phosphorylated p p38 mapk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p p38 mapk
    Phosphorylated P P38 Mapk, 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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    phosphorylated p p38 mapk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p p38 mapk
    Effects of OSM on the bFGF-induced <t>phosphorylation</t> <t>of</t> <t>p38</t> <t>MAPK,</t> SAPK/JNK and p44/p42 MAPK in MC3T3-E1 cells. The cultured cells were pretreated with 0, 30, 50 or 70 ng/ml OSM for 60 min, and then stimulated with 30 ng/ml bFGF or vehicle for (A) 10 or (B and C) 20 min. The cell extracts were then subjected to SDS-PAGE and western blot analysis with antibodies against <t>(A)</t> <t>p-p38</t> <t>MAPK,</t> <t>p38</t> <t>MAPK</t> and GAPDH; (B) p-SAPK/JNK, SAPK/JNK and GAPDH; or (C) p-p44/p42 MAPK, p44/p42 MAPK and GAPDH. The histograms show the semi-quantitative representations of the expression levels of (A) <t>p-p38</t> <t>MAPK</t> after normalization to p38 MAPK, (B) p-SAPK/JNK after normalization to SAPK/JNK, and (C) p-p44/p42 MAPK after normalization to p44/p42 MAPK obtained from densitometric analysis. The levels were expressed as the fold increase with respect to the basal levels presented in lane 1. Data are presented as the mean ± SEM of (A) quadruplicate determinations from four independent cell preparations or (B and C) triplicate determinations from three independent cell preparations. *P<0.05 vs. control; #P<0.05 vs. bFGF alone. bFGF, basic fibroblast growth factor; MAPK, mitogen-activated protein kinase; MW, molecular weight N.S., not significant; p-, phosphorylated; SAPK/JNK, stress-activated protein kinase/c-Jun N-terminal kinase.
    Phosphorylated P P38 Mapk, 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 enhances osteoprotegerin synthesis but reduces macrophage colony‑stimulating factor synthesis in bFGF‑stimulated osteoblast‑like cells"

    Article Title: Oncostatin M enhances osteoprotegerin synthesis but reduces macrophage colony‑stimulating factor synthesis in bFGF‑stimulated osteoblast‑like cells

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2023.12322

    Effects of OSM on the bFGF-induced phosphorylation of p38 MAPK, SAPK/JNK and p44/p42 MAPK in MC3T3-E1 cells. The cultured cells were pretreated with 0, 30, 50 or 70 ng/ml OSM for 60 min, and then stimulated with 30 ng/ml bFGF or vehicle for (A) 10 or (B and C) 20 min. The cell extracts were then subjected to SDS-PAGE and western blot analysis with antibodies against (A) p-p38 MAPK, p38 MAPK and GAPDH; (B) p-SAPK/JNK, SAPK/JNK and GAPDH; or (C) p-p44/p42 MAPK, p44/p42 MAPK and GAPDH. The histograms show the semi-quantitative representations of the expression levels of (A) p-p38 MAPK after normalization to p38 MAPK, (B) p-SAPK/JNK after normalization to SAPK/JNK, and (C) p-p44/p42 MAPK after normalization to p44/p42 MAPK obtained from densitometric analysis. The levels were expressed as the fold increase with respect to the basal levels presented in lane 1. Data are presented as the mean ± SEM of (A) quadruplicate determinations from four independent cell preparations or (B and C) triplicate determinations from three independent cell preparations. *P<0.05 vs. control; #P<0.05 vs. bFGF alone. bFGF, basic fibroblast growth factor; MAPK, mitogen-activated protein kinase; MW, molecular weight N.S., not significant; p-, phosphorylated; SAPK/JNK, stress-activated protein kinase/c-Jun N-terminal kinase.
    Figure Legend Snippet: Effects of OSM on the bFGF-induced phosphorylation of p38 MAPK, SAPK/JNK and p44/p42 MAPK in MC3T3-E1 cells. The cultured cells were pretreated with 0, 30, 50 or 70 ng/ml OSM for 60 min, and then stimulated with 30 ng/ml bFGF or vehicle for (A) 10 or (B and C) 20 min. The cell extracts were then subjected to SDS-PAGE and western blot analysis with antibodies against (A) p-p38 MAPK, p38 MAPK and GAPDH; (B) p-SAPK/JNK, SAPK/JNK and GAPDH; or (C) p-p44/p42 MAPK, p44/p42 MAPK and GAPDH. The histograms show the semi-quantitative representations of the expression levels of (A) p-p38 MAPK after normalization to p38 MAPK, (B) p-SAPK/JNK after normalization to SAPK/JNK, and (C) p-p44/p42 MAPK after normalization to p44/p42 MAPK obtained from densitometric analysis. The levels were expressed as the fold increase with respect to the basal levels presented in lane 1. Data are presented as the mean ± SEM of (A) quadruplicate determinations from four independent cell preparations or (B and C) triplicate determinations from three independent cell preparations. *P<0.05 vs. control; #P<0.05 vs. bFGF alone. bFGF, basic fibroblast growth factor; MAPK, mitogen-activated protein kinase; MW, molecular weight N.S., not significant; p-, phosphorylated; SAPK/JNK, stress-activated protein kinase/c-Jun N-terminal kinase.

    Techniques Used: Cell Culture, SDS Page, Western Blot, Expressing, Molecular Weight

    phosphorylated p p38 mapk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p p38 mapk
    Effects of OSM on the bFGF-induced <t>phosphorylation</t> <t>of</t> <t>p38</t> <t>MAPK,</t> SAPK/JNK and p44/p42 MAPK in MC3T3-E1 cells. The cultured cells were pretreated with 0, 30, 50 or 70 ng/ml OSM for 60 min, and then stimulated with 30 ng/ml bFGF or vehicle for (A) 10 or (B and C) 20 min. The cell extracts were then subjected to SDS-PAGE and western blot analysis with antibodies against <t>(A)</t> <t>p-p38</t> <t>MAPK,</t> <t>p38</t> <t>MAPK</t> and GAPDH; (B) p-SAPK/JNK, SAPK/JNK and GAPDH; or (C) p-p44/p42 MAPK, p44/p42 MAPK and GAPDH. The histograms show the semi-quantitative representations of the expression levels of (A) <t>p-p38</t> <t>MAPK</t> after normalization to p38 MAPK, (B) p-SAPK/JNK after normalization to SAPK/JNK, and (C) p-p44/p42 MAPK after normalization to p44/p42 MAPK obtained from densitometric analysis. The levels were expressed as the fold increase with respect to the basal levels presented in lane 1. Data are presented as the mean ± SEM of (A) quadruplicate determinations from four independent cell preparations or (B and C) triplicate determinations from three independent cell preparations. *P<0.05 vs. control; #P<0.05 vs. bFGF alone. bFGF, basic fibroblast growth factor; MAPK, mitogen-activated protein kinase; MW, molecular weight N.S., not significant; p-, phosphorylated; SAPK/JNK, stress-activated protein kinase/c-Jun N-terminal kinase.
    Phosphorylated P P38 Mapk, 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 enhances osteoprotegerin synthesis but reduces macrophage colony‑stimulating factor synthesis in bFGF‑stimulated osteoblast‑like cells"

    Article Title: Oncostatin M enhances osteoprotegerin synthesis but reduces macrophage colony‑stimulating factor synthesis in bFGF‑stimulated osteoblast‑like cells

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2023.12322

    Effects of OSM on the bFGF-induced phosphorylation of p38 MAPK, SAPK/JNK and p44/p42 MAPK in MC3T3-E1 cells. The cultured cells were pretreated with 0, 30, 50 or 70 ng/ml OSM for 60 min, and then stimulated with 30 ng/ml bFGF or vehicle for (A) 10 or (B and C) 20 min. The cell extracts were then subjected to SDS-PAGE and western blot analysis with antibodies against (A) p-p38 MAPK, p38 MAPK and GAPDH; (B) p-SAPK/JNK, SAPK/JNK and GAPDH; or (C) p-p44/p42 MAPK, p44/p42 MAPK and GAPDH. The histograms show the semi-quantitative representations of the expression levels of (A) p-p38 MAPK after normalization to p38 MAPK, (B) p-SAPK/JNK after normalization to SAPK/JNK, and (C) p-p44/p42 MAPK after normalization to p44/p42 MAPK obtained from densitometric analysis. The levels were expressed as the fold increase with respect to the basal levels presented in lane 1. Data are presented as the mean ± SEM of (A) quadruplicate determinations from four independent cell preparations or (B and C) triplicate determinations from three independent cell preparations. *P<0.05 vs. control; #P<0.05 vs. bFGF alone. bFGF, basic fibroblast growth factor; MAPK, mitogen-activated protein kinase; MW, molecular weight N.S., not significant; p-, phosphorylated; SAPK/JNK, stress-activated protein kinase/c-Jun N-terminal kinase.
    Figure Legend Snippet: Effects of OSM on the bFGF-induced phosphorylation of p38 MAPK, SAPK/JNK and p44/p42 MAPK in MC3T3-E1 cells. The cultured cells were pretreated with 0, 30, 50 or 70 ng/ml OSM for 60 min, and then stimulated with 30 ng/ml bFGF or vehicle for (A) 10 or (B and C) 20 min. The cell extracts were then subjected to SDS-PAGE and western blot analysis with antibodies against (A) p-p38 MAPK, p38 MAPK and GAPDH; (B) p-SAPK/JNK, SAPK/JNK and GAPDH; or (C) p-p44/p42 MAPK, p44/p42 MAPK and GAPDH. The histograms show the semi-quantitative representations of the expression levels of (A) p-p38 MAPK after normalization to p38 MAPK, (B) p-SAPK/JNK after normalization to SAPK/JNK, and (C) p-p44/p42 MAPK after normalization to p44/p42 MAPK obtained from densitometric analysis. The levels were expressed as the fold increase with respect to the basal levels presented in lane 1. Data are presented as the mean ± SEM of (A) quadruplicate determinations from four independent cell preparations or (B and C) triplicate determinations from three independent cell preparations. *P<0.05 vs. control; #P<0.05 vs. bFGF alone. bFGF, basic fibroblast growth factor; MAPK, mitogen-activated protein kinase; MW, molecular weight N.S., not significant; p-, phosphorylated; SAPK/JNK, stress-activated protein kinase/c-Jun N-terminal kinase.

    Techniques Used: Cell Culture, SDS Page, Western Blot, Expressing, Molecular Weight

    p p38 rabbit anti phosphorylated p38 mapk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p p38 rabbit anti phosphorylated p38 mapk
    P P38 Rabbit Anti Phosphorylated P38 Mapk, 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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    phosphorylated p38 p p38  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p38 p p38
    Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of <t>P38,</t> P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3
    Phosphorylated P38 P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Dioscin alleviates the progression of osteoarthritis: an in vitro and in vivo study"

    Article Title: Dioscin alleviates the progression of osteoarthritis: an in vitro and in vivo study

    Journal: Journal of Inflammation (London, England)

    doi: 10.1186/s12950-023-00339-w

    Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of P38, P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3
    Figure Legend Snippet: Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of P38, P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3

    Techniques Used: Activation Assay, Western Blot

    phosphorylated p p38 mapk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p p38 mapk
    Phosphorylated P P38 Mapk, 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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    mouse anti phosphorylated p38 mitogen activated protein kinase p p38  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mouse anti phosphorylated p38 mitogen activated protein kinase p p38
    Mouse Anti Phosphorylated P38 Mitogen Activated Protein Kinase P P38, 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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    phosphorylated p38 mitogen activated protein kinase p p38  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated p38 mitogen activated protein kinase p p38
    Angiogenic activities of young human EPCs after treatment with siRNA specific to PP2A (siPP2A) and western blot analysis of young human EPCs treated with PP2A siRNA. Note that (A) transcript and (B and C) protein expression levels of PP2A were suppressed in siPP2A‐treated EPCs, accompanied by attenuated cellular activities of (D) proliferation, (E) migration and (F) tube formation. n = 3 for each bar. (G) In three different clones of EPCs, <t>phosphorylated</t> <t>p38</t> <t>(p‐p38)</t> and phosphorylated JNK (p‐JNK) were upregulated after siPP2A treatment. Quantitative Analysis confirmed the activation of (H) p38 and (I) JNK signalling pathways. n = 3 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. * p < 0.05, *** p < 0.001 vs. corresponding negative control (NC). Abbreviations are as in Figure
    Phosphorylated P38 Mitogen Activated Protein Kinase P P38, 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 "Hsa‐miR ‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans"

    Article Title: Hsa‐miR ‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.17691

    Angiogenic activities of young human EPCs after treatment with siRNA specific to PP2A (siPP2A) and western blot analysis of young human EPCs treated with PP2A siRNA. Note that (A) transcript and (B and C) protein expression levels of PP2A were suppressed in siPP2A‐treated EPCs, accompanied by attenuated cellular activities of (D) proliferation, (E) migration and (F) tube formation. n = 3 for each bar. (G) In three different clones of EPCs, phosphorylated p38 (p‐p38) and phosphorylated JNK (p‐JNK) were upregulated after siPP2A treatment. Quantitative Analysis confirmed the activation of (H) p38 and (I) JNK signalling pathways. n = 3 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. * p < 0.05, *** p < 0.001 vs. corresponding negative control (NC). Abbreviations are as in Figure
    Figure Legend Snippet: Angiogenic activities of young human EPCs after treatment with siRNA specific to PP2A (siPP2A) and western blot analysis of young human EPCs treated with PP2A siRNA. Note that (A) transcript and (B and C) protein expression levels of PP2A were suppressed in siPP2A‐treated EPCs, accompanied by attenuated cellular activities of (D) proliferation, (E) migration and (F) tube formation. n = 3 for each bar. (G) In three different clones of EPCs, phosphorylated p38 (p‐p38) and phosphorylated JNK (p‐JNK) were upregulated after siPP2A treatment. Quantitative Analysis confirmed the activation of (H) p38 and (I) JNK signalling pathways. n = 3 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. * p < 0.05, *** p < 0.001 vs. corresponding negative control (NC). Abbreviations are as in Figure

    Techniques Used: Western Blot, Expressing, Migration, Clone Assay, Activation Assay, Negative Control

    Regulation of PP2A by miR‐409‐3p and the signalling proteins in young human EPCs. PP2A was downregulated by miR‐409‐3p mimic at (A) transcript and (B and C) protein levels, compared to corresponding NC. (D) Time series analysis showed, in cells treated with the mimic, (E) PP2A was downregulated for at least 72 h, while (F) p‐p38 and (G) p‐JNK were activated with peaks at 48 h. n = 5 for each bar. Data are mean ± SEM and analysed using one‐way anova followed by post hoc Fisher's least significant difference test for multiple group comparisons. * p < 0.05 vs. NC. Abbreviations are as in Figure
    Figure Legend Snippet: Regulation of PP2A by miR‐409‐3p and the signalling proteins in young human EPCs. PP2A was downregulated by miR‐409‐3p mimic at (A) transcript and (B and C) protein levels, compared to corresponding NC. (D) Time series analysis showed, in cells treated with the mimic, (E) PP2A was downregulated for at least 72 h, while (F) p‐p38 and (G) p‐JNK were activated with peaks at 48 h. n = 5 for each bar. Data are mean ± SEM and analysed using one‐way anova followed by post hoc Fisher's least significant difference test for multiple group comparisons. * p < 0.05 vs. NC. Abbreviations are as in Figure

    Techniques Used:

    Prediction of binding site of hsa‐miR‐409‐3p for protein phosphatase 2 catalytic subunit alpha (PPP2CA) gene and examination of its product protein phosphatase 2A (PP2A). (A) Diagram showing the seed sequences of hsa‐miR‐409‐3p and its predicted binding site in the 3’‐UTR of PPP2CA gene by prediction methods including TargetScan and miRanda. (B) Luciferase reporter assays of human embryonic kidney cells 293 co‐transfected with vector, wild‐type 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐WT) or mutant 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐MUT), along with mimic negative control (NC) or miR‐409‐3p mimics showed reduced activity only in the group co‐transfected with PPP2CA‐3’UTR‐WT and miR‐409‐3p mimics. Concordantly, in senescent cells, PP2A expression was downregulated at both (C) transcript and (D and E) protein levels, with activation of (F) phosphorylated p38 (p‐p38) and (G) phosphorylated JNK (p‐JNK). n = 4 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. *, p < 0.05, ***, p < 0.001 vs. corresponding control. p38, p38 mitogen‐activated protein kinase. JNK, c‐Jun N‐terminal kinase
    Figure Legend Snippet: Prediction of binding site of hsa‐miR‐409‐3p for protein phosphatase 2 catalytic subunit alpha (PPP2CA) gene and examination of its product protein phosphatase 2A (PP2A). (A) Diagram showing the seed sequences of hsa‐miR‐409‐3p and its predicted binding site in the 3’‐UTR of PPP2CA gene by prediction methods including TargetScan and miRanda. (B) Luciferase reporter assays of human embryonic kidney cells 293 co‐transfected with vector, wild‐type 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐WT) or mutant 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐MUT), along with mimic negative control (NC) or miR‐409‐3p mimics showed reduced activity only in the group co‐transfected with PPP2CA‐3’UTR‐WT and miR‐409‐3p mimics. Concordantly, in senescent cells, PP2A expression was downregulated at both (C) transcript and (D and E) protein levels, with activation of (F) phosphorylated p38 (p‐p38) and (G) phosphorylated JNK (p‐JNK). n = 4 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. *, p < 0.05, ***, p < 0.001 vs. corresponding control. p38, p38 mitogen‐activated protein kinase. JNK, c‐Jun N‐terminal kinase

    Techniques Used: Binding Assay, Luciferase, Transfection, Plasmid Preparation, Mutagenesis, Negative Control, Activity Assay, Expressing, Activation Assay

    phosphorylation p p38  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylation p p38
    Information of antibodies.
    Phosphorylation P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation"

    Article Title: Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation

    Journal: Heliyon

    doi: 10.1016/j.heliyon.2023.e12994

    Information of antibodies.
    Figure Legend Snippet: Information of antibodies.

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    protein kinases mapks p38 mapk phosphorylation p p38 mapk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc protein kinases mapks p38 mapk phosphorylation p p38 mapk
    Protein Kinases Mapks P38 Mapk Phosphorylation P P38 Mapk, 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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    P P38 Rabbit Anti Phosphorylated P38 Mapk, 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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    Cell Signaling Technology Inc phosphorylated p38 p p38
    Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of <t>P38,</t> P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3
    Phosphorylated P38 P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc mouse anti phosphorylated p38 mitogen activated protein kinase p p38
    Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of <t>P38,</t> P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3
    Mouse Anti Phosphorylated P38 Mitogen Activated Protein Kinase P P38, 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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    Cell Signaling Technology Inc phosphorylated p38 mitogen activated protein kinase p p38
    Angiogenic activities of young human EPCs after treatment with siRNA specific to PP2A (siPP2A) and western blot analysis of young human EPCs treated with PP2A siRNA. Note that (A) transcript and (B and C) protein expression levels of PP2A were suppressed in siPP2A‐treated EPCs, accompanied by attenuated cellular activities of (D) proliferation, (E) migration and (F) tube formation. n = 3 for each bar. (G) In three different clones of EPCs, <t>phosphorylated</t> <t>p38</t> <t>(p‐p38)</t> and phosphorylated JNK (p‐JNK) were upregulated after siPP2A treatment. Quantitative Analysis confirmed the activation of (H) p38 and (I) JNK signalling pathways. n = 3 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. * p < 0.05, *** p < 0.001 vs. corresponding negative control (NC). Abbreviations are as in Figure
    Phosphorylated P38 Mitogen Activated Protein Kinase P P38, 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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    Information of antibodies.
    Phosphorylation P P38, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc protein kinases mapks p38 mapk phosphorylation p p38 mapk
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    Image Search Results


    Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of P38, P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3

    Journal: Journal of Inflammation (London, England)

    Article Title: Dioscin alleviates the progression of osteoarthritis: an in vitro and in vivo study

    doi: 10.1186/s12950-023-00339-w

    Figure Lengend Snippet: Dio blocks IL-1β-induced MAPK signaling pathway activation. Chondrocytes were exposed to IL-1β (10 ng/mL) with or without Dio (200, 400, and 800 ng/mL) for 30 min. A Representative western blots and ( B ) quantitative analysis of P38, P-P38, ERK, P-ERK, JNK, and P-JNK in each group. # P < 0.05 vs. control group; * P < 0.05 vs. IL-1β group; ** P < 0.01 vs. IL-1β group; n = 3

    Article Snippet: Antibodies specific for P65 (#8242), phosphorylated P65 (P-P65) (#3033), IκBα (#4814), phosphorylated-IκBα (P-IκBα) (#2859), IKKβ (#8943), phosphorylated-IKKα/β (P-IKKα/β) (#2697), P38 (#8690), phosphorylated-p38 (p-p38) (#4511), ERK (#4695), phosphorylated-ERK (P-ERK) (#4370), JNK (#9252), and phosphorylated-JNK (P-JNK) (#4668) were procured from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Activation Assay, Western Blot

    Angiogenic activities of young human EPCs after treatment with siRNA specific to PP2A (siPP2A) and western blot analysis of young human EPCs treated with PP2A siRNA. Note that (A) transcript and (B and C) protein expression levels of PP2A were suppressed in siPP2A‐treated EPCs, accompanied by attenuated cellular activities of (D) proliferation, (E) migration and (F) tube formation. n = 3 for each bar. (G) In three different clones of EPCs, phosphorylated p38 (p‐p38) and phosphorylated JNK (p‐JNK) were upregulated after siPP2A treatment. Quantitative Analysis confirmed the activation of (H) p38 and (I) JNK signalling pathways. n = 3 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. * p < 0.05, *** p < 0.001 vs. corresponding negative control (NC). Abbreviations are as in Figure

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Hsa‐miR ‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

    doi: 10.1111/jcmm.17691

    Figure Lengend Snippet: Angiogenic activities of young human EPCs after treatment with siRNA specific to PP2A (siPP2A) and western blot analysis of young human EPCs treated with PP2A siRNA. Note that (A) transcript and (B and C) protein expression levels of PP2A were suppressed in siPP2A‐treated EPCs, accompanied by attenuated cellular activities of (D) proliferation, (E) migration and (F) tube formation. n = 3 for each bar. (G) In three different clones of EPCs, phosphorylated p38 (p‐p38) and phosphorylated JNK (p‐JNK) were upregulated after siPP2A treatment. Quantitative Analysis confirmed the activation of (H) p38 and (I) JNK signalling pathways. n = 3 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. * p < 0.05, *** p < 0.001 vs. corresponding negative control (NC). Abbreviations are as in Figure

    Article Snippet: The antibodies included phosphorylated p38 mitogen‐activated protein kinase (p‐p38), total p38, phosphorylated c‐Jun N‐terminal kinase (p‐JNK), total JNK, phosphorylated extracellular signal‐regulated kinase (p‐ERK) and total ERK from Cell Signalling Technology.

    Techniques: Western Blot, Expressing, Migration, Clone Assay, Activation Assay, Negative Control

    Regulation of PP2A by miR‐409‐3p and the signalling proteins in young human EPCs. PP2A was downregulated by miR‐409‐3p mimic at (A) transcript and (B and C) protein levels, compared to corresponding NC. (D) Time series analysis showed, in cells treated with the mimic, (E) PP2A was downregulated for at least 72 h, while (F) p‐p38 and (G) p‐JNK were activated with peaks at 48 h. n = 5 for each bar. Data are mean ± SEM and analysed using one‐way anova followed by post hoc Fisher's least significant difference test for multiple group comparisons. * p < 0.05 vs. NC. Abbreviations are as in Figure

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Hsa‐miR ‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

    doi: 10.1111/jcmm.17691

    Figure Lengend Snippet: Regulation of PP2A by miR‐409‐3p and the signalling proteins in young human EPCs. PP2A was downregulated by miR‐409‐3p mimic at (A) transcript and (B and C) protein levels, compared to corresponding NC. (D) Time series analysis showed, in cells treated with the mimic, (E) PP2A was downregulated for at least 72 h, while (F) p‐p38 and (G) p‐JNK were activated with peaks at 48 h. n = 5 for each bar. Data are mean ± SEM and analysed using one‐way anova followed by post hoc Fisher's least significant difference test for multiple group comparisons. * p < 0.05 vs. NC. Abbreviations are as in Figure

    Article Snippet: The antibodies included phosphorylated p38 mitogen‐activated protein kinase (p‐p38), total p38, phosphorylated c‐Jun N‐terminal kinase (p‐JNK), total JNK, phosphorylated extracellular signal‐regulated kinase (p‐ERK) and total ERK from Cell Signalling Technology.

    Techniques:

    Prediction of binding site of hsa‐miR‐409‐3p for protein phosphatase 2 catalytic subunit alpha (PPP2CA) gene and examination of its product protein phosphatase 2A (PP2A). (A) Diagram showing the seed sequences of hsa‐miR‐409‐3p and its predicted binding site in the 3’‐UTR of PPP2CA gene by prediction methods including TargetScan and miRanda. (B) Luciferase reporter assays of human embryonic kidney cells 293 co‐transfected with vector, wild‐type 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐WT) or mutant 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐MUT), along with mimic negative control (NC) or miR‐409‐3p mimics showed reduced activity only in the group co‐transfected with PPP2CA‐3’UTR‐WT and miR‐409‐3p mimics. Concordantly, in senescent cells, PP2A expression was downregulated at both (C) transcript and (D and E) protein levels, with activation of (F) phosphorylated p38 (p‐p38) and (G) phosphorylated JNK (p‐JNK). n = 4 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. *, p < 0.05, ***, p < 0.001 vs. corresponding control. p38, p38 mitogen‐activated protein kinase. JNK, c‐Jun N‐terminal kinase

    Journal: Journal of Cellular and Molecular Medicine

    Article Title: Hsa‐miR ‐409‐3p regulates endothelial progenitor senescence via PP2A‐P38 and is a potential ageing marker in humans

    doi: 10.1111/jcmm.17691

    Figure Lengend Snippet: Prediction of binding site of hsa‐miR‐409‐3p for protein phosphatase 2 catalytic subunit alpha (PPP2CA) gene and examination of its product protein phosphatase 2A (PP2A). (A) Diagram showing the seed sequences of hsa‐miR‐409‐3p and its predicted binding site in the 3’‐UTR of PPP2CA gene by prediction methods including TargetScan and miRanda. (B) Luciferase reporter assays of human embryonic kidney cells 293 co‐transfected with vector, wild‐type 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐WT) or mutant 3’‐UTR of PPP2CA (PPP2CA‐3’UTR‐MUT), along with mimic negative control (NC) or miR‐409‐3p mimics showed reduced activity only in the group co‐transfected with PPP2CA‐3’UTR‐WT and miR‐409‐3p mimics. Concordantly, in senescent cells, PP2A expression was downregulated at both (C) transcript and (D and E) protein levels, with activation of (F) phosphorylated p38 (p‐p38) and (G) phosphorylated JNK (p‐JNK). n = 4 for each bar. Data are mean ± SEM and analysed using unpaired Student's t test for comparison between groups. *, p < 0.05, ***, p < 0.001 vs. corresponding control. p38, p38 mitogen‐activated protein kinase. JNK, c‐Jun N‐terminal kinase

    Article Snippet: The antibodies included phosphorylated p38 mitogen‐activated protein kinase (p‐p38), total p38, phosphorylated c‐Jun N‐terminal kinase (p‐JNK), total JNK, phosphorylated extracellular signal‐regulated kinase (p‐ERK) and total ERK from Cell Signalling Technology.

    Techniques: Binding Assay, Luciferase, Transfection, Plasmid Preparation, Mutagenesis, Negative Control, Activity Assay, Expressing, Activation Assay

    Information of antibodies.

    Journal: Heliyon

    Article Title: Effects of Vigna angularis extract and its active compound hemiphloin against atopic dermatitis-like skin inflammation

    doi: 10.1016/j.heliyon.2023.e12994

    Figure Lengend Snippet: Information of antibodies.

    Article Snippet: phosphorylation(p)-p38 , rabbit monoclonal , 1:1000 , #4511S , Cell Signaling Technology.

    Techniques: