recombinant cytokines Search Results


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    R&D Systems il 17f
    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and <t>IL-17F.</t> Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Il 17f, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17f/product/R&D Systems
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17f - by Bioz Stars, 2021-05
    86/100 stars
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    97
    Thermo Fisher il 17a
    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and <t>IL-17F.</t> Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium
    Il 17a, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 1 article reviews
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    86
    Thermo Fisher interleukin 10
    Rv1523 modulates macrophage immune responses. Overexpression of M. tuberculosis Rv1523 in M. smegmatis modulates the immune pathway by suppressing production of pro-inflammatory cytokine and inducing anti-inflammatory cytokine production. PMA-differentiated THP-1 cells (2 × 106/well/ml) were infected with recombinant Ms_Vec and Ms_Rv1523 strains. After 6, 24, and 48 h infection, the infected cells and supernatant were collected. ELISA was used for detecting the production of TNF-α (A) and <t>IL-10</t> (B) . Experiments were performed at least twice; SEM is represented by error bar for biological triplicates. Two-way ANOVA was used for determining statistical significance. ns, non-significant *p
    Interleukin 10, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    interleukin 10 - by Bioz Stars, 2021-05
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    93
    PeproTech il 17f
    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or <t>IL-17F</t> for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.
    Il 17f, supplied by PeproTech, 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/il 17f/product/PeproTech
    Average 93 stars, based on 1 article reviews
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    Recombinant human CKS 1 derived from E coli
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    Image Search Results


    Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Journal:

    Article Title: Role of IL-17A, IL-17F, and the IL-17 Receptor in Regulating Growth-Related Oncogene-α and Granulocyte Colony-Stimulating Factor in Bronchial Epithelium: Implications for Airway Inflammation in Cystic Fibrosis 1

    doi:

    Figure Lengend Snippet: Effects of blocking IL-17R on GRO- α ( A ) and G-CSF ( B ) production by IL-17A and IL-17F. Primary HBE cells were pretreated with IL-17R Ab (2 μ g/ml) 30 min before IL-17A and IL-17F treatment (both at 10 ng/ml). Apical and basolateral medium

    Article Snippet: IL-17A was more potent than IL-17F on a mass basis to induce G-CSF, GRO- α , and MCP-1 at 24 h. A time course performed with 10 ng/ml IL-17A and IL-17F showed that the effect of IL-17A and IL-17F on G-CSF, GRO- α, and MCP-1 were time dependent ( ) with a maximum effect at 24 h. Based on these kinetic studies, we performed most of the next experiments using a concentration of IL-17A or IL-17F of 10 ng/ml and a incubation time of 24 h.

    Techniques: Blocking Assay

    GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Journal:

    Article Title: Role of IL-17A, IL-17F, and the IL-17 Receptor in Regulating Growth-Related Oncogene-α and Granulocyte Colony-Stimulating Factor in Bronchial Epithelium: Implications for Airway Inflammation in Cystic Fibrosis 1

    doi:

    Figure Lengend Snippet: GRO- α ( A ) and G-CSF ( B ) secreted after stimulation with IL-17F and/or TNF- α . primary HBE cells were treated with IL-17F (10 ng/ml) and TNF- α (1 ng/ml). The cytokine mixture (IL-17F + TNF- α ) was also preincubated with anti-IL-17

    Article Snippet: IL-17A was more potent than IL-17F on a mass basis to induce G-CSF, GRO- α , and MCP-1 at 24 h. A time course performed with 10 ng/ml IL-17A and IL-17F showed that the effect of IL-17A and IL-17F on G-CSF, GRO- α, and MCP-1 were time dependent ( ) with a maximum effect at 24 h. Based on these kinetic studies, we performed most of the next experiments using a concentration of IL-17A or IL-17F of 10 ng/ml and a incubation time of 24 h.

    Techniques:

    Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Journal:

    Article Title: Role of IL-17A, IL-17F, and the IL-17 Receptor in Regulating Growth-Related Oncogene-α and Granulocyte Colony-Stimulating Factor in Bronchial Epithelium: Implications for Airway Inflammation in Cystic Fibrosis 1

    doi:

    Figure Lengend Snippet: Cytokines levels in sputum from CF patients undergoing pulmonary exacerbation. Panel A: IL-17A and IL-17F concentration in sputum from CF patients at different time points, as indicated, were measured by ELISA. Panel B: IL-17- induced cytokines IL-8 (upper

    Article Snippet: IL-17A was more potent than IL-17F on a mass basis to induce G-CSF, GRO- α , and MCP-1 at 24 h. A time course performed with 10 ng/ml IL-17A and IL-17F showed that the effect of IL-17A and IL-17F on G-CSF, GRO- α, and MCP-1 were time dependent ( ) with a maximum effect at 24 h. Based on these kinetic studies, we performed most of the next experiments using a concentration of IL-17A or IL-17F of 10 ng/ml and a incubation time of 24 h.

    Techniques: Concentration Assay, Enzyme-linked Immunosorbent Assay

    A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Journal:

    Article Title: Role of IL-17A, IL-17F, and the IL-17 Receptor in Regulating Growth-Related Oncogene-α and Granulocyte Colony-Stimulating Factor in Bronchial Epithelium: Implications for Airway Inflammation in Cystic Fibrosis 1

    doi:

    Figure Lengend Snippet: A , Dose-dependent elevation of GRO- α , G-CSF, and MCP-1 protein levels by recombinant human IL-17A and IL-17F. Primary HBE cells were treated with different doses of IL-17A and IL-17F, as indicated. Basolateral media were collected 24 h after the

    Article Snippet: IL-17A was more potent than IL-17F on a mass basis to induce G-CSF, GRO- α , and MCP-1 at 24 h. A time course performed with 10 ng/ml IL-17A and IL-17F showed that the effect of IL-17A and IL-17F on G-CSF, GRO- α, and MCP-1 were time dependent ( ) with a maximum effect at 24 h. Based on these kinetic studies, we performed most of the next experiments using a concentration of IL-17A or IL-17F of 10 ng/ml and a incubation time of 24 h.

    Techniques: Recombinant

    IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Journal:

    Article Title: Role of IL-17A, IL-17F, and the IL-17 Receptor in Regulating Growth-Related Oncogene-α and Granulocyte Colony-Stimulating Factor in Bronchial Epithelium: Implications for Airway Inflammation in Cystic Fibrosis 1

    doi:

    Figure Lengend Snippet: IL-17A and IL-17F up-regulate G-CSF, GRO-α, and MCP-1 in HBE cells: kinetic studies

    Article Snippet: IL-17A was more potent than IL-17F on a mass basis to induce G-CSF, GRO- α , and MCP-1 at 24 h. A time course performed with 10 ng/ml IL-17A and IL-17F showed that the effect of IL-17A and IL-17F on G-CSF, GRO- α, and MCP-1 were time dependent ( ) with a maximum effect at 24 h. Based on these kinetic studies, we performed most of the next experiments using a concentration of IL-17A or IL-17F of 10 ng/ml and a incubation time of 24 h.

    Techniques:

    Rv1523 modulates macrophage immune responses. Overexpression of M. tuberculosis Rv1523 in M. smegmatis modulates the immune pathway by suppressing production of pro-inflammatory cytokine and inducing anti-inflammatory cytokine production. PMA-differentiated THP-1 cells (2 × 106/well/ml) were infected with recombinant Ms_Vec and Ms_Rv1523 strains. After 6, 24, and 48 h infection, the infected cells and supernatant were collected. ELISA was used for detecting the production of TNF-α (A) and IL-10 (B) . Experiments were performed at least twice; SEM is represented by error bar for biological triplicates. Two-way ANOVA was used for determining statistical significance. ns, non-significant *p

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: The M. tuberculosis Rv1523 Methyltransferase Promotes Drug Resistance Through Methylation-Mediated Cell Wall Remodeling and Modulates Macrophages Immune Responses

    doi: 10.3389/fcimb.2021.622487

    Figure Lengend Snippet: Rv1523 modulates macrophage immune responses. Overexpression of M. tuberculosis Rv1523 in M. smegmatis modulates the immune pathway by suppressing production of pro-inflammatory cytokine and inducing anti-inflammatory cytokine production. PMA-differentiated THP-1 cells (2 × 106/well/ml) were infected with recombinant Ms_Vec and Ms_Rv1523 strains. After 6, 24, and 48 h infection, the infected cells and supernatant were collected. ELISA was used for detecting the production of TNF-α (A) and IL-10 (B) . Experiments were performed at least twice; SEM is represented by error bar for biological triplicates. Two-way ANOVA was used for determining statistical significance. ns, non-significant *p

    Article Snippet: After 6, 24, and 48 h infection, culture supernatants were harvested, and the cytokines released by infected cells in the culture supernatants were quantitatively detected using ELISA kits of Tumor Necrosis Factor-α (TNF-α Invitrogen™ 88-7346-88) and interleukin-10 (IL-10 Invitrogen™ 88-7106-88).

    Techniques: Over Expression, Infection, Recombinant, Enzyme-linked Immunosorbent Assay

    Model depicting the role of Rv1523 in bacterial cell wall lipid modulation and macrophages immune response alteration. We predict the role of Rv1523 methyltransferase in cell wall lipid modulation. Recombinant M. smegmatis expressing Rv1523 (Ms_Rv1523) displayed higher survival in macrophages as compared to M. smegmatis not expressing Rv1523 (Ms_Vec). Ms_Rv1523 induced increased expression of anti-inflammatory cytokine IL-10 and reduced the expression of proinflammatory TNF- α.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: The M. tuberculosis Rv1523 Methyltransferase Promotes Drug Resistance Through Methylation-Mediated Cell Wall Remodeling and Modulates Macrophages Immune Responses

    doi: 10.3389/fcimb.2021.622487

    Figure Lengend Snippet: Model depicting the role of Rv1523 in bacterial cell wall lipid modulation and macrophages immune response alteration. We predict the role of Rv1523 methyltransferase in cell wall lipid modulation. Recombinant M. smegmatis expressing Rv1523 (Ms_Rv1523) displayed higher survival in macrophages as compared to M. smegmatis not expressing Rv1523 (Ms_Vec). Ms_Rv1523 induced increased expression of anti-inflammatory cytokine IL-10 and reduced the expression of proinflammatory TNF- α.

    Article Snippet: After 6, 24, and 48 h infection, culture supernatants were harvested, and the cytokines released by infected cells in the culture supernatants were quantitatively detected using ELISA kits of Tumor Necrosis Factor-α (TNF-α Invitrogen™ 88-7346-88) and interleukin-10 (IL-10 Invitrogen™ 88-7106-88).

    Techniques: Recombinant, Expressing

    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: shRNA, Activation Assay, In Vitro, Infection, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Standard Deviation, Negative Control

    IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: Activation Assay, In Vitro, Recombinant, Enzyme-linked Immunosorbent Assay, Expressing, Marker, Western Blot, Standard Deviation

    Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: Activation Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, shRNA, Negative Control