e4031  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 94
    Name:
    E 4031
    Description:
    E 4031 is a methsnesulfonanilide class III antiarrhythmic agent It specifically blocks hERG Kv11 1 voltage gated K channel current in heterologous systems cardiac cells and cardiac preparations
    Catalog Number:
    E-500
    Price:
    67.0
    Category:
    Small Molecule
    Source:
    Synthetic
    Applications:
    0
    Purity:
    >98%
    Size:
    0 5 mg
    Format:
    Lyophilized/solid.
    Formula:
    C21H27N3O3S•2HCl•2H2O
    Molecular Weight:
    510.5
    Molecule Name:
    (1-[2-(6-Methyl-2-pyridyl)ethyl]-4-(4-methylsulfonyl-aminobenzoyl)piperidine).
    Buy from Supplier


    Structured Review

    Alomone Labs e4031
    E 4031
    E 4031 is a methsnesulfonanilide class III antiarrhythmic agent It specifically blocks hERG Kv11 1 voltage gated K channel current in heterologous systems cardiac cells and cardiac preparations
    https://www.bioz.com/result/e4031/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    e4031 - by Bioz Stars, 2021-09
    94/100 stars

    Images

    Related Articles

    Activation Assay:

    Article Title: Mouse ERG K+ Channel Clones Reveal Differences in Protein Trafficking and Function
    Article Snippet: .. C shows normalized activation I‐V plots of mERG‐London channels without and with culture in E‐4031 studied using the same voltage protocol used for C, and the results show that E‐4031 has minimal effects on mERG‐London channel‐activation gating (V½ of 4.6±4.6 and 2.9±1.5 mV, P > 0.05; k of 7.7±0.4 and 7.4±0.2 mV/e‐fold Δ, P> 0.05, respectively). ..

    other:

    Article Title: Effects of Antipsychotic Drugs and Potassium Channel Modulators on Cognition-related Local Field Potential Spectral Properties in Mouse Hippocampus and Frontal Cortex
    Article Snippet: DrugsE-4031 (Alomone-Labs, IL) and TEA (Sigma-Aldrich, USA) were dissolved in 0.9% saline.

    Article Title: Visualizing Mutation-Specific Differences in the Trafficking-Deficient Phenotype of Kv11.1 Proteins Linked to Long QT Syndrome Type 2
    Article Snippet: E-4031 was dissolved in water.

    Article Title: Mouse ERG K+ Channel Clones Reveal Differences in Protein Trafficking and Function
    Article Snippet: Culture in E‐4031 increased the tail current amplitude.

    Incubation:

    Article Title: Visualizing Mutation-Specific Differences in the Trafficking-Deficient Phenotype of Kv11.1 Proteins Linked to Long QT Syndrome Type 2
    Article Snippet: .. For pharmacological studies, we incubated cells in nocodazole (20 μM) (Millipore, Sigma, St. Louis, MO, United States), bortezomib, lactacystin, and MG132 (Millipore, Sigma, St. Louis, MO, United States), or E-4031 (10 μM) (Alomone Laboratories, Jerusalem, Israel). ..

    Patch Clamp:

    Article Title: Mouse ERG K+ Channel Clones Reveal Differences in Protein Trafficking and Function
    Article Snippet: .. For some experiments, E‐4031 (Alomone Labs) was added to the medium (10 μmol/L) for 24 hours and washed out 1 hour to 2 hours before patch‐clamp study. ..

    Cell Culture:

    Article Title: Mouse ERG K+ Channel Clones Reveal Differences in Protein Trafficking and Function
    Article Snippet: .. B shows the mean peak tail current density for WT hERG, mERG‐London channels without culture in E‐4031, mERG‐London channels after culture in E‐4031 followed by 1 to 2 hours of drug washout, mERG‐Waterston and mERG‐Nie channels, all cultured at 37°C. ..

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    Alomone Labs snx 482
    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker <t>SNX-482</t> (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).
    Snx 482, supplied by Alomone Labs, 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/snx 482/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    snx 482 - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

    93
    Alomone Labs probdnf protein
    Schematic diagram showing how <t>proBDNF</t> dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy
    Probdnf Protein, supplied by Alomone Labs, 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/probdnf protein/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    probdnf protein - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Journal: Neuroscience

    Article Title: Regulation of glutamatergic and GABAergic neurotransmission in the chick nucleus laminaris: role of N-type calcium channels

    doi: 10.1016/j.neuroscience.2009.09.013

    Figure Lengend Snippet: Glutamatergic transmission in the NL is predominantly triggered by Ca 2+ entry through N-type VGCCs. A : Both the ipsilateral (open circles) and the contralateral (filled circles) EPSCs recorded from the same NL neuron were largely and irreversibly blocked by the N-type blocker ω-Conotoxin-GVIA (ω-CTx-GVIA, 2.5 μM), with nearly identical time courses. Averaged traces under control (thin traces) and drug (thick traces) conditions are shown on the right. Stimulus artifacts are truncated for clarity. B-C : No inhibition of EPSCs was produced by the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga-IVA, 0.1 μM) or the L-type blocker nimodipine (10 μM). D: A small and reversible inhibition of the EPSCs by the R-type blocker SNX-482 (50 nM) was observed. The different time courses of the EPSCs observed in the sampled neurons may be due to different locations of the neurons along the tonotopic frequency axis. E : Summary of the effects of different VGCC blockers on EPSCs of NL neurons. ω-CTx-GVIA inhibited the ipsilateral and the contralateral EPSCs by 88% and 86%, respectively. Blockers for P/Q- and L-type VGCCs had no effects on EPSCs. SNX-482 produced a small inhibition with a large variation among cells. No differences in the percent inhibition by either drug were detected between the ipsilateral and the contralateral EPSCs. Error bars represent standard deviations. n.s.: non-significant (paired t-test, p > 0.05; the number of cells is indicated in parentheses).

    Article Snippet: All chemicals and drugs were obtained from Sigma (Saint Louis, MO), except for SNX-482, ω-Conotoxin-GVIA (ω-CTx-GVIA) and tACPD, which were obtained from Peptide International (Louisville, KY), Alomone Labs (Jerusalem, Israel), and Tocris (Ballwin, MO), respectively.

    Techniques: Transmission Assay, Inhibition, Produced

    Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Journal: Journal of Neurophysiology

    Article Title: Low-threshold calcium currents contribute to locomotor-like activity in neonatal mice

    doi: 10.1152/jn.00583.2011

    Figure Lengend Snippet: Application of the selective R-type calcium channel blocker SNX-482 does not alter fictive locomotor-like activity. A : paired extracellular recordings from iL2 and iL5 in an isolated whole-cord preparation with cocktail (3–10 μM NMDA,

    Article Snippet: The cycle frequency was not significantly affected by SNX-482 (control, mean = 0.24 ± 0.04 Hz; SNX-482, mean = 0.23 ± 0.02 Hz; n = 3; t = 0.39; P = 0.72; ).

    Techniques: Activity Assay, Isolation

    Effects of amiloride and SNX-482 on bursting

    Journal: The Journal of Physiology

    Article Title: Recruitment of apical dendritic T-type Ca2+ channels by backpropagating spikes underlies de novo intrinsic bursting in hippocampal epileptogenesis

    doi: 10.1113/jphysiol.2007.127670

    Figure Lengend Snippet: Effects of amiloride and SNX-482 on bursting

    Article Snippet: We also examined the effects of SNX-482 on bursting in se -experienced neurons.

    Techniques:

    Schematic diagram showing how proBDNF dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Schematic diagram showing how proBDNF dampens CD4 + T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4 + T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Activity Assay, Expressing

    Exogenous proBDNF protein reduced CD4 + T cells but increased CD8 + T cells of septic mice in vitro. Mice injected with saline or LPS (5 mg kg −1 ) for 5 days and the splenocytes were isolated and cultured for 3 days in vitro. Exogenous proBDNF did not alter the percentage of a CD3 + T cells in CD45 + cells or the percentage of b CD4 + T cells or c CD8 + T cells in CD3 + T cells in splenocytes from mice treated with saline. d Exogenous proBDNF did not alter the percentage of CD3 + T cells in CD45 + cells in splenocytes in septic mice. e–f ProBDNF treatment significantly decreased the percentage of e CD4 + T cells but increased the percentage of f CD8 + T cells in CD3 + T cells in splenocytes in LPS-treated mice. n = 4 in each group. Data were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Exogenous proBDNF protein reduced CD4 + T cells but increased CD8 + T cells of septic mice in vitro. Mice injected with saline or LPS (5 mg kg −1 ) for 5 days and the splenocytes were isolated and cultured for 3 days in vitro. Exogenous proBDNF did not alter the percentage of a CD3 + T cells in CD45 + cells or the percentage of b CD4 + T cells or c CD8 + T cells in CD3 + T cells in splenocytes from mice treated with saline. d Exogenous proBDNF did not alter the percentage of CD3 + T cells in CD45 + cells in splenocytes in septic mice. e–f ProBDNF treatment significantly decreased the percentage of e CD4 + T cells but increased the percentage of f CD8 + T cells in CD3 + T cells in splenocytes in LPS-treated mice. n = 4 in each group. Data were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Mouse Assay, In Vitro, Injection, Isolation, Cell Culture

    Increased proBDNF expression in meningeal and peripheral blood immune cells in septic mice. Mice were i.p. injected with LPS (5 mg kg −1 ) and meninges and peripheral blood were harvested for immunofluorescence staining or flow cytometry. a Representative whole mount meningeal immunofluorescence images showed markedly increased proBDNF-positive staining cells in the meninges in mice at 1 day after LPS injection compared to saline injected mice. The high magnification images around the arrows are displayed in a white square as insets. Bar = 100 μm. b – f Representative meningeal single cell flow cytometry images ( upper panel ) and its statistical analysis ( lower panel ) indicated that proBDNF MFI was increased in meningeal b CD3 + T cells, c CD4 + T cells, d CD8 + T cells, and f CD11b + monocytes/macrophages at 1 day after LPS injection. proBDNF in meningeal e CD19 + B cells upregulated until 5 days after LPS injection. n = 10 in the Con group, n = 6 in LPS groups. g – k Upregulation of proBDNF in g CD3 + T cells, h CD4 + T cells, i CD8 + T cells, j CD19 + B cells, and k CD11b + monocytes/macrophages in peripheral blood in LPS-injected mice were detected. n = 9 in Con group, n = 8 in the LPS1d group, n = 4 in the LPS 5d group. Data b – k were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Increased proBDNF expression in meningeal and peripheral blood immune cells in septic mice. Mice were i.p. injected with LPS (5 mg kg −1 ) and meninges and peripheral blood were harvested for immunofluorescence staining or flow cytometry. a Representative whole mount meningeal immunofluorescence images showed markedly increased proBDNF-positive staining cells in the meninges in mice at 1 day after LPS injection compared to saline injected mice. The high magnification images around the arrows are displayed in a white square as insets. Bar = 100 μm. b – f Representative meningeal single cell flow cytometry images ( upper panel ) and its statistical analysis ( lower panel ) indicated that proBDNF MFI was increased in meningeal b CD3 + T cells, c CD4 + T cells, d CD8 + T cells, and f CD11b + monocytes/macrophages at 1 day after LPS injection. proBDNF in meningeal e CD19 + B cells upregulated until 5 days after LPS injection. n = 10 in the Con group, n = 6 in LPS groups. g – k Upregulation of proBDNF in g CD3 + T cells, h CD4 + T cells, i CD8 + T cells, j CD19 + B cells, and k CD11b + monocytes/macrophages in peripheral blood in LPS-injected mice were detected. n = 9 in Con group, n = 8 in the LPS1d group, n = 4 in the LPS 5d group. Data b – k were analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Expressing, Mouse Assay, Injection, Immunofluorescence, Staining, Flow Cytometry

    Effect of i.c.v. injection of anti-proBDNF antibody on fear memory and meningeal immune activity in the septic mice. Mice were bilateral i.c.v. injected with 1 μg McAb-proB 3 days before LPS injection. Behavior tests were performed 1 day after LPS injection. a Representative images showed the broad and thorough diffusion of drugs in cerebroventricular lumen following i.c.v. injection with methylene blue. b McAb-proB i.c.v. injection did not influence weight of mice. c–e There was no difference of c fear conditioning acquiring performance in each group, nor McAb-proB increased the freezing time of d contextual or e cued fear conditioning test as compared to IgG control after LPS injection. n = 6 in each group. Data b , c , and e were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc test and data d was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Effect of i.c.v. injection of anti-proBDNF antibody on fear memory and meningeal immune activity in the septic mice. Mice were bilateral i.c.v. injected with 1 μg McAb-proB 3 days before LPS injection. Behavior tests were performed 1 day after LPS injection. a Representative images showed the broad and thorough diffusion of drugs in cerebroventricular lumen following i.c.v. injection with methylene blue. b McAb-proB i.c.v. injection did not influence weight of mice. c–e There was no difference of c fear conditioning acquiring performance in each group, nor McAb-proB increased the freezing time of d contextual or e cued fear conditioning test as compared to IgG control after LPS injection. n = 6 in each group. Data b , c , and e were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc test and data d was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Injection, Activity Assay, Mouse Assay, Diffusion-based Assay

    Systemic blockade of proBDNF ameliorated cognitive dysfunction and restored meningeal and peripheral CD4 + T cell ratio in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Fear conditioning testing was performed 1 day after LPS injection. Meninges and peripheral blood were harvested 5 days after LPS injection for flow cytometry. a McAb-proB did not influence the weight of mice or b fear conditioning acquiring. c , d McAb-proB greatly alleviated memory deficit induced by LPS injection in mice as indicated by the increased freezing time in ( c ) contextual and ( d ) cued fear conditioning tests in the McAb-proB group relative to the IgG control. n = 8 in each group. Data a , b , and d were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc tests. Data c was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Systemic blockade of proBDNF ameliorated cognitive dysfunction and restored meningeal and peripheral CD4 + T cell ratio in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Fear conditioning testing was performed 1 day after LPS injection. Meninges and peripheral blood were harvested 5 days after LPS injection for flow cytometry. a McAb-proB did not influence the weight of mice or b fear conditioning acquiring. c , d McAb-proB greatly alleviated memory deficit induced by LPS injection in mice as indicated by the increased freezing time in ( c ) contextual and ( d ) cued fear conditioning tests in the McAb-proB group relative to the IgG control. n = 8 in each group. Data a , b , and d were analyzed by repeated measures ANOVA and followed by Bonferroni post hoc tests. Data c was analyzed by one-way ANOVA and followed by Tukey post hoc test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Mouse Assay, Injection, Flow Cytometry

    Systemic blockade of proBDNF restored meningeal pro-inflammatory microenvironment in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Meninges were harvested 5 days after LPS injection for qPCR. a The level of CD4 gene expression was higher in the meninges of the McAb-proB group than in IgG controls in septic mice. b–f Gene levels were significantly lower in b IL-1β and c IL-6 but higher in d IL-4, e IFN-γ, and f IL-13 in the meninges after LPS injection in the McAb-proB group as compared to IgG control. n = 5 in each group. All experiments were performed at least in triplicate. Data were analyzed by unpaired T test, * P

    Journal: Journal of Neuroinflammation

    Article Title: ProBDNF promotes sepsis-associated encephalopathy in mice by dampening the immune activity of meningeal CD4+ T cells

    doi: 10.1186/s12974-020-01850-0

    Figure Lengend Snippet: Systemic blockade of proBDNF restored meningeal pro-inflammatory microenvironment in septic mice. Mice were i.p. injected with proBDNF 30 min before LPS (5 mg kg −1 ) injection. Meninges were harvested 5 days after LPS injection for qPCR. a The level of CD4 gene expression was higher in the meninges of the McAb-proB group than in IgG controls in septic mice. b–f Gene levels were significantly lower in b IL-1β and c IL-6 but higher in d IL-4, e IFN-γ, and f IL-13 in the meninges after LPS injection in the McAb-proB group as compared to IgG control. n = 5 in each group. All experiments were performed at least in triplicate. Data were analyzed by unpaired T test, * P

    Article Snippet: 4 × 105 cells were put in each well of a 96-well flat-bottom plate and stimulated with 100, 200, or 500 ng ml−1 proBDNF protein (Alomone Labs, Israel, catalog: B243) as introduced by our previous studies [ ], respectively.

    Techniques: Mouse Assay, Injection, Real-time Polymerase Chain Reaction, Expressing