erk inhibitor u0126 Millipore Search Results


  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95
    Millipore mitogen activated protein kinases mek inhibitor u0126
    Analysis of LH/hCG-induced ERK and CREB phosphorylation in the presence/absence of specific inhibitors. Murine primary Leydig cells were stimulated 15 min by EC 80 LH or hCG, in the presence or in the absence of PKA and <t>MEK</t> inhibitors (H-89 and <t>U0126,</t> respectively). pERK and pCREB levels were evaluated by Western blotting (image representative of three independent experiments)
    Mitogen Activated Protein Kinases Mek Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mitogen activated protein kinases mek inhibitor u0126/product/Millipore
    Average 95 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    mitogen activated protein kinases mek inhibitor u0126 - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    98
    Millipore erk inhibitor u0126
    CCR7 regulates <t>ERK</t> expression in different cells. (A) Western blot analysis of pERK in OE and NC cells pretreated with or without CCL21 and <t>U0126.</t> GAPDH was used as a loading control. (B) Transcription levels of ERK1/2 in OE and NC cells with or without pretreatment with CCL21 and U0126. **P
    Erk Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 98/100, based on 184 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk inhibitor u0126/product/Millipore
    Average 98 stars, based on 184 article reviews
    Price from $9.99 to $1999.99
    erk inhibitor u0126 - by Bioz Stars, 2020-02
    98/100 stars
      Buy from Supplier

    99
    Millipore erk inhibitor
    Transcription of proinflammatory cytokines is regulated by endoplasmic reticulum (ER) stress induction, as well as by <t>JNK</t> and <t>ERK</t> signaling. A , Quantitative polymerase chain reaction (qPCR) analysis of il8 and il23a , as well as atf3 and chop , in cells
    Erk Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 317 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk inhibitor/product/Millipore
    Average 99 stars, based on 317 article reviews
    Price from $9.99 to $1999.99
    erk inhibitor - by Bioz Stars, 2020-02
    99/100 stars
      Buy from Supplier

    80
    Millipore mek erk inhibitor u0126
    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a <t>MEK/ERK</t> inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.
    Mek Erk Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 80/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mek erk inhibitor u0126/product/Millipore
    Average 80 stars, based on 9 article reviews
    Price from $9.99 to $1999.99
    mek erk inhibitor u0126 - by Bioz Stars, 2020-02
    80/100 stars
      Buy from Supplier

    76
    Millipore mapk erk inhibitor u0126
    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a <t>MEK/ERK</t> inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.
    Mapk Erk Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 76/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mapk erk inhibitor u0126/product/Millipore
    Average 76 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mapk erk inhibitor u0126 - by Bioz Stars, 2020-02
    76/100 stars
      Buy from Supplier

    87
    Merck KGaA erk inhibitor u0126
    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a <t>MEK/ERK</t> inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.
    Erk Inhibitor U0126, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 87/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk inhibitor u0126/product/Merck KGaA
    Average 87 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    erk inhibitor u0126 - by Bioz Stars, 2020-02
    87/100 stars
      Buy from Supplier

    85
    Millipore mapk erk inhibitor
    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a <t>MEK/ERK</t> inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.
    Mapk Erk Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mapk erk inhibitor/product/Millipore
    Average 85 stars, based on 13 article reviews
    Price from $9.99 to $1999.99
    mapk erk inhibitor - by Bioz Stars, 2020-02
    85/100 stars
      Buy from Supplier

    82
    Millipore extracellular signal regulated kinase erk inhibitor u0126
    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a <t>MEK/ERK</t> inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.
    Extracellular Signal Regulated Kinase Erk Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 82/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/extracellular signal regulated kinase erk inhibitor u0126/product/Millipore
    Average 82 stars, based on 10 article reviews
    Price from $9.99 to $1999.99
    extracellular signal regulated kinase erk inhibitor u0126 - by Bioz Stars, 2020-02
    82/100 stars
      Buy from Supplier

    77
    Millipore mek mapk erk inhibitor u0126
    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a <t>MEK/ERK</t> inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.
    Mek Mapk Erk Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mek mapk erk inhibitor u0126/product/Millipore
    Average 77 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    mek mapk erk inhibitor u0126 - by Bioz Stars, 2020-02
    77/100 stars
      Buy from Supplier

    77
    Millipore erk phosphorylation inhibitor u0126
    Scavenge of NO with C-PTIO (A) and inhibition of <t>ERK</t> signal pathway with <t>U0126</t> (B) recover the same levels of fibronectin (Fb) and laminin β-1(LMN β-1) in the cells treated with control (Ctrl), OGD, tPA, and OGD+tPA (O+t). Upper panel: representative immunoblots, β-actin served as loading control; Bottom panel: band intensity was quantitated after normalization to β-actin and the data were expressed as mean ± SD, ANOVA, N = 4.
    Erk Phosphorylation Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/erk phosphorylation inhibitor u0126/product/Millipore
    Average 77 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    erk phosphorylation inhibitor u0126 - by Bioz Stars, 2020-02
    77/100 stars
      Buy from Supplier

    75
    Millipore r d erk kinase inhibitor u0126
    Inhibition of <t>ERK</t> pathway abolished [Ca 2+ ] o -induced proliferation of pBMSCs. (a) Effects of <t>U0126</t> (1 μ M), an inhibitor of MEK, on the proliferation of pBMSCs after 5-day incubation ( n = 8). (b) The mRNA expression levels of cyclins (cyclin A2, cyclin D3, and cyclin E2), PCNA, and p21 in response to 4 mM [Ca 2+ ] o and/or 1 μ M U0126. (c) Western blot analysis of cyclin D1, p21, phosphor-ERK (p-ERK), and ERK in pBMSCs after 5-day culture. β -actin was used as loading control. (d) Mean ± SEM of immunoblotting bands of cyclin D1, p21, and p-ERK/ERK. The intensities of the bands were expressed as the arbitrary units ( n = 4). ∗ P
    R D Erk Kinase Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 75/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/r d erk kinase inhibitor u0126/product/Millipore
    Average 75 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    r d erk kinase inhibitor u0126 - by Bioz Stars, 2020-02
    75/100 stars
      Buy from Supplier

    89
    Millipore mapk erk kinase inhibitor u0126
    Scrapie responsive gene 1 (SCRG1) suppresses lipopolysaccharide (LPS)-induced CC-chemokine ligand 22 (CCL22) production through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in Raw264.7 cells. Raw264.7 cells were stimulated with or without 10 ng/ml LPS, 100 ng/ml rmSCRG1, and 1 mM <t>U0126</t> for either 6 h (A) or 48 h (B). (A) Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed with specific oligonucleotide primers. mRNA expression level of Ccl22 was normalized to glyceraldehyde-3-phosphate dehydrogenase, and the results are expressed as the fold change relative to the unstimulated control. (B) The amount of secreted CCL22 in the culture medium was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) for mouse CCL22. In (A) and (B), data are presented as the means ± SD. *P
    Mapk Erk Kinase Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 89/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mapk erk kinase inhibitor u0126/product/Millipore
    Average 89 stars, based on 10 article reviews
    Price from $9.99 to $1999.99
    mapk erk kinase inhibitor u0126 - by Bioz Stars, 2020-02
    89/100 stars
      Buy from Supplier

    99
    Millipore u0126
    Oleuropein increased phosphorylation of Akt (a) and ERK1/2 (b) in neonatal rat cardiomyocytes subjected to SI/R. The effects of oleuropein were blocked by LY294002 (PI3K inhibitor) or <t>U0126</t> (ERK inhibitor). Total ERK1/2 and Akt levels were not significantly different among the groups. All data were presented as mean ± SE ( n = 4). SI/R: simulated ischemia/reperfusion. # P
    U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 6337 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u0126/product/Millipore
    Average 99 stars, based on 6337 article reviews
    Price from $9.99 to $1999.99
    u0126 - by Bioz Stars, 2020-02
    99/100 stars
      Buy from Supplier

    89
    Millipore u0125
    Oleuropein increased phosphorylation of Akt (a) and ERK1/2 (b) in neonatal rat cardiomyocytes subjected to SI/R. The effects of oleuropein were blocked by LY294002 (PI3K inhibitor) or <t>U0126</t> (ERK inhibitor). Total ERK1/2 and Akt levels were not significantly different among the groups. All data were presented as mean ± SE ( n = 4). SI/R: simulated ischemia/reperfusion. # P
    U0125, supplied by Millipore, used in various techniques. Bioz Stars score: 89/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u0125/product/Millipore
    Average 89 stars, based on 17 article reviews
    Price from $9.99 to $1999.99
    u0125 - by Bioz Stars, 2020-02
    89/100 stars
      Buy from Supplier

    82
    Millipore m u0126
    Signal pathway and transcription factor involved in miR-210 upregulation. ROS generators induce miR-210 level not only by HIF-1 α stabilization but also by phosphorylation of PDGFR- β , Akt and ERK1/2. In addition, NF- κ B and Elk1 are involved in the transcription of miR-210. ( a ) Although hypoxia (Hyp.) (2%) induced HIF-1 α level, low concentrations of antimycin (Ama.) and rotenone (Rot.) did not in western blot analysis. ( b ) HIF-1 α was not reduced by ROS scavenger, NAC. ( c ) Hypoxia-induced miR-210 expression was not reduced by an HIF-1 α inhibitor (Yc-1, 50 and 100 μ M). ( d ) Phosphorylation of PDGFR- β , Akt and ERK 1/2 molecules was significantly increased by antimycin (10 nM) and rotenone (10 pM) treatment according to western blot analysis. ( e , f ) Antimycin- ( e ) and rotenone- ( f ) induced miR-210 expressions were significantly reduced by AG1296 (a PDGFR inhibitor, 10 μ M), LY-294002 (a PI3K/Akt inhibitor, 5 μ M) and <t>U0126</t> (an MAPK/ERK inhibitor, 5 μ M). ( g ) The promoter region upstream of miR-210 was analyzed using Patch 1.0 and AliBaba 2.1 program, and NF- κ B and Elk1 were found to be candidates for miR-210 transcription factors. ( h , i ) Phosphorylation of NF- κ B and Elk1 was induced by antimycin (10 nM, h ) and rotenone (10 pM, i ) treatment. ( j , k ) In addition, antimycin- ( j ) and rotenone- ( k ) induced miR-210 expression was significantly attenuated by transfection of siRNA for NF- κ B (20 nM) and Elk1 (20 nM). ( l ) ChIP assay shows that antimycin and rotenone treatment significantly increased the signal intensity of PCR products, which indicated that phosphorylated NF- κ B and Elk1 could bind to the upstream region of miR-210 promoter. ** P
    M U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 82/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/m u0126/product/Millipore
    Average 82 stars, based on 27 article reviews
    Price from $9.99 to $1999.99
    m u0126 - by Bioz Stars, 2020-02
    82/100 stars
      Buy from Supplier

    78
    Millipore mapk kinase mek 1 2 inhibitor u 0126
    Signal pathway and transcription factor involved in miR-210 upregulation. ROS generators induce miR-210 level not only by HIF-1 α stabilization but also by phosphorylation of PDGFR- β , Akt and ERK1/2. In addition, NF- κ B and Elk1 are involved in the transcription of miR-210. ( a ) Although hypoxia (Hyp.) (2%) induced HIF-1 α level, low concentrations of antimycin (Ama.) and rotenone (Rot.) did not in western blot analysis. ( b ) HIF-1 α was not reduced by ROS scavenger, NAC. ( c ) Hypoxia-induced miR-210 expression was not reduced by an HIF-1 α inhibitor (Yc-1, 50 and 100 μ M). ( d ) Phosphorylation of PDGFR- β , Akt and ERK 1/2 molecules was significantly increased by antimycin (10 nM) and rotenone (10 pM) treatment according to western blot analysis. ( e , f ) Antimycin- ( e ) and rotenone- ( f ) induced miR-210 expressions were significantly reduced by AG1296 (a PDGFR inhibitor, 10 μ M), LY-294002 (a PI3K/Akt inhibitor, 5 μ M) and <t>U0126</t> (an MAPK/ERK inhibitor, 5 μ M). ( g ) The promoter region upstream of miR-210 was analyzed using Patch 1.0 and AliBaba 2.1 program, and NF- κ B and Elk1 were found to be candidates for miR-210 transcription factors. ( h , i ) Phosphorylation of NF- κ B and Elk1 was induced by antimycin (10 nM, h ) and rotenone (10 pM, i ) treatment. ( j , k ) In addition, antimycin- ( j ) and rotenone- ( k ) induced miR-210 expression was significantly attenuated by transfection of siRNA for NF- κ B (20 nM) and Elk1 (20 nM). ( l ) ChIP assay shows that antimycin and rotenone treatment significantly increased the signal intensity of PCR products, which indicated that phosphorylated NF- κ B and Elk1 could bind to the upstream region of miR-210 promoter. ** P
    Mapk Kinase Mek 1 2 Inhibitor U 0126, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mapk kinase mek 1 2 inhibitor u 0126/product/Millipore
    Average 78 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    mapk kinase mek 1 2 inhibitor u 0126 - by Bioz Stars, 2020-02
    78/100 stars
      Buy from Supplier

    77
    Millipore mitogen activated protein extracellular signal regulated kinase mek inhibitors u0126
    Signal pathway and transcription factor involved in miR-210 upregulation. ROS generators induce miR-210 level not only by HIF-1 α stabilization but also by phosphorylation of PDGFR- β , Akt and ERK1/2. In addition, NF- κ B and Elk1 are involved in the transcription of miR-210. ( a ) Although hypoxia (Hyp.) (2%) induced HIF-1 α level, low concentrations of antimycin (Ama.) and rotenone (Rot.) did not in western blot analysis. ( b ) HIF-1 α was not reduced by ROS scavenger, NAC. ( c ) Hypoxia-induced miR-210 expression was not reduced by an HIF-1 α inhibitor (Yc-1, 50 and 100 μ M). ( d ) Phosphorylation of PDGFR- β , Akt and ERK 1/2 molecules was significantly increased by antimycin (10 nM) and rotenone (10 pM) treatment according to western blot analysis. ( e , f ) Antimycin- ( e ) and rotenone- ( f ) induced miR-210 expressions were significantly reduced by AG1296 (a PDGFR inhibitor, 10 μ M), LY-294002 (a PI3K/Akt inhibitor, 5 μ M) and <t>U0126</t> (an MAPK/ERK inhibitor, 5 μ M). ( g ) The promoter region upstream of miR-210 was analyzed using Patch 1.0 and AliBaba 2.1 program, and NF- κ B and Elk1 were found to be candidates for miR-210 transcription factors. ( h , i ) Phosphorylation of NF- κ B and Elk1 was induced by antimycin (10 nM, h ) and rotenone (10 pM, i ) treatment. ( j , k ) In addition, antimycin- ( j ) and rotenone- ( k ) induced miR-210 expression was significantly attenuated by transfection of siRNA for NF- κ B (20 nM) and Elk1 (20 nM). ( l ) ChIP assay shows that antimycin and rotenone treatment significantly increased the signal intensity of PCR products, which indicated that phosphorylated NF- κ B and Elk1 could bind to the upstream region of miR-210 promoter. ** P
    Mitogen Activated Protein Extracellular Signal Regulated Kinase Mek Inhibitors U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mitogen activated protein extracellular signal regulated kinase mek inhibitors u0126/product/Millipore
    Average 77 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    mitogen activated protein extracellular signal regulated kinase mek inhibitors u0126 - by Bioz Stars, 2020-02
    77/100 stars
      Buy from Supplier

    83
    Millipore extracellular signal regulated kinase erk
    F. hepatica Teg suppresses NF-κBp65 activation, but the activation of JNK, <t>p38,</t> or <t>ERK</t> cannot account for the broad suppressive effect of F. hepatica Teg (FhTeg) on DCs. DCs were treated as described in the legend to Fig. . (A)
    Extracellular Signal Regulated Kinase Erk, supplied by Millipore, used in various techniques. Bioz Stars score: 83/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/extracellular signal regulated kinase erk/product/Millipore
    Average 83 stars, based on 8 article reviews
    Price from $9.99 to $1999.99
    extracellular signal regulated kinase erk - by Bioz Stars, 2020-02
    83/100 stars
      Buy from Supplier

    95
    Millipore mitogen activated protein kinase
    F. hepatica Teg suppresses NF-κBp65 activation, but the activation of JNK, <t>p38,</t> or <t>ERK</t> cannot account for the broad suppressive effect of F. hepatica Teg (FhTeg) on DCs. DCs were treated as described in the legend to Fig. . (A)
    Mitogen Activated Protein Kinase, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 85 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mitogen activated protein kinase/product/Millipore
    Average 95 stars, based on 85 article reviews
    Price from $9.99 to $1999.99
    mitogen activated protein kinase - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    78
    Millipore mek1 2 erk1 2 inhibitor
    F. hepatica Teg suppresses NF-κBp65 activation, but the activation of JNK, <t>p38,</t> or <t>ERK</t> cannot account for the broad suppressive effect of F. hepatica Teg (FhTeg) on DCs. DCs were treated as described in the legend to Fig. . (A)
    Mek1 2 Erk1 2 Inhibitor, supplied by Millipore, used in various techniques. Bioz Stars score: 78/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mek1 2 erk1 2 inhibitor/product/Millipore
    Average 78 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    mek1 2 erk1 2 inhibitor - by Bioz Stars, 2020-02
    78/100 stars
      Buy from Supplier

    95
    Millipore mek1 2
    F. hepatica Teg suppresses NF-κBp65 activation, but the activation of JNK, <t>p38,</t> or <t>ERK</t> cannot account for the broad suppressive effect of F. hepatica Teg (FhTeg) on DCs. DCs were treated as described in the legend to Fig. . (A)
    Mek1 2, supplied by Millipore, used in various techniques. Bioz Stars score: 95/100, based on 202 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mek1 2/product/Millipore
    Average 95 stars, based on 202 article reviews
    Price from $9.99 to $1999.99
    mek1 2 - by Bioz Stars, 2020-02
    95/100 stars
      Buy from Supplier

    76
    Millipore 20um erk1 2 pathway inhibitor u0126
    STAT3 and p38MAPK pathway are involved in the combination of 17β-estradiol and TCDD-induced M2 polarization of macrophages. Co-cultured ESC and U937 cells were incubated with <t>20uM</t> STAT3 pathway inhibitor D4071, 20uM <t>ERK1/2</t> pathway inhibitor <t>U0126,</t> 20uM JNK pathway inhibitor SP600125 or 20uM p38MAPK pathway inhibitor SB203580. After 30 minutes, 1nM 17β-estradiol and 1nM TCDD were added to the cells, with PBS serving as the control. 48 hours later, western blot was performed to analyze the levels of the phosphorylated forms and total amounts of STAT3 and P38 in U937 cells(A). IL-10 was measured by ELISA. Surface expression of CD86 and HLA-DR in U937 cells was determined by flow cytometry(B). STAT3i: STAT3 pathway inhibitor; ERK1/2i: ERK1/2 pathway inhibitor; JNKi: JNK pathway inhibitor; P38MAPKi: P38MAPK pathway inhibitor.
    20um Erk1 2 Pathway Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 76/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/20um erk1 2 pathway inhibitor u0126/product/Millipore
    Average 76 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    20um erk1 2 pathway inhibitor u0126 - by Bioz Stars, 2020-02
    76/100 stars
      Buy from Supplier

    77
    Millipore map kinase kinase mek1 2 inhibitor u0126
    METH decreased basal pERK1/2 levels and potentiated ERK1/2 phosphorylation induced by 6-OHDA. (A) Western blot analysis showing pERK levels at different time points after exposure to sub-lethal concentration of METH (0.5 mM) for up to 24 hr. Lysates were collected at 15 min, 30 min, 1 hr, 6 hr, and 24 hr. Shown are the 15 min and 30 min time points. (B) pERK1/2 levels decreased by 15 min post METH exposure and lasted for up to 24 hr. METH decreased activation of ERK 1/2 in a concentration-dependent manner (0, 0.5, and 1 mM at the 24 hr time point) and enhanced the activation of ERK1/2 after 6-OHDA exposure. This activation lasted from 15 to at least 24 hr. (C) Quantification of ERK1/2 activation in response to 6-OHDA. (D) MN9D cells were treated with sub-lethal concentration of METH (0.5 mM) for 24 hr, the medium was removed and the cells treated with the <t>MEK1/2</t> inhibitor <t>U0126</t> (10 µM) for 1 hr before and during the 20 min 6-OHDA exposure. Western blot analysis confirmed the activation of ERK1/2 by 6-OHDA and its enhancement by METH preconditioning and confirmed that U0126 blocked the phosphorylation of ERK1/2. (E) Viability assay looking at ATP levels and performed 24 hr post 6-OHDA treatment showed that METH protected MN9D cells against 6-OHDA toxicity and U0126 abolishes this protection. α-tubulin was used as a loading control. Data are presented as means ± SEM (N = 3). *p
    Map Kinase Kinase Mek1 2 Inhibitor U0126, supplied by Millipore, used in various techniques. Bioz Stars score: 77/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/map kinase kinase mek1 2 inhibitor u0126/product/Millipore
    Average 77 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    map kinase kinase mek1 2 inhibitor u0126 - by Bioz Stars, 2020-02
    77/100 stars
      Buy from Supplier

    85
    Millipore mapk kinase
    METH decreased basal pERK1/2 levels and potentiated ERK1/2 phosphorylation induced by 6-OHDA. (A) Western blot analysis showing pERK levels at different time points after exposure to sub-lethal concentration of METH (0.5 mM) for up to 24 hr. Lysates were collected at 15 min, 30 min, 1 hr, 6 hr, and 24 hr. Shown are the 15 min and 30 min time points. (B) pERK1/2 levels decreased by 15 min post METH exposure and lasted for up to 24 hr. METH decreased activation of ERK 1/2 in a concentration-dependent manner (0, 0.5, and 1 mM at the 24 hr time point) and enhanced the activation of ERK1/2 after 6-OHDA exposure. This activation lasted from 15 to at least 24 hr. (C) Quantification of ERK1/2 activation in response to 6-OHDA. (D) MN9D cells were treated with sub-lethal concentration of METH (0.5 mM) for 24 hr, the medium was removed and the cells treated with the <t>MEK1/2</t> inhibitor <t>U0126</t> (10 µM) for 1 hr before and during the 20 min 6-OHDA exposure. Western blot analysis confirmed the activation of ERK1/2 by 6-OHDA and its enhancement by METH preconditioning and confirmed that U0126 blocked the phosphorylation of ERK1/2. (E) Viability assay looking at ATP levels and performed 24 hr post 6-OHDA treatment showed that METH protected MN9D cells against 6-OHDA toxicity and U0126 abolishes this protection. α-tubulin was used as a loading control. Data are presented as means ± SEM (N = 3). *p
    Mapk Kinase, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mapk kinase/product/Millipore
    Average 85 stars, based on 19 article reviews
    Price from $9.99 to $1999.99
    mapk kinase - by Bioz Stars, 2020-02
    85/100 stars
      Buy from Supplier

    Image Search Results


    Analysis of LH/hCG-induced ERK and CREB phosphorylation in the presence/absence of specific inhibitors. Murine primary Leydig cells were stimulated 15 min by EC 80 LH or hCG, in the presence or in the absence of PKA and MEK inhibitors (H-89 and U0126, respectively). pERK and pCREB levels were evaluated by Western blotting (image representative of three independent experiments)

    Journal: Reproductive Biology and Endocrinology : RB & E

    Article Title: Human LH and hCG stimulate differently the early signalling pathways but result in equal testosterone synthesis in mouse Leydig cells in vitro

    doi: 10.1186/s12958-016-0224-3

    Figure Lengend Snippet: Analysis of LH/hCG-induced ERK and CREB phosphorylation in the presence/absence of specific inhibitors. Murine primary Leydig cells were stimulated 15 min by EC 80 LH or hCG, in the presence or in the absence of PKA and MEK inhibitors (H-89 and U0126, respectively). pERK and pCREB levels were evaluated by Western blotting (image representative of three independent experiments)

    Article Snippet: 10 μM of the mitogen-activated protein kinases (Mek) inhibitor U0126 (#U120, Sigma-Aldrich), or 10 μM of the PKA inhibitor H-89 (#B1427, Sigma-Aldrich) [ ] were also used where appropriate.

    Techniques: Western Blot

    CCR7 regulates ERK expression in different cells. (A) Western blot analysis of pERK in OE and NC cells pretreated with or without CCL21 and U0126. GAPDH was used as a loading control. (B) Transcription levels of ERK1/2 in OE and NC cells with or without pretreatment with CCL21 and U0126. **P

    Journal: Oncology Letters

    Article Title: CCR7 regulates ANO6 to promote migration of pancreatic ductal adenocarcinoma cells via the ERK signaling pathway

    doi: 10.3892/ol.2018.8962

    Figure Lengend Snippet: CCR7 regulates ERK expression in different cells. (A) Western blot analysis of pERK in OE and NC cells pretreated with or without CCL21 and U0126. GAPDH was used as a loading control. (B) Transcription levels of ERK1/2 in OE and NC cells with or without pretreatment with CCL21 and U0126. **P

    Article Snippet: The ERK inhibitor U0126 was obtained from Sigma-Aldrich; Merck KGaA (Darmstadt, Germany).

    Techniques: Expressing, Western Blot

    Effects of CCL21/CCR7 axis and the extracellular signal-regulated kinase inhibitor, U0126, on proliferation and migration. OE cells were pretreated with or without U0126 for 2 h, followed by stimulation with CCL21 for 16 h. (A) Proliferative ability of OE cells and NC cells pretreated with or without CCL21 and U0126. (B) Migratory ability of OE and NC cells pretreated with or without CCL21 and U0126. (C) Transwell migration assay was used to evaluate the migration capacity of different cells (magnification, ×100). **P

    Journal: Oncology Letters

    Article Title: CCR7 regulates ANO6 to promote migration of pancreatic ductal adenocarcinoma cells via the ERK signaling pathway

    doi: 10.3892/ol.2018.8962

    Figure Lengend Snippet: Effects of CCL21/CCR7 axis and the extracellular signal-regulated kinase inhibitor, U0126, on proliferation and migration. OE cells were pretreated with or without U0126 for 2 h, followed by stimulation with CCL21 for 16 h. (A) Proliferative ability of OE cells and NC cells pretreated with or without CCL21 and U0126. (B) Migratory ability of OE and NC cells pretreated with or without CCL21 and U0126. (C) Transwell migration assay was used to evaluate the migration capacity of different cells (magnification, ×100). **P

    Article Snippet: The ERK inhibitor U0126 was obtained from Sigma-Aldrich; Merck KGaA (Darmstadt, Germany).

    Techniques: Migration, Transwell Migration Assay

    ERK 1/2 in C26 CM and LIF-induced myotube atrophy. A , the ERK 1/2 inhibitor U0126 (3 μ m ) blocks the atrophy produced by C26 CM. B , the ERK 1/2 inhibitor U0126 (3 μ m ) blocks the atrophy produced by LIF (370 pg/ml). C , time course of the

    Journal: The Journal of Biological Chemistry

    Article Title: A Key Role for Leukemia Inhibitory Factor in C26 Cancer Cachexia *

    doi: 10.1074/jbc.M115.638411

    Figure Lengend Snippet: ERK 1/2 in C26 CM and LIF-induced myotube atrophy. A , the ERK 1/2 inhibitor U0126 (3 μ m ) blocks the atrophy produced by C26 CM. B , the ERK 1/2 inhibitor U0126 (3 μ m ) blocks the atrophy produced by LIF (370 pg/ml). C , time course of the

    Article Snippet: The inhibitors used were ruxolitinib/INCB-18424 (ChemieTek, Indianapolis IN), JAK2 inhibitors, Tyrphostin AG490 and WP1066 (Sigma), and the ERK 1/2 inhibitor U0126 (EMD/Millipore, Danvers MA).

    Techniques: Produced

    Transcription of proinflammatory cytokines is regulated by endoplasmic reticulum (ER) stress induction, as well as by JNK and ERK signaling. A , Quantitative polymerase chain reaction (qPCR) analysis of il8 and il23a , as well as atf3 and chop , in cells

    Journal: The Journal of Infectious Diseases

    Article Title: Pneumococcal Hydrogen Peroxide–Induced Stress Signaling Regulates Inflammatory Genes

    doi: 10.1093/infdis/jiu428

    Figure Lengend Snippet: Transcription of proinflammatory cytokines is regulated by endoplasmic reticulum (ER) stress induction, as well as by JNK and ERK signaling. A , Quantitative polymerase chain reaction (qPCR) analysis of il8 and il23a , as well as atf3 and chop , in cells

    Article Snippet: Cells were pretreated with JNK and ERK inhibitor (SP600125 10 µM, U0126 50 µM; Sigma), as well as p38 inhibitor (SB203580 10 µM; Tocris, Bristol, United Kingdom) and salubrinal (50 µM; Sigma) 30 minutes before infection.

    Techniques: Real-time Polymerase Chain Reaction

    A. hydrophila -induced ERK 1/2 phosphorylation is PKA mediated and is pro-apoptotic in HKM. (A) HKM were transfected with PKACA-siRNA, scrambled siRNA or pre-treated with H-89, U 0126 then infected with  A. hydrophila  and checked for total ERK and pERK activity 24 h p.i. using EIA based kits. HKM were pre-treated with or without U 0126 then infected with  A. hydrophila  and checked for (B) Hoechst 33342 positive cells and caspase-3 activity and (C) AV-PI staining 24 h p.i. Vertical bars represent mean ± SE (n = 6).  * P

    Journal: PLoS Pathogens

    Article Title: Role of Calmodulin-Calmodulin Kinase II, cAMP/Protein Kinase A and ERK 1/2 on Aeromonas hydrophila-Induced Apoptosis of Head Kidney Macrophages

    doi: 10.1371/journal.ppat.1004018

    Figure Lengend Snippet: A. hydrophila -induced ERK 1/2 phosphorylation is PKA mediated and is pro-apoptotic in HKM. (A) HKM were transfected with PKACA-siRNA, scrambled siRNA or pre-treated with H-89, U 0126 then infected with A. hydrophila and checked for total ERK and pERK activity 24 h p.i. using EIA based kits. HKM were pre-treated with or without U 0126 then infected with A. hydrophila and checked for (B) Hoechst 33342 positive cells and caspase-3 activity and (C) AV-PI staining 24 h p.i. Vertical bars represent mean ± SE (n = 6). * P

    Article Snippet: For inhibitor studies, HKM were pre-treated with or without 10 μM caspase-3 inhibitor (Acetyl-Asp-Glu-Val-Asp-aldehyde, Ac-DEVD-CHO, Promega), 50 μM calpain-2 inhibitor (N-acetyl-leucyl-leucyl-methioninal, calpain-2i ), 4 nM CaM inhibitor (calmidazolium chloride, CMZ), 20 μM CaMKII inhibitor (KN-93, Calbiochem), 20 μM inactive analogue of KN-93 (KN-92), 20 μM cAMP dependent PKA inhibitor (H-89) for 1 h or 5 mM intracellular calcium chelator {[1,2-bis-(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid tetra (acetoxymethyl) ester], BAPTA/AM)}, 10 mM extracellular calcium chelator [Ethyleneglycol-bis (β-aminoethyl-N,N,N′,N′-tetraacetic acid), EGTA], 10 μM calcium channel blocker nifedipine (Nf), 5 μM calcium channel blocker verapamil (Vp), 100 μM CaMKK inhibitor (STO-609), 20 μM ERK 1/2 inhibitor (U 0126, Calbiochem) for 2 h followed by A. hydrophila infection as mentioned above and checked for apoptotic studies and protein assays.

    Techniques: Transfection, Infection, Activity Assay, Enzyme-linked Immunosorbent Assay, Staining

    CaM-CaMKII-cAMP/PKA-ERK 1/2 axis leads to caspase-3 mediated apoptosis of  A. hydrophila -infected HKM. A. hydrophila -elevated Ca 2+  leads to downstream calpain-2 activation and CaM expression. The pathways converge at CaMKII g  to induce cAMP/PKA mediated activation of ERK 1/2 leading to caspase-3 mediated apoptosis of  A. hydrophila -infected HKM.

    Journal: PLoS Pathogens

    Article Title: Role of Calmodulin-Calmodulin Kinase II, cAMP/Protein Kinase A and ERK 1/2 on Aeromonas hydrophila-Induced Apoptosis of Head Kidney Macrophages

    doi: 10.1371/journal.ppat.1004018

    Figure Lengend Snippet: CaM-CaMKII-cAMP/PKA-ERK 1/2 axis leads to caspase-3 mediated apoptosis of A. hydrophila -infected HKM. A. hydrophila -elevated Ca 2+ leads to downstream calpain-2 activation and CaM expression. The pathways converge at CaMKII g to induce cAMP/PKA mediated activation of ERK 1/2 leading to caspase-3 mediated apoptosis of A. hydrophila -infected HKM.

    Article Snippet: For inhibitor studies, HKM were pre-treated with or without 10 μM caspase-3 inhibitor (Acetyl-Asp-Glu-Val-Asp-aldehyde, Ac-DEVD-CHO, Promega), 50 μM calpain-2 inhibitor (N-acetyl-leucyl-leucyl-methioninal, calpain-2i ), 4 nM CaM inhibitor (calmidazolium chloride, CMZ), 20 μM CaMKII inhibitor (KN-93, Calbiochem), 20 μM inactive analogue of KN-93 (KN-92), 20 μM cAMP dependent PKA inhibitor (H-89) for 1 h or 5 mM intracellular calcium chelator {[1,2-bis-(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid tetra (acetoxymethyl) ester], BAPTA/AM)}, 10 mM extracellular calcium chelator [Ethyleneglycol-bis (β-aminoethyl-N,N,N′,N′-tetraacetic acid), EGTA], 10 μM calcium channel blocker nifedipine (Nf), 5 μM calcium channel blocker verapamil (Vp), 100 μM CaMKK inhibitor (STO-609), 20 μM ERK 1/2 inhibitor (U 0126, Calbiochem) for 2 h followed by A. hydrophila infection as mentioned above and checked for apoptotic studies and protein assays.

    Techniques: Chick Chorioallantoic Membrane Assay, Infection, Activation Assay, Expressing

    Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a MEK/ERK inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.

    Journal: The EMBO Journal

    Article Title: A G1‐like state allows HIV‐1 to bypass SAMHD1 restriction in macrophages

    doi: 10.15252/embj.201696025

    Figure Lengend Snippet: Bidirectional transitions shape SAMHD 1‐mediated restriction of HIV ‐1 MDM from three donors (D1, D2, D3) were used for immunoblotting to detect SAMHD1 and CDK proteins. The blot for D1 is the same as that in Fig 1 G in order to facilitate comparison of different cell cycle‐associated proteins and SAMHD1. MDM were co‐infected with VSV‐G HIV‐1 GFP and SIVmac virus‐like particles containing vpx (VLP‐vpx). Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). MDM were transfected with control or pool of SAMHD1 siRNAs and infected 3 days later with VSV‐G‐pseudotyped HIV‐1 GFP. Cells from a representative donor were used for immunoblotting. The percentage of infected cells was quantified by FACS 48 h post‐infection ( n = 2, mean ± s.e.m.; **P‐ value ≤ 0.01; (ns) non‐significant, unpaired t ‐test). Experimental approach used to model MDM bidirectional G0–G1‐like transitions. MDM were as follows: (unstim) cultured in HS or (stim) cultured in FCS as described in Materials and Methods ; [stim (day 3)] grown in HS conditions for 3 days and changed to stimulating FCS conditions for 3 days; [unstim (3 days)] grown in stimulating FCS condition for the 3 days and changed to non‐stimulating HS for the remaining 3 days. Single round of infection of MDM with full‐length HIV‐1 BaL. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins. Graph is a representative example of n ≥ 3, mean ± s.e.m. Proposed signalling pathway leading to SAMHD1 phosphorylation in stimulated MDM. Unstimulated (G) and stimulated (H) MDM were treated with inhibitors of RAF (2 μM), B‐RAF (3 μM), MEK1/2 (AS‐703026, 1 μM), JAK 1–3 (1 μM), GSK3 (2 μM), PIM 1–3 (3 μM) and CDK4/6 (1 μM) for 18 h before infection and infected with VSV‐G HIV‐1 GFP. The percentage of infected cells was quantified by FACS 48 h post‐infection. Graphs are representative example of n ≥ 3, mean ± s.e.m., *P‐ value ≤ 0.05; **P‐ value ≤ 0.01; calculated from triplicates, unpaired t ‐test). MDM were treated with a MEK/ERK inhibitor (U0126, 10 μM) for 18 h before infection and where indicated VLP‐vpx was added at the time of infection. Percentage of infected cells were detected by FACS 48 h post‐infection. Cells were used for immunoblotting to detect CDKs, SAMHD1 and MCM2 proteins ( n = 3, mean ± s.e.m.; (ns) non‐significant; ***P‐ value ≤ 0.001, unpaired t ‐test). Source data are available online for this figure.

    Article Snippet: Kinase inhibitors used: CDK4/6 inhibitor (PD 0332991, Palbociclib) from Sigma; MEK/ERK inhibitor U0126 from Calbiochem (San Diego, USA); JAK 1–3 (ruxolitinib), PIM 1–3 (AZD1897), GSK3 (CT99021), and MEK1/2 (AS‐703026), RAF (TAK‐632), B‐RAF (PXL4032) from Selleckchem (Houston, TX, USA), SAHA (vorinostat) from Sigma and panobinostat from Cayman Chemicals (Ann Arbor, MI, USA).

    Techniques: Infection, FACS, Transfection, Cell Culture

    Scavenge of NO with C-PTIO (A) and inhibition of ERK signal pathway with U0126 (B) recover the same levels of fibronectin (Fb) and laminin β-1(LMN β-1) in the cells treated with control (Ctrl), OGD, tPA, and OGD+tPA (O+t). Upper panel: representative immunoblots, β-actin served as loading control; Bottom panel: band intensity was quantitated after normalization to β-actin and the data were expressed as mean ± SD, ANOVA, N = 4.

    Journal: PLoS ONE

    Article Title: Release of Matrix Metalloproteinases-2 and 9 by S-Nitrosylated Caveolin-1 Contributes to Degradation of Extracellular Matrix in tPA-Treated Hypoxic Endothelial Cells

    doi: 10.1371/journal.pone.0149269

    Figure Lengend Snippet: Scavenge of NO with C-PTIO (A) and inhibition of ERK signal pathway with U0126 (B) recover the same levels of fibronectin (Fb) and laminin β-1(LMN β-1) in the cells treated with control (Ctrl), OGD, tPA, and OGD+tPA (O+t). Upper panel: representative immunoblots, β-actin served as loading control; Bottom panel: band intensity was quantitated after normalization to β-actin and the data were expressed as mean ± SD, ANOVA, N = 4.

    Article Snippet: For mechanistic studies, MMP2 and 9 specific inhibitor SB-3CT (10 μM, Calbiochem) or specific ERK phosphorylation inhibitor U0126 (0.5 U/ml, Sigma) was applied at the beginning of tPA treatment, while Carboxy-PTIO (C-PTIO) (10 μM, Cayman), a scavenger of NO, was added to cells at the same times of OGD treatment.

    Techniques: Inhibition, Western Blot

    Inhibition of ERK pathway abolished [Ca 2+ ] o -induced proliferation of pBMSCs. (a) Effects of U0126 (1 μ M), an inhibitor of MEK, on the proliferation of pBMSCs after 5-day incubation ( n = 8). (b) The mRNA expression levels of cyclins (cyclin A2, cyclin D3, and cyclin E2), PCNA, and p21 in response to 4 mM [Ca 2+ ] o and/or 1 μ M U0126. (c) Western blot analysis of cyclin D1, p21, phosphor-ERK (p-ERK), and ERK in pBMSCs after 5-day culture. β -actin was used as loading control. (d) Mean ± SEM of immunoblotting bands of cyclin D1, p21, and p-ERK/ERK. The intensities of the bands were expressed as the arbitrary units ( n = 4). ∗ P

    Journal: Stem Cells International

    Article Title: Enhanced Proliferation of Porcine Bone Marrow Mesenchymal Stem Cells Induced by Extracellular Calcium is Associated with the Activation of the Calcium-Sensing Receptor and ERK Signaling Pathway

    doi: 10.1155/2016/6570671

    Figure Lengend Snippet: Inhibition of ERK pathway abolished [Ca 2+ ] o -induced proliferation of pBMSCs. (a) Effects of U0126 (1 μ M), an inhibitor of MEK, on the proliferation of pBMSCs after 5-day incubation ( n = 8). (b) The mRNA expression levels of cyclins (cyclin A2, cyclin D3, and cyclin E2), PCNA, and p21 in response to 4 mM [Ca 2+ ] o and/or 1 μ M U0126. (c) Western blot analysis of cyclin D1, p21, phosphor-ERK (p-ERK), and ERK in pBMSCs after 5-day culture. β -actin was used as loading control. (d) Mean ± SEM of immunoblotting bands of cyclin D1, p21, and p-ERK/ERK. The intensities of the bands were expressed as the arbitrary units ( n = 4). ∗ P

    Article Snippet: Chemicals and Antibodies Calcium acetate, CaSR antagonist NPS2143, calcium indicator Fluo 3-AM, and ERK kinase inhibitor U0126 were purchased from Sigma-Aldrich.

    Techniques: Inhibition, Incubation, Expressing, Western Blot

    Scrapie responsive gene 1 (SCRG1) suppresses lipopolysaccharide (LPS)-induced CC-chemokine ligand 22 (CCL22) production through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in Raw264.7 cells. Raw264.7 cells were stimulated with or without 10 ng/ml LPS, 100 ng/ml rmSCRG1, and 1 mM U0126 for either 6 h (A) or 48 h (B). (A) Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed with specific oligonucleotide primers. mRNA expression level of Ccl22 was normalized to glyceraldehyde-3-phosphate dehydrogenase, and the results are expressed as the fold change relative to the unstimulated control. (B) The amount of secreted CCL22 in the culture medium was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) for mouse CCL22. In (A) and (B), data are presented as the means ± SD. *P

    Journal: Molecular Medicine Reports

    Article Title: SCRG1 suppresses LPS-induced CCL22 production through ERK1/2 activation in mouse macrophage Raw264.7 cells

    doi: 10.3892/mmr.2017.6492

    Figure Lengend Snippet: Scrapie responsive gene 1 (SCRG1) suppresses lipopolysaccharide (LPS)-induced CC-chemokine ligand 22 (CCL22) production through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in Raw264.7 cells. Raw264.7 cells were stimulated with or without 10 ng/ml LPS, 100 ng/ml rmSCRG1, and 1 mM U0126 for either 6 h (A) or 48 h (B). (A) Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed with specific oligonucleotide primers. mRNA expression level of Ccl22 was normalized to glyceraldehyde-3-phosphate dehydrogenase, and the results are expressed as the fold change relative to the unstimulated control. (B) The amount of secreted CCL22 in the culture medium was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) for mouse CCL22. In (A) and (B), data are presented as the means ± SD. *P

    Article Snippet: The MAPK/ERK kinase inhibitor U0126 was purchased from Calbiochem (Merck Millipore, Darmstadt, Germany).

    Techniques: Activation Assay, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Expressing, Sandwich ELISA, Enzyme-linked Immunosorbent Assay

    Oleuropein increased phosphorylation of Akt (a) and ERK1/2 (b) in neonatal rat cardiomyocytes subjected to SI/R. The effects of oleuropein were blocked by LY294002 (PI3K inhibitor) or U0126 (ERK inhibitor). Total ERK1/2 and Akt levels were not significantly different among the groups. All data were presented as mean ± SE ( n = 4). SI/R: simulated ischemia/reperfusion. # P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Oleuropein Protects Cardiomyocyte against Apoptosis via Activating the Reperfusion Injury Salvage Kinase Pathway In Vitro

    doi: 10.1155/2017/2109018

    Figure Lengend Snippet: Oleuropein increased phosphorylation of Akt (a) and ERK1/2 (b) in neonatal rat cardiomyocytes subjected to SI/R. The effects of oleuropein were blocked by LY294002 (PI3K inhibitor) or U0126 (ERK inhibitor). Total ERK1/2 and Akt levels were not significantly different among the groups. All data were presented as mean ± SE ( n = 4). SI/R: simulated ischemia/reperfusion. # P

    Article Snippet: LY294002 (PI3K inhibitor) and U0126 (ERK inhibitor) were purchased from Sigma (Sigma, USA).

    Techniques:

    Signal pathway and transcription factor involved in miR-210 upregulation. ROS generators induce miR-210 level not only by HIF-1 α stabilization but also by phosphorylation of PDGFR- β , Akt and ERK1/2. In addition, NF- κ B and Elk1 are involved in the transcription of miR-210. ( a ) Although hypoxia (Hyp.) (2%) induced HIF-1 α level, low concentrations of antimycin (Ama.) and rotenone (Rot.) did not in western blot analysis. ( b ) HIF-1 α was not reduced by ROS scavenger, NAC. ( c ) Hypoxia-induced miR-210 expression was not reduced by an HIF-1 α inhibitor (Yc-1, 50 and 100 μ M). ( d ) Phosphorylation of PDGFR- β , Akt and ERK 1/2 molecules was significantly increased by antimycin (10 nM) and rotenone (10 pM) treatment according to western blot analysis. ( e , f ) Antimycin- ( e ) and rotenone- ( f ) induced miR-210 expressions were significantly reduced by AG1296 (a PDGFR inhibitor, 10 μ M), LY-294002 (a PI3K/Akt inhibitor, 5 μ M) and U0126 (an MAPK/ERK inhibitor, 5 μ M). ( g ) The promoter region upstream of miR-210 was analyzed using Patch 1.0 and AliBaba 2.1 program, and NF- κ B and Elk1 were found to be candidates for miR-210 transcription factors. ( h , i ) Phosphorylation of NF- κ B and Elk1 was induced by antimycin (10 nM, h ) and rotenone (10 pM, i ) treatment. ( j , k ) In addition, antimycin- ( j ) and rotenone- ( k ) induced miR-210 expression was significantly attenuated by transfection of siRNA for NF- κ B (20 nM) and Elk1 (20 nM). ( l ) ChIP assay shows that antimycin and rotenone treatment significantly increased the signal intensity of PCR products, which indicated that phosphorylated NF- κ B and Elk1 could bind to the upstream region of miR-210 promoter. ** P

    Journal: Cell Death & Disease

    Article Title: Reactive oxygen species-responsive miR-210 regulates proliferation and migration of adipose-derived stem cells via PTPN2

    doi: 10.1038/cddis.2013.117

    Figure Lengend Snippet: Signal pathway and transcription factor involved in miR-210 upregulation. ROS generators induce miR-210 level not only by HIF-1 α stabilization but also by phosphorylation of PDGFR- β , Akt and ERK1/2. In addition, NF- κ B and Elk1 are involved in the transcription of miR-210. ( a ) Although hypoxia (Hyp.) (2%) induced HIF-1 α level, low concentrations of antimycin (Ama.) and rotenone (Rot.) did not in western blot analysis. ( b ) HIF-1 α was not reduced by ROS scavenger, NAC. ( c ) Hypoxia-induced miR-210 expression was not reduced by an HIF-1 α inhibitor (Yc-1, 50 and 100 μ M). ( d ) Phosphorylation of PDGFR- β , Akt and ERK 1/2 molecules was significantly increased by antimycin (10 nM) and rotenone (10 pM) treatment according to western blot analysis. ( e , f ) Antimycin- ( e ) and rotenone- ( f ) induced miR-210 expressions were significantly reduced by AG1296 (a PDGFR inhibitor, 10 μ M), LY-294002 (a PI3K/Akt inhibitor, 5 μ M) and U0126 (an MAPK/ERK inhibitor, 5 μ M). ( g ) The promoter region upstream of miR-210 was analyzed using Patch 1.0 and AliBaba 2.1 program, and NF- κ B and Elk1 were found to be candidates for miR-210 transcription factors. ( h , i ) Phosphorylation of NF- κ B and Elk1 was induced by antimycin (10 nM, h ) and rotenone (10 pM, i ) treatment. ( j , k ) In addition, antimycin- ( j ) and rotenone- ( k ) induced miR-210 expression was significantly attenuated by transfection of siRNA for NF- κ B (20 nM) and Elk1 (20 nM). ( l ) ChIP assay shows that antimycin and rotenone treatment significantly increased the signal intensity of PCR products, which indicated that phosphorylated NF- κ B and Elk1 could bind to the upstream region of miR-210 promoter. ** P

    Article Snippet: For the inhibition study, 0.1 mM NAC (ROS scavenger; Sigma-Aldrich, St. Louis, MO, USA), 50 and 100 μ M Yc-1 (an HIF-1α inhibitor; Sigma), 5 μ M LY294002 (PI3K/Akt inhibitor; Calbiochem, San Diego, CA, USA), 5 μ M U0126 (MAPK/ERK inhibitor; Calbiochem), 10 μ M AG1296 (PDGFR inhibitor; Calbiochem) and 0.001–1 μ M ethyl-3,4-dephostatin (PTPN2 inhibitor; Santa Cruz Biotechnology, Santa Cruz, CA, USA) were used.

    Techniques: Western Blot, Expressing, Transfection, Chromatin Immunoprecipitation, Polymerase Chain Reaction

    F. hepatica Teg suppresses NF-κBp65 activation, but the activation of JNK, p38, or ERK cannot account for the broad suppressive effect of F. hepatica Teg (FhTeg) on DCs. DCs were treated as described in the legend to Fig. . (A)

    Journal: Infection and Immunity

    Article Title: The Fasciola hepatica Tegumental Antigen Suppresses Dendritic Cell Maturation and Function ▿

    doi: 10.1128/IAI.00919-08

    Figure Lengend Snippet: F. hepatica Teg suppresses NF-κBp65 activation, but the activation of JNK, p38, or ERK cannot account for the broad suppressive effect of F. hepatica Teg (FhTeg) on DCs. DCs were treated as described in the legend to Fig. . (A)

    Article Snippet: In the MAPK inhibitor studies, cells were incubated with extracellular signal-regulated kinase (ERK) (U0126; Sigma Aldrich), p38 (SB 202190; Sigma Aldrich), or Jun N-terminal protein kinase (JNK) inhibitors [JNK inhibitor I (L)-form; Calbiochem] (all 5 μM) 1 hour prior to TLR ligand stimulation.

    Techniques: Activation Assay

    STAT3 and p38MAPK pathway are involved in the combination of 17β-estradiol and TCDD-induced M2 polarization of macrophages. Co-cultured ESC and U937 cells were incubated with 20uM STAT3 pathway inhibitor D4071, 20uM ERK1/2 pathway inhibitor U0126, 20uM JNK pathway inhibitor SP600125 or 20uM p38MAPK pathway inhibitor SB203580. After 30 minutes, 1nM 17β-estradiol and 1nM TCDD were added to the cells, with PBS serving as the control. 48 hours later, western blot was performed to analyze the levels of the phosphorylated forms and total amounts of STAT3 and P38 in U937 cells(A). IL-10 was measured by ELISA. Surface expression of CD86 and HLA-DR in U937 cells was determined by flow cytometry(B). STAT3i: STAT3 pathway inhibitor; ERK1/2i: ERK1/2 pathway inhibitor; JNKi: JNK pathway inhibitor; P38MAPKi: P38MAPK pathway inhibitor.

    Journal: PLoS ONE

    Article Title: Combined 17β-Estradiol with TCDD Promotes M2 Polarization of Macrophages in the Endometriotic Milieu with Aid of the Interaction between Endometrial Stromal Cells and Macrophages

    doi: 10.1371/journal.pone.0125559

    Figure Lengend Snippet: STAT3 and p38MAPK pathway are involved in the combination of 17β-estradiol and TCDD-induced M2 polarization of macrophages. Co-cultured ESC and U937 cells were incubated with 20uM STAT3 pathway inhibitor D4071, 20uM ERK1/2 pathway inhibitor U0126, 20uM JNK pathway inhibitor SP600125 or 20uM p38MAPK pathway inhibitor SB203580. After 30 minutes, 1nM 17β-estradiol and 1nM TCDD were added to the cells, with PBS serving as the control. 48 hours later, western blot was performed to analyze the levels of the phosphorylated forms and total amounts of STAT3 and P38 in U937 cells(A). IL-10 was measured by ELISA. Surface expression of CD86 and HLA-DR in U937 cells was determined by flow cytometry(B). STAT3i: STAT3 pathway inhibitor; ERK1/2i: ERK1/2 pathway inhibitor; JNKi: JNK pathway inhibitor; P38MAPKi: P38MAPK pathway inhibitor.

    Article Snippet: Treatment with STAT3, ERK1/2, JNK, or p38MAPK Pathway inhibitors ESCs and U937 cells were co-cultured as described previously, and 20uM STAT3 pathway inhibitor D4071(Sigma, St. Louis, MO, USA), 20uM ERK1/2 pathway inhibitor U0126 (Calbiochem, San Diego, CA, USA), 20uM JNK pathway inhibitor SP600125 or 20uM p38MAPK pathway inhibitor SB203580 (both from Sigma, St. Louis, MO, USA) were added to the culture supernatants.

    Techniques: Cell Culture, Incubation, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Flow Cytometry, Cytometry

    METH decreased basal pERK1/2 levels and potentiated ERK1/2 phosphorylation induced by 6-OHDA. (A) Western blot analysis showing pERK levels at different time points after exposure to sub-lethal concentration of METH (0.5 mM) for up to 24 hr. Lysates were collected at 15 min, 30 min, 1 hr, 6 hr, and 24 hr. Shown are the 15 min and 30 min time points. (B) pERK1/2 levels decreased by 15 min post METH exposure and lasted for up to 24 hr. METH decreased activation of ERK 1/2 in a concentration-dependent manner (0, 0.5, and 1 mM at the 24 hr time point) and enhanced the activation of ERK1/2 after 6-OHDA exposure. This activation lasted from 15 to at least 24 hr. (C) Quantification of ERK1/2 activation in response to 6-OHDA. (D) MN9D cells were treated with sub-lethal concentration of METH (0.5 mM) for 24 hr, the medium was removed and the cells treated with the MEK1/2 inhibitor U0126 (10 µM) for 1 hr before and during the 20 min 6-OHDA exposure. Western blot analysis confirmed the activation of ERK1/2 by 6-OHDA and its enhancement by METH preconditioning and confirmed that U0126 blocked the phosphorylation of ERK1/2. (E) Viability assay looking at ATP levels and performed 24 hr post 6-OHDA treatment showed that METH protected MN9D cells against 6-OHDA toxicity and U0126 abolishes this protection. α-tubulin was used as a loading control. Data are presented as means ± SEM (N = 3). *p

    Journal: PLoS ONE

    Article Title: Low Concentrations of Methamphetamine Can Protect Dopaminergic Cells against a Larger Oxidative Stress Injury: Mechanistic Study

    doi: 10.1371/journal.pone.0024722

    Figure Lengend Snippet: METH decreased basal pERK1/2 levels and potentiated ERK1/2 phosphorylation induced by 6-OHDA. (A) Western blot analysis showing pERK levels at different time points after exposure to sub-lethal concentration of METH (0.5 mM) for up to 24 hr. Lysates were collected at 15 min, 30 min, 1 hr, 6 hr, and 24 hr. Shown are the 15 min and 30 min time points. (B) pERK1/2 levels decreased by 15 min post METH exposure and lasted for up to 24 hr. METH decreased activation of ERK 1/2 in a concentration-dependent manner (0, 0.5, and 1 mM at the 24 hr time point) and enhanced the activation of ERK1/2 after 6-OHDA exposure. This activation lasted from 15 to at least 24 hr. (C) Quantification of ERK1/2 activation in response to 6-OHDA. (D) MN9D cells were treated with sub-lethal concentration of METH (0.5 mM) for 24 hr, the medium was removed and the cells treated with the MEK1/2 inhibitor U0126 (10 µM) for 1 hr before and during the 20 min 6-OHDA exposure. Western blot analysis confirmed the activation of ERK1/2 by 6-OHDA and its enhancement by METH preconditioning and confirmed that U0126 blocked the phosphorylation of ERK1/2. (E) Viability assay looking at ATP levels and performed 24 hr post 6-OHDA treatment showed that METH protected MN9D cells against 6-OHDA toxicity and U0126 abolishes this protection. α-tubulin was used as a loading control. Data are presented as means ± SEM (N = 3). *p

    Article Snippet: When the MAP kinase kinase (MEK1/2) inhibitor U0126 (Calbiochem, EMD Chemicals Inc. San Diego, CA) was used, cells were pretreated for 1 hr with 10 µM U0126 or its vehicle before and during the time of 6-OHDA exposure.

    Techniques: Western Blot, Concentration Assay, Activation Assay, Viability Assay