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antibodies for detecting map2k3, p38 mapk, p-p38 mapk, hsp 27, p-hsp 27, and gapdh  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibodies for detecting map2k3, p38 mapk, p-p38 mapk, hsp 27, p-hsp 27, and gapdh
    Antibodies For Detecting Map2k3, P38 Mapk, P P38 Mapk, Hsp 27, P Hsp 27, And Gapdh, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies for detecting map2k3, p38 mapk, p-p38 mapk, hsp 27, p-hsp 27, and gapdh/product/Cell Signaling Technology Inc
    Average 90 stars, based on 1 article reviews
    antibodies for detecting map2k3, p38 mapk, p-p38 mapk, hsp 27, p-hsp 27, and gapdh - by Bioz Stars, 2026-04
    90/100 stars

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    Effects of BI2B on cAMP-PKA and p38 MAPK -MSK1 axes in α-MSH-induced melanogenic programs. B16F0 cells were pretreated with BI2B for 2 h and stimulated with α-MSH for 30 min in the presence of BI2B. (A) BI2B did not alter α-MSH-induced PKA activity. (B) BI2B inhibited α-MSH-induced phosphorylation of p38 MAPK but did not alter those of ERK and JNK. (C) BI2B inhibited α-MSH-induced phosphorylation of MSK1. (D) BI2B did not alter α-MSH-induced phosphorylation of MKK3/6. (E) Catalytically active <t>rhMKK3</t> was treated with BI2B for 10 min, and its kinase activity was measured in cell-free reactions. BI2B inhibited MKK3-catalyzed kinase activity on p38 MAPK . * P < 0.05 vs. α-MSH alone or rhMKK3 alone.
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    DUPS1 regulates p38 MAPK signaling after CPT1 inhibition in postnatal cardiomyocytes. (A) The expression of <t>Map2k3</t> , mitogen-activated protein kinase kinase 6 ( Map2k6 ), and dual specificity phosphatase family ( Dusp1 , Dusp2 , Dusp3 , Dusp4 , Dusp5 , Dusp6 , Dusp7 , Dusp8 , Dusp9 , Dusp10 , Dusp11 , Dusp12 , Dusp13 , Dusp14 , Dusp15 , Dusp16 , Dusp18 , Dusp19 , Dusp21 , Dusp22 ) in P1 and P7 cardiomyocytes ( n = 6, ∗ P < 0.05 vs. P1). (B) The effect of ETX treatment and Dusp1 siRNA (si Dusp1 ) on DUSP1 expression and p38 MAPK phosphorylation in P7 cardiomyocytes ( n = 3, ∗ P < 0.05 vs. Control, # P < 0.05 vs. ETX). (C) The effect of ETX treatment on the interaction of DUSP1 and p38 MAPK in P7 cardiomyocytes ( n = 6, ∗ P < 0.05 vs. Control). Error bars indicate SEM.
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    Image Search Results


    Effects of BI2B on cAMP-PKA and p38 MAPK -MSK1 axes in α-MSH-induced melanogenic programs. B16F0 cells were pretreated with BI2B for 2 h and stimulated with α-MSH for 30 min in the presence of BI2B. (A) BI2B did not alter α-MSH-induced PKA activity. (B) BI2B inhibited α-MSH-induced phosphorylation of p38 MAPK but did not alter those of ERK and JNK. (C) BI2B inhibited α-MSH-induced phosphorylation of MSK1. (D) BI2B did not alter α-MSH-induced phosphorylation of MKK3/6. (E) Catalytically active rhMKK3 was treated with BI2B for 10 min, and its kinase activity was measured in cell-free reactions. BI2B inhibited MKK3-catalyzed kinase activity on p38 MAPK . * P < 0.05 vs. α-MSH alone or rhMKK3 alone.

    Journal: International Journal of Biological Sciences

    Article Title: Interruption of p38 MAPK -MSK1-CREB-MITF-M pathway to prevent hyperpigmentation in the skin

    doi: 10.7150/ijbs.93120

    Figure Lengend Snippet: Effects of BI2B on cAMP-PKA and p38 MAPK -MSK1 axes in α-MSH-induced melanogenic programs. B16F0 cells were pretreated with BI2B for 2 h and stimulated with α-MSH for 30 min in the presence of BI2B. (A) BI2B did not alter α-MSH-induced PKA activity. (B) BI2B inhibited α-MSH-induced phosphorylation of p38 MAPK but did not alter those of ERK and JNK. (C) BI2B inhibited α-MSH-induced phosphorylation of MSK1. (D) BI2B did not alter α-MSH-induced phosphorylation of MKK3/6. (E) Catalytically active rhMKK3 was treated with BI2B for 10 min, and its kinase activity was measured in cell-free reactions. BI2B inhibited MKK3-catalyzed kinase activity on p38 MAPK . * P < 0.05 vs. α-MSH alone or rhMKK3 alone.

    Article Snippet: To determine in vitro kinase activity of MKK3 in cell-free conditions, catalytically active rhMKK3 (SignalChem, M04-10G) was reacted with p38α MAPK (SignalChem, M37-14G) as a substrate in presence of 10 μCi [γ- 32 P]-ATP as a probe for 30 min at 30°C.

    Techniques: Activity Assay, Phospho-proteomics

    DUPS1 regulates p38 MAPK signaling after CPT1 inhibition in postnatal cardiomyocytes. (A) The expression of Map2k3 , mitogen-activated protein kinase kinase 6 ( Map2k6 ), and dual specificity phosphatase family ( Dusp1 , Dusp2 , Dusp3 , Dusp4 , Dusp5 , Dusp6 , Dusp7 , Dusp8 , Dusp9 , Dusp10 , Dusp11 , Dusp12 , Dusp13 , Dusp14 , Dusp15 , Dusp16 , Dusp18 , Dusp19 , Dusp21 , Dusp22 ) in P1 and P7 cardiomyocytes ( n = 6, ∗ P < 0.05 vs. P1). (B) The effect of ETX treatment and Dusp1 siRNA (si Dusp1 ) on DUSP1 expression and p38 MAPK phosphorylation in P7 cardiomyocytes ( n = 3, ∗ P < 0.05 vs. Control, # P < 0.05 vs. ETX). (C) The effect of ETX treatment on the interaction of DUSP1 and p38 MAPK in P7 cardiomyocytes ( n = 6, ∗ P < 0.05 vs. Control). Error bars indicate SEM.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regeneration via DUSP1 ADP-ribosylation-mediated p38 MAPK phosphorylation

    doi: 10.1016/j.apsb.2024.11.001

    Figure Lengend Snippet: DUPS1 regulates p38 MAPK signaling after CPT1 inhibition in postnatal cardiomyocytes. (A) The expression of Map2k3 , mitogen-activated protein kinase kinase 6 ( Map2k6 ), and dual specificity phosphatase family ( Dusp1 , Dusp2 , Dusp3 , Dusp4 , Dusp5 , Dusp6 , Dusp7 , Dusp8 , Dusp9 , Dusp10 , Dusp11 , Dusp12 , Dusp13 , Dusp14 , Dusp15 , Dusp16 , Dusp18 , Dusp19 , Dusp21 , Dusp22 ) in P1 and P7 cardiomyocytes ( n = 6, ∗ P < 0.05 vs. P1). (B) The effect of ETX treatment and Dusp1 siRNA (si Dusp1 ) on DUSP1 expression and p38 MAPK phosphorylation in P7 cardiomyocytes ( n = 3, ∗ P < 0.05 vs. Control, # P < 0.05 vs. ETX). (C) The effect of ETX treatment on the interaction of DUSP1 and p38 MAPK in P7 cardiomyocytes ( n = 6, ∗ P < 0.05 vs. Control). Error bars indicate SEM.

    Article Snippet: The primary antibodies were: anti-phospho p38 mitogen-activated protein kinase (p-p38 MAPK) alpha Thr180/Tyr182 antibody (Thermo Fisher Scientific; 36-8500, Rabbit, 1:500), anti-p38 MAPK antibody (Cell Signaling Technology; 9212, Rabbit, 1:1000), anti-dual-specificity phosphatases 1 (DUSP1) antibody (Cell Signaling Technology; 48625, Rabbit, 1:1000), anti-dual-specificity phosphatases 4 (DUSP4) antibody (Cell Signaling Technology; 5149, Rabbit, 1:1000), anti-dual-specificity phosphatases 12 (DUSP12) antibody (Proteintech, Wuhan, China; 67101-1-Ig, Mouse, 1:1000), anti-Poly/Mono-ADP ribose antibody (Cell Signaling Technology; 83732, Rabbit, 1:1000), anti-poly(ADP-ribose) polymerase family, member 1 (PARP1) antibody (Proteintech; 66520-1-Ig, Mouse, 1:1000), anti-mitogen-activated protein kinase 3 (MAP2K3) antibody (Proteintech; 80137-1-RR, Rabbit, 1:1000), anti-CPT1A antibody (Abcam; ab234111, Rabbit, 1:1000), anti-CPT1B antibody (Proteintech; 22170-1-AP, Rabbit, 1:1000), and anti-glucokinase (GCK) antibody (Proteintech; 19666-1-AP, Rabbit, 1:1000).

    Techniques: Inhibition, Expressing, Phospho-proteomics, Control

    Journal: iScience

    Article Title: TRAF7 is an essential regulator of blood vessel integrity during mouse embryonic and neonatal development

    doi: 10.1016/j.isci.2023.107474

    Figure Lengend Snippet:

    Article Snippet: MISSION® esiRNA targeting human MAP2K3 , Sigma-Aldrich , EHU088281-20UG.

    Techniques: Produced, Affinity Purification, Recombinant, Transfection, Mutagenesis, Expressing, esiRNA, TaqMan Assay, Real-time Polymerase Chain Reaction, Knock-Out, Plasmid Preparation, Software