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nf κb p65 l8f6 mouse mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc nf κb p65 l8f6 mouse mab
    Effects of the MEK inhibitor, Trametinib, and PKC inhibitor, RO-317549, on ERK <t>and</t> <t>NF-κB</t> phosphorylation. BAs were incubated in OC for 6 h. (a) Western blot analysis of total ERK and p-ERK, (b) Quantitative data of ERK, (c) Western blot of total NF-κB and pNF-κB (d) Quantitative data of NF-κB Data are shown as mean ± SEM (Biological replicate; n = 5) and protein expression was compared by one-way ANOVA, with Dunnett's post-test. * = p < 0.05. Please note that the order of the inhibitor is not the same across the figures, due to the original experimental setup.
    Nf κb P65 L8f6 Mouse Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 785 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nf κb p65 l8f6 mouse mab/product/Cell Signaling Technology Inc
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    nf κb p65 l8f6 mouse mab - by Bioz Stars, 2026-02
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    1) Product Images from "Independent and synergistic roles of MEK-ERK1/2 and PKC pathways in regulating functional changes in vascular tissue following flow cessation"

    Article Title: Independent and synergistic roles of MEK-ERK1/2 and PKC pathways in regulating functional changes in vascular tissue following flow cessation

    Journal: Journal of Molecular and Cellular Cardiology Plus

    doi: 10.1016/j.jmccpl.2025.100300

    Effects of the MEK inhibitor, Trametinib, and PKC inhibitor, RO-317549, on ERK and NF-κB phosphorylation. BAs were incubated in OC for 6 h. (a) Western blot analysis of total ERK and p-ERK, (b) Quantitative data of ERK, (c) Western blot of total NF-κB and pNF-κB (d) Quantitative data of NF-κB Data are shown as mean ± SEM (Biological replicate; n = 5) and protein expression was compared by one-way ANOVA, with Dunnett's post-test. * = p < 0.05. Please note that the order of the inhibitor is not the same across the figures, due to the original experimental setup.
    Figure Legend Snippet: Effects of the MEK inhibitor, Trametinib, and PKC inhibitor, RO-317549, on ERK and NF-κB phosphorylation. BAs were incubated in OC for 6 h. (a) Western blot analysis of total ERK and p-ERK, (b) Quantitative data of ERK, (c) Western blot of total NF-κB and pNF-κB (d) Quantitative data of NF-κB Data are shown as mean ± SEM (Biological replicate; n = 5) and protein expression was compared by one-way ANOVA, with Dunnett's post-test. * = p < 0.05. Please note that the order of the inhibitor is not the same across the figures, due to the original experimental setup.

    Techniques Used: Phospho-proteomics, Incubation, Western Blot, Expressing

    The effect of NF-κB inhibitors in the contractility of BAs incubated for 48 h in OC. (a) Log concentration-response curves in response S6c, following incubation with the NF-κB inhibitors SP100030, BMS 345541, IMD 0354 (10 −6 M) the E max was compared by a multiple t -test with a Holm-Sidak correction (b) Log-concentration-response curves in response to S6c following incubation with 10 −5 M and 10 −6 M BMS 345541, the E max was compared by a multiple t-test with a Holm-Sidak correction (c) E max(S6c) contractions of RO317549 10 −6 M, BMS 345541 10 −6 M and their combination, compared with Trametinib 10 −8 M and its combination with BMS 345541 10 −6 M. E max were compared by one-way ANOVA, with Dunnett's post-test. Data are shown as mean ± SEM (Biological replicate; n = 4–18). * = p < 0.05.
    Figure Legend Snippet: The effect of NF-κB inhibitors in the contractility of BAs incubated for 48 h in OC. (a) Log concentration-response curves in response S6c, following incubation with the NF-κB inhibitors SP100030, BMS 345541, IMD 0354 (10 −6 M) the E max was compared by a multiple t -test with a Holm-Sidak correction (b) Log-concentration-response curves in response to S6c following incubation with 10 −5 M and 10 −6 M BMS 345541, the E max was compared by a multiple t-test with a Holm-Sidak correction (c) E max(S6c) contractions of RO317549 10 −6 M, BMS 345541 10 −6 M and their combination, compared with Trametinib 10 −8 M and its combination with BMS 345541 10 −6 M. E max were compared by one-way ANOVA, with Dunnett's post-test. Data are shown as mean ± SEM (Biological replicate; n = 4–18). * = p < 0.05.

    Techniques Used: Incubation, Concentration Assay

    Signaling pathways involved in ET B receptor upregulation and VSMC contraction. Extracellular stimuli such as flow cessation activate the MAPK/ERK pathway, which is disrupted by MEK inhibition (Trametinib) or ERK inhibition (Ulixertinib). In parallel, intracellular Ca 2+ increase leads to delayed PKC activation, promoting NF-κB signaling via the IKK complex. PKC and NF-κB inhibition (RO-317549 and BMS345541, respectively) remain effective when applied up to 6 h post-stimulus. Combined inhibition further suppresses ET B upregulation on VSMCs and reduces receptor-mediated contraction, indicating that both pathways contribute independently and are required for full functional response . Abbreviations: ET B : endothelin type B receptor; VSMC: vascular smooth muscle cell; NF-κB: nuclear factor. Created in BioRender. Kazantzi, S. (2025) https://BioRender.com/u89c445
    Figure Legend Snippet: Signaling pathways involved in ET B receptor upregulation and VSMC contraction. Extracellular stimuli such as flow cessation activate the MAPK/ERK pathway, which is disrupted by MEK inhibition (Trametinib) or ERK inhibition (Ulixertinib). In parallel, intracellular Ca 2+ increase leads to delayed PKC activation, promoting NF-κB signaling via the IKK complex. PKC and NF-κB inhibition (RO-317549 and BMS345541, respectively) remain effective when applied up to 6 h post-stimulus. Combined inhibition further suppresses ET B upregulation on VSMCs and reduces receptor-mediated contraction, indicating that both pathways contribute independently and are required for full functional response . Abbreviations: ET B : endothelin type B receptor; VSMC: vascular smooth muscle cell; NF-κB: nuclear factor. Created in BioRender. Kazantzi, S. (2025) https://BioRender.com/u89c445

    Techniques Used: Protein-Protein interactions, Inhibition, Activation Assay, Functional Assay



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    Image Search Results


    Effects of the MEK inhibitor, Trametinib, and PKC inhibitor, RO-317549, on ERK and NF-κB phosphorylation. BAs were incubated in OC for 6 h. (a) Western blot analysis of total ERK and p-ERK, (b) Quantitative data of ERK, (c) Western blot of total NF-κB and pNF-κB (d) Quantitative data of NF-κB Data are shown as mean ± SEM (Biological replicate; n = 5) and protein expression was compared by one-way ANOVA, with Dunnett's post-test. * = p < 0.05. Please note that the order of the inhibitor is not the same across the figures, due to the original experimental setup.

    Journal: Journal of Molecular and Cellular Cardiology Plus

    Article Title: Independent and synergistic roles of MEK-ERK1/2 and PKC pathways in regulating functional changes in vascular tissue following flow cessation

    doi: 10.1016/j.jmccpl.2025.100300

    Figure Lengend Snippet: Effects of the MEK inhibitor, Trametinib, and PKC inhibitor, RO-317549, on ERK and NF-κB phosphorylation. BAs were incubated in OC for 6 h. (a) Western blot analysis of total ERK and p-ERK, (b) Quantitative data of ERK, (c) Western blot of total NF-κB and pNF-κB (d) Quantitative data of NF-κB Data are shown as mean ± SEM (Biological replicate; n = 5) and protein expression was compared by one-way ANOVA, with Dunnett's post-test. * = p < 0.05. Please note that the order of the inhibitor is not the same across the figures, due to the original experimental setup.

    Article Snippet: The membranes were then transferred to a rocking table in room temperature with Blocking Buffer (EveryBlot Blocking Buffer, Cat. #: 12010020, Bio-Rad) for 10 min and then, the membranes were incubated with primary antibody dilutions overnight in 4 °C (1:1000 Mouse Anti-p44 / 42 MAP Kinase Monoclonal Antibody, Unconjugated, Clone L34F12 [Cell Signaling Technology Cat# 4696, lot: 29, RRID: AB_390780 ], 1:1000 Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (D13.14.4E) XP® Rabbit mAb [Cell Signaling Technology Cat# 4370, Lot: 28, RRID: AB_2315112 ), 1:1000 NF-κB p65 (L8F6) Mouse mAb [Cell Signaling Technology Cat# 6956, Lot:10, RRID: AB_10828935 ], 1:1000 Phospho-NF-κB p65 (Ser536) (93H1) Rabbit mAb [Cell Signaling Technology Cat# 3033,Lot: 19, RRID: AB_331284 ], GAPDH (D16H11) XP Rabbit mAb, [Cell Signaling Technology Cat# 5174, Lot: 8, RRID: AB_10622025 ], 1:1000 Actin, Smooth Muscle (1A4) Mouse Monoclonal Antibody [Cell Marque Cat# 202 M-94, Lot:0000243213, RRID: AB_1157937 ], 1:1000 alpha smooth muscle Actin antibody (EPR5368) [Abcam Cat# ab124964, Lot: GR303485 –26, RRID: AB_11129103 ]).

    Techniques: Phospho-proteomics, Incubation, Western Blot, Expressing

    The effect of NF-κB inhibitors in the contractility of BAs incubated for 48 h in OC. (a) Log concentration-response curves in response S6c, following incubation with the NF-κB inhibitors SP100030, BMS 345541, IMD 0354 (10 −6 M) the E max was compared by a multiple t -test with a Holm-Sidak correction (b) Log-concentration-response curves in response to S6c following incubation with 10 −5 M and 10 −6 M BMS 345541, the E max was compared by a multiple t-test with a Holm-Sidak correction (c) E max(S6c) contractions of RO317549 10 −6 M, BMS 345541 10 −6 M and their combination, compared with Trametinib 10 −8 M and its combination with BMS 345541 10 −6 M. E max were compared by one-way ANOVA, with Dunnett's post-test. Data are shown as mean ± SEM (Biological replicate; n = 4–18). * = p < 0.05.

    Journal: Journal of Molecular and Cellular Cardiology Plus

    Article Title: Independent and synergistic roles of MEK-ERK1/2 and PKC pathways in regulating functional changes in vascular tissue following flow cessation

    doi: 10.1016/j.jmccpl.2025.100300

    Figure Lengend Snippet: The effect of NF-κB inhibitors in the contractility of BAs incubated for 48 h in OC. (a) Log concentration-response curves in response S6c, following incubation with the NF-κB inhibitors SP100030, BMS 345541, IMD 0354 (10 −6 M) the E max was compared by a multiple t -test with a Holm-Sidak correction (b) Log-concentration-response curves in response to S6c following incubation with 10 −5 M and 10 −6 M BMS 345541, the E max was compared by a multiple t-test with a Holm-Sidak correction (c) E max(S6c) contractions of RO317549 10 −6 M, BMS 345541 10 −6 M and their combination, compared with Trametinib 10 −8 M and its combination with BMS 345541 10 −6 M. E max were compared by one-way ANOVA, with Dunnett's post-test. Data are shown as mean ± SEM (Biological replicate; n = 4–18). * = p < 0.05.

    Article Snippet: The membranes were then transferred to a rocking table in room temperature with Blocking Buffer (EveryBlot Blocking Buffer, Cat. #: 12010020, Bio-Rad) for 10 min and then, the membranes were incubated with primary antibody dilutions overnight in 4 °C (1:1000 Mouse Anti-p44 / 42 MAP Kinase Monoclonal Antibody, Unconjugated, Clone L34F12 [Cell Signaling Technology Cat# 4696, lot: 29, RRID: AB_390780 ], 1:1000 Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (D13.14.4E) XP® Rabbit mAb [Cell Signaling Technology Cat# 4370, Lot: 28, RRID: AB_2315112 ), 1:1000 NF-κB p65 (L8F6) Mouse mAb [Cell Signaling Technology Cat# 6956, Lot:10, RRID: AB_10828935 ], 1:1000 Phospho-NF-κB p65 (Ser536) (93H1) Rabbit mAb [Cell Signaling Technology Cat# 3033,Lot: 19, RRID: AB_331284 ], GAPDH (D16H11) XP Rabbit mAb, [Cell Signaling Technology Cat# 5174, Lot: 8, RRID: AB_10622025 ], 1:1000 Actin, Smooth Muscle (1A4) Mouse Monoclonal Antibody [Cell Marque Cat# 202 M-94, Lot:0000243213, RRID: AB_1157937 ], 1:1000 alpha smooth muscle Actin antibody (EPR5368) [Abcam Cat# ab124964, Lot: GR303485 –26, RRID: AB_11129103 ]).

    Techniques: Incubation, Concentration Assay

    Signaling pathways involved in ET B receptor upregulation and VSMC contraction. Extracellular stimuli such as flow cessation activate the MAPK/ERK pathway, which is disrupted by MEK inhibition (Trametinib) or ERK inhibition (Ulixertinib). In parallel, intracellular Ca 2+ increase leads to delayed PKC activation, promoting NF-κB signaling via the IKK complex. PKC and NF-κB inhibition (RO-317549 and BMS345541, respectively) remain effective when applied up to 6 h post-stimulus. Combined inhibition further suppresses ET B upregulation on VSMCs and reduces receptor-mediated contraction, indicating that both pathways contribute independently and are required for full functional response . Abbreviations: ET B : endothelin type B receptor; VSMC: vascular smooth muscle cell; NF-κB: nuclear factor. Created in BioRender. Kazantzi, S. (2025) https://BioRender.com/u89c445

    Journal: Journal of Molecular and Cellular Cardiology Plus

    Article Title: Independent and synergistic roles of MEK-ERK1/2 and PKC pathways in regulating functional changes in vascular tissue following flow cessation

    doi: 10.1016/j.jmccpl.2025.100300

    Figure Lengend Snippet: Signaling pathways involved in ET B receptor upregulation and VSMC contraction. Extracellular stimuli such as flow cessation activate the MAPK/ERK pathway, which is disrupted by MEK inhibition (Trametinib) or ERK inhibition (Ulixertinib). In parallel, intracellular Ca 2+ increase leads to delayed PKC activation, promoting NF-κB signaling via the IKK complex. PKC and NF-κB inhibition (RO-317549 and BMS345541, respectively) remain effective when applied up to 6 h post-stimulus. Combined inhibition further suppresses ET B upregulation on VSMCs and reduces receptor-mediated contraction, indicating that both pathways contribute independently and are required for full functional response . Abbreviations: ET B : endothelin type B receptor; VSMC: vascular smooth muscle cell; NF-κB: nuclear factor. Created in BioRender. Kazantzi, S. (2025) https://BioRender.com/u89c445

    Article Snippet: The membranes were then transferred to a rocking table in room temperature with Blocking Buffer (EveryBlot Blocking Buffer, Cat. #: 12010020, Bio-Rad) for 10 min and then, the membranes were incubated with primary antibody dilutions overnight in 4 °C (1:1000 Mouse Anti-p44 / 42 MAP Kinase Monoclonal Antibody, Unconjugated, Clone L34F12 [Cell Signaling Technology Cat# 4696, lot: 29, RRID: AB_390780 ], 1:1000 Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (D13.14.4E) XP® Rabbit mAb [Cell Signaling Technology Cat# 4370, Lot: 28, RRID: AB_2315112 ), 1:1000 NF-κB p65 (L8F6) Mouse mAb [Cell Signaling Technology Cat# 6956, Lot:10, RRID: AB_10828935 ], 1:1000 Phospho-NF-κB p65 (Ser536) (93H1) Rabbit mAb [Cell Signaling Technology Cat# 3033,Lot: 19, RRID: AB_331284 ], GAPDH (D16H11) XP Rabbit mAb, [Cell Signaling Technology Cat# 5174, Lot: 8, RRID: AB_10622025 ], 1:1000 Actin, Smooth Muscle (1A4) Mouse Monoclonal Antibody [Cell Marque Cat# 202 M-94, Lot:0000243213, RRID: AB_1157937 ], 1:1000 alpha smooth muscle Actin antibody (EPR5368) [Abcam Cat# ab124964, Lot: GR303485 –26, RRID: AB_11129103 ]).

    Techniques: Protein-Protein interactions, Inhibition, Activation Assay, Functional Assay