phosphorylated nfκb  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated nfκb
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    Phosphorylated Nfκb, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice"

    Article Title: Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice

    Journal: Molecular Vision

    doi:

    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta (NFκB). F : Western blot results for inhibitor of kappa beta (IκB). n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    Figure Legend Snippet: Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta (NFκB). F : Western blot results for inhibitor of kappa beta (IκB). n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.

    Techniques Used: In Vitro, Western Blot, Enzyme-linked Immunosorbent Assay

    Epac1 regulates NFκB phosphorylation in the mouse retina. Whole retinal lysates from exchange protein for cAMP 1 (Epac1) floxed versus Epac1 Cre-Lox mice were processed for western blot analyses for phosphorylated nuclear factor kappa beta (NFκB (Ser536) versus total NFκB ( A ) or inhibitor of kappa beta (IκB; B ). n = 5 for each group. Data are mean ± standard error of the mean (SEM). *p<0.05 versus Epac1 floxed.
    Figure Legend Snippet: Epac1 regulates NFκB phosphorylation in the mouse retina. Whole retinal lysates from exchange protein for cAMP 1 (Epac1) floxed versus Epac1 Cre-Lox mice were processed for western blot analyses for phosphorylated nuclear factor kappa beta (NFκB (Ser536) versus total NFκB ( A ) or inhibitor of kappa beta (IκB; B ). n = 5 for each group. Data are mean ± standard error of the mean (SEM). *p<0.05 versus Epac1 floxed.

    Techniques Used: Western Blot

    phosphorylated nfκb  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated nfκb
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    Phosphorylated Nfκb, supplied by Cell Signaling Technology Inc, 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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    Images

    1) Product Images from "Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice"

    Article Title: Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice

    Journal: Molecular Vision

    doi:

    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta (NFκB). F : Western blot results for inhibitor of kappa beta (IκB). n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    Figure Legend Snippet: Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta (NFκB). F : Western blot results for inhibitor of kappa beta (IκB). n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.

    Techniques Used: In Vitro, Western Blot, Enzyme-linked Immunosorbent Assay

    Epac1 regulates NFκB phosphorylation in the mouse retina. Whole retinal lysates from exchange protein for cAMP 1 (Epac1) floxed versus Epac1 Cre-Lox mice were processed for western blot analyses for phosphorylated nuclear factor kappa beta (NFκB (Ser536) versus total NFκB ( A ) or inhibitor of kappa beta (IκB; B ). n = 5 for each group. Data are mean ± standard error of the mean (SEM). *p<0.05 versus Epac1 floxed.
    Figure Legend Snippet: Epac1 regulates NFκB phosphorylation in the mouse retina. Whole retinal lysates from exchange protein for cAMP 1 (Epac1) floxed versus Epac1 Cre-Lox mice were processed for western blot analyses for phosphorylated nuclear factor kappa beta (NFκB (Ser536) versus total NFκB ( A ) or inhibitor of kappa beta (IκB; B ). n = 5 for each group. Data are mean ± standard error of the mean (SEM). *p<0.05 versus Epac1 floxed.

    Techniques Used: Western Blot

    anti pp65  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti pp65
    Anti Pp65, supplied by Cell Signaling Technology Inc, 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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    anti phospho nfκb p65  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho nfκb p65
    Anti Phospho Nfκb P65, supplied by Cell Signaling Technology Inc, 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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    hspa4  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc hspa4
    Hspa4, supplied by Cell Signaling Technology Inc, 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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    p p65  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p p65
    P P65, supplied by Cell Signaling Technology Inc, 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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    p p65  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p p65
    The activation of AMPK was increased in the differentiated osteoclast after LPS treatment. The phosphorylation of AMPK was increased with LPS stimulation in osteoclasts (A). Quantitative levels of inflammatory genes TNF‐α (B) and iNOS (C) expression were measured by qPCR in osteoclasts after exposure to 1 µg/ml LPS for 6 h. The MAPK (D–F: ERK (D), JNK (E), and p38(F)) and NF‐κB (G,H; IKKα/β (G) and <t>p65(H))</t> pathways were activated with LPS stimulation. Each column represents the mean ± SEM of at least three independent experiments. Symbols indicate significance difference between treatment with/without LPS (* p < .05, ** p < .002, *** p < .001). AMPK, AMP‐activated protein kinase; ERK, extracellular signal‐regulated kinases; iNOS, inducible nitric oxide synthase; JNK, c‐Jun N‐terminal kinase; LPS, lipopolysaccharide; MAPK, mitogen‐activated protein kinase; NF‐κB, nuclear factor kappa B; qPCR, quantitative polymerase chain reaction; TNF‐α, tumor necrosis factor‐α
    P P65, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "AMP‐activated protein kinase mediates lipopolysaccharide‐induced proinflammatory responses and elevated bone resorption in differentiated osteoclasts"

    Article Title: AMP‐activated protein kinase mediates lipopolysaccharide‐induced proinflammatory responses and elevated bone resorption in differentiated osteoclasts

    Journal: Journal of Cellular Biochemistry

    doi: 10.1002/jcb.30165

    The activation of AMPK was increased in the differentiated osteoclast after LPS treatment. The phosphorylation of AMPK was increased with LPS stimulation in osteoclasts (A). Quantitative levels of inflammatory genes TNF‐α (B) and iNOS (C) expression were measured by qPCR in osteoclasts after exposure to 1 µg/ml LPS for 6 h. The MAPK (D–F: ERK (D), JNK (E), and p38(F)) and NF‐κB (G,H; IKKα/β (G) and p65(H)) pathways were activated with LPS stimulation. Each column represents the mean ± SEM of at least three independent experiments. Symbols indicate significance difference between treatment with/without LPS (* p < .05, ** p < .002, *** p < .001). AMPK, AMP‐activated protein kinase; ERK, extracellular signal‐regulated kinases; iNOS, inducible nitric oxide synthase; JNK, c‐Jun N‐terminal kinase; LPS, lipopolysaccharide; MAPK, mitogen‐activated protein kinase; NF‐κB, nuclear factor kappa B; qPCR, quantitative polymerase chain reaction; TNF‐α, tumor necrosis factor‐α
    Figure Legend Snippet: The activation of AMPK was increased in the differentiated osteoclast after LPS treatment. The phosphorylation of AMPK was increased with LPS stimulation in osteoclasts (A). Quantitative levels of inflammatory genes TNF‐α (B) and iNOS (C) expression were measured by qPCR in osteoclasts after exposure to 1 µg/ml LPS for 6 h. The MAPK (D–F: ERK (D), JNK (E), and p38(F)) and NF‐κB (G,H; IKKα/β (G) and p65(H)) pathways were activated with LPS stimulation. Each column represents the mean ± SEM of at least three independent experiments. Symbols indicate significance difference between treatment with/without LPS (* p < .05, ** p < .002, *** p < .001). AMPK, AMP‐activated protein kinase; ERK, extracellular signal‐regulated kinases; iNOS, inducible nitric oxide synthase; JNK, c‐Jun N‐terminal kinase; LPS, lipopolysaccharide; MAPK, mitogen‐activated protein kinase; NF‐κB, nuclear factor kappa B; qPCR, quantitative polymerase chain reaction; TNF‐α, tumor necrosis factor‐α

    Techniques Used: Activation Assay, Expressing, Real-time Polymerase Chain Reaction

    anti phospho nf kb p65 ser536  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho nf kb p65 ser536
    Anti Phospho Nf Kb P65 Ser536, supplied by Cell Signaling Technology Inc, 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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    hspa4  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc hspa4
    Protein levels of heat shock proteins determined by western blot. (A–C) Show representative western blot images. (D–K) Display quantified protein levels for HSPA1, HSPA2, HSPD1, HSPB1, HSPB5, HSPB7, <t>HSPA4,</t> and HSP90, respectively. Data were statistically analyzed by unpaired two-tailed t -test. Dashed line indicates protein levels in the NF IVS . Western blot dataset is partly derived from Dorsch et al. and re-analyzed for the age-matched samples included in the current study .
    Hspa4, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "Sex-Related Differences in Protein Expression in Sarcomere Mutation-Positive Hypertrophic Cardiomyopathy"

    Article Title: Sex-Related Differences in Protein Expression in Sarcomere Mutation-Positive Hypertrophic Cardiomyopathy

    Journal: Frontiers in Cardiovascular Medicine

    doi: 10.3389/fcvm.2021.612215

    Protein levels of heat shock proteins determined by western blot. (A–C) Show representative western blot images. (D–K) Display quantified protein levels for HSPA1, HSPA2, HSPD1, HSPB1, HSPB5, HSPB7, HSPA4, and HSP90, respectively. Data were statistically analyzed by unpaired two-tailed t -test. Dashed line indicates protein levels in the NF IVS . Western blot dataset is partly derived from Dorsch et al. and re-analyzed for the age-matched samples included in the current study .
    Figure Legend Snippet: Protein levels of heat shock proteins determined by western blot. (A–C) Show representative western blot images. (D–K) Display quantified protein levels for HSPA1, HSPA2, HSPD1, HSPB1, HSPB5, HSPB7, HSPA4, and HSP90, respectively. Data were statistically analyzed by unpaired two-tailed t -test. Dashed line indicates protein levels in the NF IVS . Western blot dataset is partly derived from Dorsch et al. and re-analyzed for the age-matched samples included in the current study .

    Techniques Used: Western Blot, Two Tailed Test, Derivative Assay

    Normalized counts of proteins that are significantly upregulated in HCM female compared to HCM male and are uniquely upregulated in females when compared to NF IVS . (A) CRK, (B) HSPA4, (C) TUBB6, (D) ALDH1B1, (E) DMD, (F) LMOD2, (G) HNRNPA3 and (H) TFRC. # p < 0.05, ## p < 0.01, unpaired two-tailed t -test.
    Figure Legend Snippet: Normalized counts of proteins that are significantly upregulated in HCM female compared to HCM male and are uniquely upregulated in females when compared to NF IVS . (A) CRK, (B) HSPA4, (C) TUBB6, (D) ALDH1B1, (E) DMD, (F) LMOD2, (G) HNRNPA3 and (H) TFRC. # p < 0.05, ## p < 0.01, unpaired two-tailed t -test.

    Techniques Used: Two Tailed Test

    hspa4  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc hspa4
    Hspa4, supplied by Cell Signaling Technology Inc, 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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    phosphorylated p p65  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p p65
    JNK-IN-8 suppresses the JNK/NF-κB signaling pathway in LPS-induced acute lung injury in vivo and in vitro . (A) Primary macrophages stimulated by LPS and JNK-IN-8 (10 mM) for 2 h were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, <t>p65</t> and <t>p-p65</t> were assessed and (B) analyzed by densitometry. (C) Primary macrophages, stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 0, 30, 60 or 120 min, were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (D) analyzed by densitometry. (E) Protein expression levels of JNK, p-JNK, p65 and p-p65 in lung tissue were assessed and (F) analyzed by densitometry. β-actin was used as the internal loading control. (G) Primary macrophages were stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 2 h. Cytoplasmic and nuclear NF-κB p65 protein expression levels were determined and (H) analyzed by densitometry. β-actin and Lamin B were used as internal loading controls. Data are presented as the mean ± SD (n=3). ***P<0.001 vs. Sham; ## P<0.01 and ### P<0.001 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.
    Phosphorylated P P65, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "JNK-IN-8 treatment alleviates lipopolysaccharide-induced acute lung injury via suppression of inflammation and oxidative stress regulated by JNK/NF-κB signaling"

    Article Title: JNK-IN-8 treatment alleviates lipopolysaccharide-induced acute lung injury via suppression of inflammation and oxidative stress regulated by JNK/NF-κB signaling

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2020.11789

    JNK-IN-8 suppresses the JNK/NF-κB signaling pathway in LPS-induced acute lung injury in vivo and in vitro . (A) Primary macrophages stimulated by LPS and JNK-IN-8 (10 mM) for 2 h were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (B) analyzed by densitometry. (C) Primary macrophages, stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 0, 30, 60 or 120 min, were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (D) analyzed by densitometry. (E) Protein expression levels of JNK, p-JNK, p65 and p-p65 in lung tissue were assessed and (F) analyzed by densitometry. β-actin was used as the internal loading control. (G) Primary macrophages were stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 2 h. Cytoplasmic and nuclear NF-κB p65 protein expression levels were determined and (H) analyzed by densitometry. β-actin and Lamin B were used as internal loading controls. Data are presented as the mean ± SD (n=3). ***P<0.001 vs. Sham; ## P<0.01 and ### P<0.001 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.
    Figure Legend Snippet: JNK-IN-8 suppresses the JNK/NF-κB signaling pathway in LPS-induced acute lung injury in vivo and in vitro . (A) Primary macrophages stimulated by LPS and JNK-IN-8 (10 mM) for 2 h were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (B) analyzed by densitometry. (C) Primary macrophages, stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 0, 30, 60 or 120 min, were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (D) analyzed by densitometry. (E) Protein expression levels of JNK, p-JNK, p65 and p-p65 in lung tissue were assessed and (F) analyzed by densitometry. β-actin was used as the internal loading control. (G) Primary macrophages were stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 2 h. Cytoplasmic and nuclear NF-κB p65 protein expression levels were determined and (H) analyzed by densitometry. β-actin and Lamin B were used as internal loading controls. Data are presented as the mean ± SD (n=3). ***P<0.001 vs. Sham; ## P<0.01 and ### P<0.001 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.

    Techniques Used: In Vivo, In Vitro, Western Blot, Expressing

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    Cell Signaling Technology Inc phosphorylated nfκb
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
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    Cell Signaling Technology Inc anti pp65
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
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    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    Anti Phospho Nfκb P65, supplied by Cell Signaling Technology Inc, 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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    Cell Signaling Technology Inc hspa4
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    Hspa4, supplied by Cell Signaling Technology Inc, 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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    Cell Signaling Technology Inc p p65
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
    P P65, supplied by Cell Signaling Technology Inc, 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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    Cell Signaling Technology Inc anti phospho nf kb p65 ser536
    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta <t>(NFκB).</t> F : Western blot results for inhibitor of kappa <t>beta</t> <t>(IκB).</t> n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.
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    Cell Signaling Technology Inc phosphorylated p p65
    JNK-IN-8 suppresses the JNK/NF-κB signaling pathway in LPS-induced acute lung injury in vivo and in vitro . (A) Primary macrophages stimulated by LPS and JNK-IN-8 (10 mM) for 2 h were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, <t>p65</t> and <t>p-p65</t> were assessed and (B) analyzed by densitometry. (C) Primary macrophages, stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 0, 30, 60 or 120 min, were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (D) analyzed by densitometry. (E) Protein expression levels of JNK, p-JNK, p65 and p-p65 in lung tissue were assessed and (F) analyzed by densitometry. β-actin was used as the internal loading control. (G) Primary macrophages were stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 2 h. Cytoplasmic and nuclear NF-κB p65 protein expression levels were determined and (H) analyzed by densitometry. β-actin and Lamin B were used as internal loading controls. Data are presented as the mean ± SD (n=3). ***P<0.001 vs. Sham; ## P<0.01 and ### P<0.001 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.
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    Image Search Results


    Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta (NFκB). F : Western blot results for inhibitor of kappa beta (IκB). n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.

    Journal: Molecular Vision

    Article Title: Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice

    doi:

    Figure Lengend Snippet: Epac1 agonist decreased TNF-α and IL-1β in vitro. Data show results from retinal endothelial cells (RECs) grown in normal glucose (NG) or high glucose (HG) only, grown in NG or HG and treated with CPT-2’-O-Me-cAMP, an exchange protein for cAMP 1 (Epac1)-specific agonist (NG or HG+8CPT-cAMP), and grown in NG and HG and treated with scrambled (NG or HG+Sc) or Epac1 siRNA (NG or HG+Epac1 siRNA). A : Western blot data show successful knockdown of Epac1. B : Western blot data for Epac2 show that CPT-2’-O-Me-cAMP is specific for Epac1. C : Enzyme-linked immunosorbent assay (ELISA) data for tumor necrosis factor alpha (TNF-α). D : Data for interleukin-1β (IL-1β). E : Western blot results for nuclear factor kappa beta (NFκB). F : Western blot results for inhibitor of kappa beta (IκB). n = 4 for each group. Data are mean ± standard error of the mean (SEM). * p<0.05 versus NG, #p<0.05 versus HG, $p<0.05 versus HG+8CPT-cAMP.

    Article Snippet: After blocking in Tris-buffered saline and Tween 20 (TBST; 10 mM Tris-HCl buffer, pH 8.0, 150 mM NaCl, 0.1% Tween-20) and 5% (w/v) bovine serum albumin, the membranes were treated with Epac1 (ab109415), Epac 2 (ab193665, Abcam), total nuclear factor kappa beta (NFκB; #4764), phosphorylated NFκB (Ser 536, #3303), phosphorylated IκB (Ser32, #2859), total IκB (#4812, Cell Signaling, Danvers, MA), and beta actin (sc-47778, Santa Cruz Biotechnology, Santa Cruz, CA) primary antibodies followed by incubation with secondary antibodies labeled with horseradish peroxidase.

    Techniques: In Vitro, Western Blot, Enzyme-linked Immunosorbent Assay

    Epac1 regulates NFκB phosphorylation in the mouse retina. Whole retinal lysates from exchange protein for cAMP 1 (Epac1) floxed versus Epac1 Cre-Lox mice were processed for western blot analyses for phosphorylated nuclear factor kappa beta (NFκB (Ser536) versus total NFκB ( A ) or inhibitor of kappa beta (IκB; B ). n = 5 for each group. Data are mean ± standard error of the mean (SEM). *p<0.05 versus Epac1 floxed.

    Journal: Molecular Vision

    Article Title: Epac1 agonist decreased inflammatory proteins in retinal endothelial cells, and loss of Epac1 increased inflammatory proteins in the retinal vasculature of mice

    doi:

    Figure Lengend Snippet: Epac1 regulates NFκB phosphorylation in the mouse retina. Whole retinal lysates from exchange protein for cAMP 1 (Epac1) floxed versus Epac1 Cre-Lox mice were processed for western blot analyses for phosphorylated nuclear factor kappa beta (NFκB (Ser536) versus total NFκB ( A ) or inhibitor of kappa beta (IκB; B ). n = 5 for each group. Data are mean ± standard error of the mean (SEM). *p<0.05 versus Epac1 floxed.

    Article Snippet: After blocking in Tris-buffered saline and Tween 20 (TBST; 10 mM Tris-HCl buffer, pH 8.0, 150 mM NaCl, 0.1% Tween-20) and 5% (w/v) bovine serum albumin, the membranes were treated with Epac1 (ab109415), Epac 2 (ab193665, Abcam), total nuclear factor kappa beta (NFκB; #4764), phosphorylated NFκB (Ser 536, #3303), phosphorylated IκB (Ser32, #2859), total IκB (#4812, Cell Signaling, Danvers, MA), and beta actin (sc-47778, Santa Cruz Biotechnology, Santa Cruz, CA) primary antibodies followed by incubation with secondary antibodies labeled with horseradish peroxidase.

    Techniques: Western Blot

    JNK-IN-8 suppresses the JNK/NF-κB signaling pathway in LPS-induced acute lung injury in vivo and in vitro . (A) Primary macrophages stimulated by LPS and JNK-IN-8 (10 mM) for 2 h were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (B) analyzed by densitometry. (C) Primary macrophages, stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 0, 30, 60 or 120 min, were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (D) analyzed by densitometry. (E) Protein expression levels of JNK, p-JNK, p65 and p-p65 in lung tissue were assessed and (F) analyzed by densitometry. β-actin was used as the internal loading control. (G) Primary macrophages were stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 2 h. Cytoplasmic and nuclear NF-κB p65 protein expression levels were determined and (H) analyzed by densitometry. β-actin and Lamin B were used as internal loading controls. Data are presented as the mean ± SD (n=3). ***P<0.001 vs. Sham; ## P<0.01 and ### P<0.001 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.

    Journal: Molecular Medicine Reports

    Article Title: JNK-IN-8 treatment alleviates lipopolysaccharide-induced acute lung injury via suppression of inflammation and oxidative stress regulated by JNK/NF-κB signaling

    doi: 10.3892/mmr.2020.11789

    Figure Lengend Snippet: JNK-IN-8 suppresses the JNK/NF-κB signaling pathway in LPS-induced acute lung injury in vivo and in vitro . (A) Primary macrophages stimulated by LPS and JNK-IN-8 (10 mM) for 2 h were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (B) analyzed by densitometry. (C) Primary macrophages, stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 0, 30, 60 or 120 min, were extracted and subjected to western blot analysis. The protein expression levels of JNK, p-JNK, p65 and p-p65 were assessed and (D) analyzed by densitometry. (E) Protein expression levels of JNK, p-JNK, p65 and p-p65 in lung tissue were assessed and (F) analyzed by densitometry. β-actin was used as the internal loading control. (G) Primary macrophages were stimulated with LPS in the presence or absence of JNK-IN-8 (10 mM) for 2 h. Cytoplasmic and nuclear NF-κB p65 protein expression levels were determined and (H) analyzed by densitometry. β-actin and Lamin B were used as internal loading controls. Data are presented as the mean ± SD (n=3). ***P<0.001 vs. Sham; ## P<0.01 and ### P<0.001 vs. LPS. LPS, lipopolysaccharide; p-, phosphorylated.

    Article Snippet: Specific primary antibodies against NF-κB p65 (cat. no. 8242), phosphorylated (p)-p65 (Ser536; cat. no. 3303), JNK (cat. no. 9252), p-JNK (Thr183/Tyr185; cat. no. 4668) and β-actin (cat. no. 3700) were purchased from Cell Signaling Technology, Inc.

    Techniques: In Vivo, In Vitro, Western Blot, Expressing