082) and MAPK inhibitors (SP600125 and SB202190) were purchased from TargetMol (Shanghai, China).

Techniques: Reverse Transcription Polymerase Chain Reaction, Infection

PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BAY11-7082 (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6

Journal: Respiratory Research

Article Title: Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

doi: 10.1186/s12931-021-01793-x

Figure Lengend Snippet: PCTR1 regulates HPA and EXT-1 expression in LPS- triggered sepsis in mice. a – e Mice were treated with LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. The levels of HPA, EXT-1, SIRT1 and p65 in the lung tissue were quantified by western blot. f – h BOC-2 (ALX receptor inhibitor, 600 ng/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BAY11-7082 (NF-κB inhibitor, 20 mg/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse). The protein levels of HPA and EXT-1 were measured by western blot. * P < .05, ** P < .01 relative to the CONTROL group, # P < .05, ## P < .01 relative to the LPS group, & P < .05, relative to the LPS + PCTR1 group. n = 6

Article Snippet: BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence.

Techniques: Expressing, Western Blot, Injection

PCTR1 protects the endothelial glycocalyx by modulating SIRT1/NF-κB pathways via ALX receptor. The level of HPA, EXT-1, SIRT1 and p65 in lung tissues was quantified using western blotting assay. BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence. HUVECs were administered with 1 µg/ml LPS and 100 nM PCTR1 for 6 h. After treatment with EX527 or DMSO, HS in HUVECs was determined by immunofluorescence ( c, d ). Scar bar = 50 μm. ** P < .01 in comparison to the CONTROL group, # P < .05, ## P < .01 in comparison to the LPS group, & P < .05, && P < .01, in comparison to the LPS + PCTR1 group. n = 6

Journal: Respiratory Research

Article Title: Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

doi: 10.1186/s12931-021-01793-x

Figure Lengend Snippet: PCTR1 protects the endothelial glycocalyx by modulating SIRT1/NF-κB pathways via ALX receptor. The level of HPA, EXT-1, SIRT1 and p65 in lung tissues was quantified using western blotting assay. BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence. HUVECs were administered with 1 µg/ml LPS and 100 nM PCTR1 for 6 h. After treatment with EX527 or DMSO, HS in HUVECs was determined by immunofluorescence ( c, d ). Scar bar = 50 μm. ** P < .01 in comparison to the CONTROL group, # P < .05, ## P < .01 in comparison to the LPS group, & P < .05, && P < .01, in comparison to the LPS + PCTR1 group. n = 6

Article Snippet: BAY11-7082 (NF-κB inhibitor, 20 mg/kg) or EX527 (SIRT1 inhibitor, 10 mg/kg) or BOC-2(ALX receptor inhibitor, 600 ng/kg) was injected 1 h followed by LPS (10 mg/kg) with or without PCTR1 (100 ng/mouse) for 6 h. ( a, b ) The expression of HS in tissue was examined by immunofluorescence.

Techniques: Western Blot, Injection, Expressing, Immunofluorescence