Review



mouse monoclonal antibody against ep4  (Proteintech)


Bioz Verified Symbol Proteintech is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Proteintech mouse monoclonal antibody against ep4
    Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the <t>EP4</t> receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as
    Mouse Monoclonal Antibody Against Ep4, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse monoclonal antibody against ep4/product/Proteintech
    Average 93 stars, based on 12 article reviews
    mouse monoclonal antibody against ep4 - by Bioz Stars, 2026-03
    93/100 stars

    Images

    1) Product Images from "NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling."

    Article Title: NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling.

    Journal: Nature neuroscience

    doi: 10.1038/s41593-024-01663-x

    Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the EP4 receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as
    Figure Legend Snippet: Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the EP4 receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as

    Techniques Used: Live Cell Imaging, Infection, Expressing, Control, Immunofluorescence



    Similar Products

    mouse monoclonal antibody against ep4  (Proteintech)
    93
    Proteintech mouse monoclonal antibody against ep4
    Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the <t>EP4</t> receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as
    Mouse Monoclonal Antibody Against Ep4, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse monoclonal antibody against ep4/product/Proteintech
    Average 93 stars, based on 1 article reviews
    mouse monoclonal antibody against ep4 - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier
    primary antibodies (at 1:50 dilution) against ca-125, ca-19.9, muc1, and ber-ep4 and mouse monoclonal anti-human e-cadherin and n-cadherin  (Thermo Fisher)
    90
    Thermo Fisher primary antibodies (at 1:50 dilution) against ca-125, ca-19.9, muc1, and ber-ep4 and mouse monoclonal anti-human e-cadherin and n-cadherin
    Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the <t>EP4</t> receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as
    Primary Antibodies (At 1:50 Dilution) Against Ca 125, Ca 19.9, Muc1, And Ber Ep4 And Mouse Monoclonal Anti Human E Cadherin And N Cadherin, supplied by Thermo Fisher, 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/primary antibodies (at 1:50 dilution) against ca-125, ca-19.9, muc1, and ber-ep4 and mouse monoclonal anti-human e-cadherin and n-cadherin/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    primary antibodies (at 1:50 dilution) against ca-125, ca-19.9, muc1, and ber-ep4 and mouse monoclonal anti-human e-cadherin and n-cadherin - by Bioz Stars, 2026-03
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the EP4 receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as

    Journal: Nature neuroscience

    Article Title: NG2 glia protect against prion neurotoxicity by inhibiting microglia-to-neuron prostaglandin E2 signaling.

    doi: 10.1038/s41593-024-01663-x

    Figure Lengend Snippet: Fig. 7 | PGE2 enhances prion neurotoxicity mainly through the EP4 receptor (Ptger4). a,b, Live-cell imaging (a) and quantitative analysis (b) of chronically prion-infected HovS cells expressing control (Ctrl) transgene or one of the four PGE2 receptors (Ptger1–4). Effects of PGE2 treatment on prion-induced cell toxicity were measured with the ratio of GFP signals under the PGE2 condition against the DMSO condition; n = 4 independent experiments. Data are presented as mean ± s.e.m. One-way ANOVA with Benjamini–Hochberg FDR adjustment for multiple comparisons: P < 0.0001 (Ptger1 versus Ctrl); P = 0.2246 (Ptger2 versus Ctrl); P = 0.3351 (Ptger3 versus Ctrl); P < 0.0001 (Ptger4 versus Ctrl). c, Immunofluorescence of NeuN, Map2 and Tau showing cellular damage of prion- infected primary neurons treated with different concentrations of Ptger4 agonist L902688. d, Quantification of neuronal density as well as Map2-positive and Tau positive areas shown in c; n = 6 independent experiments. Data are presented as

    Article Snippet: The following primary antibodies were used: rabbit polyclonal antibody against NG2 (1:500, a gift from W. Stallcup), rabbit monoclonal antibody against NeuN (1:1,000, Abcam, cat. no. ab177487), rabbit polyclonal antibody against Iba1 (1:500, Wako, cat. no. 019-19741), rat monoclonal antibody against Cd68 (1:200, BioRad, cat. no. MCA1957), rabbit polyclonal antibody against Map2 (1:200, Biolegend, cat. no. 840601), mouse monoclonal antibody against Tau (1:200, ThermoFisher Scientific, cat. no. MN1010), chicken polyclonal antibody against NeuN (1:1,000, Merck, cat. no. ABN91), mouse monoclonal antibody against Cox2 (1:200, Santa Cruz, cat. no. sc-166475), mouse monoclonal antibody against Ptges (1:200, Santa Cruz, cat. no. sc-365844), rabbit polyclonal antibody against EP1 (1:200, Bioss Antibodies, cat. no. BS-6316R), rabbit monoclonal antibody against EP2 (1:200, Abcam, cat. no. ab167171), rabbit polyclonal antibody against EP3 (1:200, Cayman Chemical, cat. no. 101760) and mouse monoclonal antibody against EP4 (1:200, ProteinTech, cat. no. 66921-1-Ig).

    Techniques: Live Cell Imaging, Infection, Expressing, Control, Immunofluorescence