extracellular signal regulated kinase erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc extracellular signal regulated kinase erk 1 2
    Extracellular Signal Regulated Kinase Erk 1 2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phosphorylated extracellular signal regulated protein kinases erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated extracellular signal regulated protein kinases erk 1 2
    Phosphorylated Extracellular Signal Regulated Protein Kinases Erk 1 2, supplied by Cell Signaling Technology Inc, 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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    extracellular signal regulated kinase erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc extracellular signal regulated kinase erk 1 2
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    phosphorylated extracellular signal regulated kinase p erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated extracellular signal regulated kinase p erk 1 2
    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) <t>p-ERK1/2,</t> ERK1/2, and <t>p-ERK/ERK</t> ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
    Phosphorylated Extracellular Signal Regulated Kinase P Erk 1 2, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "Dietary Curcumin Attenuates Hepatic Cellular Senescence by Suppressing the MAPK/NF-κB Signaling Pathway in Aged Mice"

    Article Title: Dietary Curcumin Attenuates Hepatic Cellular Senescence by Suppressing the MAPK/NF-κB Signaling Pathway in Aged Mice

    Journal: Antioxidants

    doi: 10.3390/antiox12061165

    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) p-ERK1/2, ERK1/2, and p-ERK/ERK ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
    Figure Legend Snippet: Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) p-ERK1/2, ERK1/2, and p-ERK/ERK ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).

    Techniques Used: Western Blot, Expressing

    anti extracellular signal regulated kinase erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti extracellular signal regulated kinase erk 1 2
    Anti Extracellular Signal Regulated Kinase Erk 1 2, supplied by Cell Signaling Technology Inc, 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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    anti phospho extracellular signal regulated kinase erk 1 2 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho extracellular signal regulated kinase erk 1 2 antibody
    Anti Phospho Extracellular Signal Regulated Kinase Erk 1 2 Antibody, supplied by Cell Signaling Technology Inc, 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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    anti phospho extracellular signal regulated kinase erk 1 2 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho extracellular signal regulated kinase erk 1 2 antibody
    Anti Phospho Extracellular Signal Regulated Kinase Erk 1 2 Antibody, supplied by Cell Signaling Technology Inc, 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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    rabbit anti phospho extracellular signal regulated kinase erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti phospho extracellular signal regulated kinase erk 1 2
    Rabbit Anti Phospho Extracellular Signal Regulated Kinase Erk 1 2, supplied by Cell Signaling Technology Inc, 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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    extracellular signal regulated kinase erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc extracellular signal regulated kinase erk 1 2
    Effect of recombinant IL-6 on Akt, MEK 1/2, and ERK 1/2 phosphorylation in ERα-positive and ERα-negative cell lines. Notes: Cell lines were treated with IL-6 and analyzed at baseline and 24 hours posttreatment. Each blot represents independent experiments and bands were digitally excised without modification and rearranged for presentation. Abbreviations: IL-6, interleukin-6; Akt, serine-threonine kinase; MEK, MAPK/ERK kinase; ERK, extracellular signal regulated kinase; ER, estrogen receptor.
    Extracellular Signal Regulated Kinase Erk 1 2, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "Interleukin-6 is a potential therapeutic target in interleukin-6 dependent, estrogen receptor-α-positive breast cancer"

    Article Title: Interleukin-6 is a potential therapeutic target in interleukin-6 dependent, estrogen receptor-α-positive breast cancer

    Journal: Breast Cancer : Targets and Therapy

    doi: 10.2147/BCTT.S92414

    Effect of recombinant IL-6 on Akt, MEK 1/2, and ERK 1/2 phosphorylation in ERα-positive and ERα-negative cell lines. Notes: Cell lines were treated with IL-6 and analyzed at baseline and 24 hours posttreatment. Each blot represents independent experiments and bands were digitally excised without modification and rearranged for presentation. Abbreviations: IL-6, interleukin-6; Akt, serine-threonine kinase; MEK, MAPK/ERK kinase; ERK, extracellular signal regulated kinase; ER, estrogen receptor.
    Figure Legend Snippet: Effect of recombinant IL-6 on Akt, MEK 1/2, and ERK 1/2 phosphorylation in ERα-positive and ERα-negative cell lines. Notes: Cell lines were treated with IL-6 and analyzed at baseline and 24 hours posttreatment. Each blot represents independent experiments and bands were digitally excised without modification and rearranged for presentation. Abbreviations: IL-6, interleukin-6; Akt, serine-threonine kinase; MEK, MAPK/ERK kinase; ERK, extracellular signal regulated kinase; ER, estrogen receptor.

    Techniques Used: Recombinant, Modification

    11587 1 ap phospho extracellular signal regulated kinase p erk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 11587 1 ap phospho extracellular signal regulated kinase p erk
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    extracellular signal regulated kinase erk 1 2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc extracellular signal regulated kinase erk 1 2
    (A) Stimulation with OSM (100 ng/mL) resulted in increased phosphorylation of <t>ERK-1/2,</t> SAPK/JNK-1/2 kinases and induced PI3 kinase-dependent Akt phosphorylation. One representative experiment (n = 3) is shown. TNF-α (50 ng/mL) served as positive control. (B) Activation and expression of phospho-STATs and protein loading of the respective STAT proteins were assessed by immunoblotting. STAT1 and STAT3 phosphorylation was detected with a maximum at 10–30 min after stimulation with OSM (100 ng/mL). One representative experiment (n = 3) is shown. IL-22 (100 ng/mL), for which we previously demonstrated STAT1 and STAT3 activation in IEC , served as positive control. (C) MEK inhibition did not alter OSM-mediated STAT3 upregulation. Similarly, STAT3 inhibition had no significant effect on ERK-1/2 regulation. PCNA served as house keeping control. (D) Knockdown of OSMR, but not LIFR in HCT116 cells resulted in decrease of STAT3-phosphorylation after OSM stimulation compared to cells treated with control siRNA (co siRNA). One representative experiment (n = 3) is shown.
    Extracellular Signal Regulated Kinase Erk 1 2, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "Oncostatin M Mediates STAT3-Dependent Intestinal Epithelial Restitution via Increased Cell Proliferation, Decreased Apoptosis and Upregulation of SERPIN Family Members"

    Article Title: Oncostatin M Mediates STAT3-Dependent Intestinal Epithelial Restitution via Increased Cell Proliferation, Decreased Apoptosis and Upregulation of SERPIN Family Members

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0093498

    (A) Stimulation with OSM (100 ng/mL) resulted in increased phosphorylation of ERK-1/2, SAPK/JNK-1/2 kinases and induced PI3 kinase-dependent Akt phosphorylation. One representative experiment (n = 3) is shown. TNF-α (50 ng/mL) served as positive control. (B) Activation and expression of phospho-STATs and protein loading of the respective STAT proteins were assessed by immunoblotting. STAT1 and STAT3 phosphorylation was detected with a maximum at 10–30 min after stimulation with OSM (100 ng/mL). One representative experiment (n = 3) is shown. IL-22 (100 ng/mL), for which we previously demonstrated STAT1 and STAT3 activation in IEC , served as positive control. (C) MEK inhibition did not alter OSM-mediated STAT3 upregulation. Similarly, STAT3 inhibition had no significant effect on ERK-1/2 regulation. PCNA served as house keeping control. (D) Knockdown of OSMR, but not LIFR in HCT116 cells resulted in decrease of STAT3-phosphorylation after OSM stimulation compared to cells treated with control siRNA (co siRNA). One representative experiment (n = 3) is shown.
    Figure Legend Snippet: (A) Stimulation with OSM (100 ng/mL) resulted in increased phosphorylation of ERK-1/2, SAPK/JNK-1/2 kinases and induced PI3 kinase-dependent Akt phosphorylation. One representative experiment (n = 3) is shown. TNF-α (50 ng/mL) served as positive control. (B) Activation and expression of phospho-STATs and protein loading of the respective STAT proteins were assessed by immunoblotting. STAT1 and STAT3 phosphorylation was detected with a maximum at 10–30 min after stimulation with OSM (100 ng/mL). One representative experiment (n = 3) is shown. IL-22 (100 ng/mL), for which we previously demonstrated STAT1 and STAT3 activation in IEC , served as positive control. (C) MEK inhibition did not alter OSM-mediated STAT3 upregulation. Similarly, STAT3 inhibition had no significant effect on ERK-1/2 regulation. PCNA served as house keeping control. (D) Knockdown of OSMR, but not LIFR in HCT116 cells resulted in decrease of STAT3-phosphorylation after OSM stimulation compared to cells treated with control siRNA (co siRNA). One representative experiment (n = 3) is shown.

    Techniques Used: Positive Control, Activation Assay, Expressing, Western Blot, Inhibition

    After stimulation with 100/mL OSM for 48 hours, cell proliferation was significantly higher in OSM-treated cells in comparison to unstimulated cells as determined by WST-1 assay; * p = 0.02 vs. control. Pretreatment with the ERK-1/2-inhibitor PD98059 and transfection with STAT3 siRNA reduced OSM-mediated cell proliferation, while there was no effect by the PI3 kinase inhibitor wortmannin; ** p = 0.01, # p = 0.006, ‡ p = 0.57 vs. OSM-stimulated. In all experiments, proliferation in unstimulated control cells was arbitrarily set to 1.0.
    Figure Legend Snippet: After stimulation with 100/mL OSM for 48 hours, cell proliferation was significantly higher in OSM-treated cells in comparison to unstimulated cells as determined by WST-1 assay; * p = 0.02 vs. control. Pretreatment with the ERK-1/2-inhibitor PD98059 and transfection with STAT3 siRNA reduced OSM-mediated cell proliferation, while there was no effect by the PI3 kinase inhibitor wortmannin; ** p = 0.01, # p = 0.006, ‡ p = 0.57 vs. OSM-stimulated. In all experiments, proliferation in unstimulated control cells was arbitrarily set to 1.0.

    Techniques Used: WST-1 Assay, Transfection

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    Cell Signaling Technology Inc extracellular signal regulated kinase erk 1 2
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    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) <t>p-ERK1/2,</t> ERK1/2, and <t>p-ERK/ERK</t> ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
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    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) <t>p-ERK1/2,</t> ERK1/2, and <t>p-ERK/ERK</t> ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
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    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) <t>p-ERK1/2,</t> ERK1/2, and <t>p-ERK/ERK</t> ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
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    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) <t>p-ERK1/2,</t> ERK1/2, and <t>p-ERK/ERK</t> ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
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    Cell Signaling Technology Inc 11587 1 ap phospho extracellular signal regulated kinase p erk
    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) <t>p-ERK1/2,</t> ERK1/2, and <t>p-ERK/ERK</t> ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).
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    Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) p-ERK1/2, ERK1/2, and p-ERK/ERK ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).

    Journal: Antioxidants

    Article Title: Dietary Curcumin Attenuates Hepatic Cellular Senescence by Suppressing the MAPK/NF-κB Signaling Pathway in Aged Mice

    doi: 10.3390/antiox12061165

    Figure Lengend Snippet: Curcumin ameliorates hepatic cellular senescence by regulating the p38-MAPK signaling pathway in HFHSD-fed aged mice. Immunoblots and protein expression levels in the liver tissue lysates after 15 weeks of dietary interventions: ( A ) p-ERK1/2, ERK1/2, and p-ERK/ERK ratio; ( B ) p-JNK, JNK, and p-JNK/JNK ratio; ( C ) p-p38, p38, and p-p38/p38 ratio; and ( D ) p-MK2, MK2, and p-MK2/MK2 ratio. The results are expressed as mean ± SEM (* p < 0.05).

    Article Snippet: The membranes were blocked in a blocking reagent (LI-COR, Lincoln, NE, USA) at room temperature for 1 h and incubated with the primary antibodies at 4 °C overnight as follows: phosphorylated extracellular signal-regulated kinase (p-ERK) 1/2, ERK1/2, phosphorylated c-Jun N-terminal kinase (p-JNK) 1/2, JNK1/2, p-p38, p38, phosphorylated MAP kinase-activated protein kinase 2 (p-MK2), MK2, p-p65, p65, p53, cyclophilin B, histone deacetylase 1 (HDAC1), β-tubulin, and β-actin from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Western Blot, Expressing