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dusp1 phosphatase  (Staples)

 
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    Staples dusp1 phosphatase
    Dusp1 Phosphatase, supplied by Staples, 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/dusp1 phosphatase/product/Staples
    Average 90 stars, based on 1 article reviews
    dusp1 phosphatase - by Bioz Stars, 2026-03
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    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 ( <t>Dusp1</t> , 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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    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 ( <t>Dusp1</t> , 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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    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

    CPT1 inhibition suppresses p38 MAPK phosphorylation mediated by ADP-ribosylation of DUSP1. (A) The effect of ETX treatment on the interaction between DUSP1 and PARP1 in P7 cardiomyocytes ( n = 4, ∗ P < 0.05 vs. Control). (B) The effect of ETX treatment on the on ADP-ribosylation of DUSP1 in P7 cardiomyocytes ( n = 4, ∗ P < 0.05 vs. Control). (C) The effect of ETX treatment and/or PARP1 OE on ADP-ribosylation of DUSP1 and the interaction between DUSP1 and p38 MAPK in P7 cardiomyocytes ( n = 3, ∗ P < 0.05, NS=Not significant). (D) LVEF, LVFS, LVIDd and LVIDs at 4 weeks after MI were measured in MADM mice after treatment with ETX and/or PARP1 AAV9 (PARP1 overexpression, PARP1 OE) ( n = 5, ∗ P < 0.05, NS=Not significant). (E) The infarcted area of the heart in mice 4 weeks after MI treated with control (Vector), ETX, and/or PARP1 OE ( n = 5, ∗ P < 0.05, NS=Not significant; Scale bars = 1 mm). (F) Representative immunofluorescence and quantification of single-labeled (red or green, white arrow) cardiomyocytes in MADM mice after MI for 4 weeks treated with control (Vector), ETX, and/or PARP1 OE ( n = 5, ∗ P < 0.05, NS=Not significant; Scale bars = 20 μm). (G) The effect of ETX and PARP1 OE on ADP-ribosylation of DUSP1 and the interaction between DUSP1 and p38 MAPK in mice hearts ( n = 3, ∗ P < 0.05, NS=Not significant). 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: CPT1 inhibition suppresses p38 MAPK phosphorylation mediated by ADP-ribosylation of DUSP1. (A) The effect of ETX treatment on the interaction between DUSP1 and PARP1 in P7 cardiomyocytes ( n = 4, ∗ P < 0.05 vs. Control). (B) The effect of ETX treatment on the on ADP-ribosylation of DUSP1 in P7 cardiomyocytes ( n = 4, ∗ P < 0.05 vs. Control). (C) The effect of ETX treatment and/or PARP1 OE on ADP-ribosylation of DUSP1 and the interaction between DUSP1 and p38 MAPK in P7 cardiomyocytes ( n = 3, ∗ P < 0.05, NS=Not significant). (D) LVEF, LVFS, LVIDd and LVIDs at 4 weeks after MI were measured in MADM mice after treatment with ETX and/or PARP1 AAV9 (PARP1 overexpression, PARP1 OE) ( n = 5, ∗ P < 0.05, NS=Not significant). (E) The infarcted area of the heart in mice 4 weeks after MI treated with control (Vector), ETX, and/or PARP1 OE ( n = 5, ∗ P < 0.05, NS=Not significant; Scale bars = 1 mm). (F) Representative immunofluorescence and quantification of single-labeled (red or green, white arrow) cardiomyocytes in MADM mice after MI for 4 weeks treated with control (Vector), ETX, and/or PARP1 OE ( n = 5, ∗ P < 0.05, NS=Not significant; Scale bars = 20 μm). (G) The effect of ETX and PARP1 OE on ADP-ribosylation of DUSP1 and the interaction between DUSP1 and p38 MAPK in mice hearts ( n = 3, ∗ P < 0.05, NS=Not significant). 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, Phospho-proteomics, Control, Over Expression, Plasmid Preparation, Immunofluorescence, Labeling

    Schematic representation of the proposed effect of reversing metabolic reprogramming by CPT1 inhibition on cardiomyocyte proliferation and heart regeneration. Inhibition of FAO by CPT1 KO or Etomoxir decreases PARP1 expression, negatively regulates ADP-ribosylation modification of DUSP1 and dephosphorylates p38 MAPK which increases cell cycle gene expression and promotes cardiomyocyte proliferation. The suppression of postnatal cardiomyocyte cell-cycle arrest increases cardiac regeneration post myocardial infraction injury.

    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: Schematic representation of the proposed effect of reversing metabolic reprogramming by CPT1 inhibition on cardiomyocyte proliferation and heart regeneration. Inhibition of FAO by CPT1 KO or Etomoxir decreases PARP1 expression, negatively regulates ADP-ribosylation modification of DUSP1 and dephosphorylates p38 MAPK which increases cell cycle gene expression and promotes cardiomyocyte proliferation. The suppression of postnatal cardiomyocyte cell-cycle arrest increases cardiac regeneration post myocardial infraction injury.

    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, Modification, Gene Expression