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anti il28a  (R&D Systems)


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    R&D Systems anti il28a
    Anti Il28a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+il28a/Human+IL-28A%2FIFN-lambda+2+Antibody/10__1158_slash_0008___5472__can___22___0736-111-57-58
    Average 94 stars, based on 6 article reviews
    anti il28a - by Bioz Stars, 2026-10
    94/100 stars

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    Control:

    Article Title: PRC2-Mediated Epigenetic Suppression of Type I IFN-STAT2 Signaling Impairs Antitumor Immunity in Luminal Breast Cancer
    Article Snippet: .. Neutralizing antibodies were added into the culture media at the following final concentrations: 2 mg/mL for IgG isotype control [(R&D Systems, #AB-108-C) or (Invitrogen, #31903)], 0.5 mg/mL for anti-IFNa (R&D Systems, #21100-1), 2 mg/mL for anti-IFNb (R&D Systems, #AF814), 2 mg/mL for anti-IFNg (R&D Systems, #MAB2851), 4 mg/mL for anti-IL29 (R&D Systems, #MAB15981), and 1 mg/mL for anti-IL28A (R&D Systems, #MAB1587). ..



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    <t>IL28A</t> expression was activated by ATG10S and ATG10 mutants with Cys 44 -Cys 135 mutation, and mediated autolysosome formation and HCV degradation. (A) Protein levels of the immune factors (IL28A, IRF3, and IRF7) and autophagy flux-related proteins (LC3B, P62, and LAMP2) were analyzed by Western blotting. (B) Transcription levels of IL28A, IRF3, and IRF7 were tested by qPCR. (C) Co-Immunoprecipitation showed the interactions among LAMP2, IL28A, P62, and LC3B using anti-LAMP2 antibody, and the interactions among IL28A with ATG10 mutant proteins and LAMP2 using anti-Flag antibody (labeling the ATG10, ATG10S, and the ATG10 mutants). (D) Immunofluorescence analysis shows co-localization of IL28A with LAMP2 by using anti-IL28A and anti-LAMP2 antibodies and co-localization of ATG10 mutants with IL28A by using anti-Flag and anti-IL28A antibodies in the HCV subreplicon cells. (E) The interactions between autophagosomes and lysosomes were disappeared in IL28A-knockdown cells by immunoprecipitation with anti-LC3B antibody (upper two panels). The replication of HCV subgenomic replicon was restored in IL28A-knockdown cells detected by Western blotting and RT-PCR tests in which HCV CORE and NS5B proteins and core RNA were obviously elevated via IL28A downregulation (lower two panels). Scale bars, 15 μm. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Ctrl; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. the replicon model.
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    IL28A expression was activated by ATG10S and ATG10 mutants with Cys 44 -Cys 135 mutation, and mediated autolysosome formation and HCV degradation. (A) Protein levels of the immune factors (IL28A, IRF3, and IRF7) and autophagy flux-related proteins (LC3B, P62, and LAMP2) were analyzed by Western blotting. (B) Transcription levels of IL28A, IRF3, and IRF7 were tested by qPCR. (C) Co-Immunoprecipitation showed the interactions among LAMP2, IL28A, P62, and LC3B using anti-LAMP2 antibody, and the interactions among IL28A with ATG10 mutant proteins and LAMP2 using anti-Flag antibody (labeling the ATG10, ATG10S, and the ATG10 mutants). (D) Immunofluorescence analysis shows co-localization of IL28A with LAMP2 by using anti-IL28A and anti-LAMP2 antibodies and co-localization of ATG10 mutants with IL28A by using anti-Flag and anti-IL28A antibodies in the HCV subreplicon cells. (E) The interactions between autophagosomes and lysosomes were disappeared in IL28A-knockdown cells by immunoprecipitation with anti-LC3B antibody (upper two panels). The replication of HCV subgenomic replicon was restored in IL28A-knockdown cells detected by Western blotting and RT-PCR tests in which HCV CORE and NS5B proteins and core RNA were obviously elevated via IL28A downregulation (lower two panels). Scale bars, 15 μm. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Ctrl; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. the replicon model.

    Journal: Frontiers in Immunology

    Article Title: Differential Effects of Autophagy-Related 10 Protein on HCV Replication and Autophagy Flux Are Mediated by Its Cysteine 44 and Cysteine 135

    doi: 10.3389/fimmu.2018.02176

    Figure Lengend Snippet: IL28A expression was activated by ATG10S and ATG10 mutants with Cys 44 -Cys 135 mutation, and mediated autolysosome formation and HCV degradation. (A) Protein levels of the immune factors (IL28A, IRF3, and IRF7) and autophagy flux-related proteins (LC3B, P62, and LAMP2) were analyzed by Western blotting. (B) Transcription levels of IL28A, IRF3, and IRF7 were tested by qPCR. (C) Co-Immunoprecipitation showed the interactions among LAMP2, IL28A, P62, and LC3B using anti-LAMP2 antibody, and the interactions among IL28A with ATG10 mutant proteins and LAMP2 using anti-Flag antibody (labeling the ATG10, ATG10S, and the ATG10 mutants). (D) Immunofluorescence analysis shows co-localization of IL28A with LAMP2 by using anti-IL28A and anti-LAMP2 antibodies and co-localization of ATG10 mutants with IL28A by using anti-Flag and anti-IL28A antibodies in the HCV subreplicon cells. (E) The interactions between autophagosomes and lysosomes were disappeared in IL28A-knockdown cells by immunoprecipitation with anti-LC3B antibody (upper two panels). The replication of HCV subgenomic replicon was restored in IL28A-knockdown cells detected by Western blotting and RT-PCR tests in which HCV CORE and NS5B proteins and core RNA were obviously elevated via IL28A downregulation (lower two panels). Scale bars, 15 μm. * P < 0.05, ** P < 0.01, *** P < 0.001 vs. Ctrl; # P < 0.05, ## P < 0.01, ### P < 0.001 vs. the replicon model.

    Article Snippet: Anti-IL28A (sc-365834) antibody for IF and anti-Lamin B (sc-6216) for Western blotting was purchased from Santa Cruz.

    Techniques: Expressing, Mutagenesis, Western Blot, Immunoprecipitation, Antibody Labeling, Immunofluorescence, Knockdown, Reverse Transcription Polymerase Chain Reaction

    ATG10 mutants with Cys 44 and/or Cys 135 mutation function as a kind of transcription factors. (A,B) Immunofluorescence by using anti-Flag antibody and nuclear–cytoplasmic fractionation analysis show the nuclear translocation of the ATG10 mutants without Cys 44 or/and Cys 135 . Scale bars: 15 μm. (C) The ATG10 mutants and ATG10S docking to IL28A promoter were confirmed by ChIP assay with anti-Flag, in which.a 400 bp fragment of IL28A promoter was amplified from the precipitates of the groups of ATGS and the ATG10 mutants without Cys 44 or/and Cys 135 compared with four groups of the control, the subreplicon model, and the model plus native ATG10 or plus ATG10 ΔM43 .

    Journal: Frontiers in Immunology

    Article Title: Differential Effects of Autophagy-Related 10 Protein on HCV Replication and Autophagy Flux Are Mediated by Its Cysteine 44 and Cysteine 135

    doi: 10.3389/fimmu.2018.02176

    Figure Lengend Snippet: ATG10 mutants with Cys 44 and/or Cys 135 mutation function as a kind of transcription factors. (A,B) Immunofluorescence by using anti-Flag antibody and nuclear–cytoplasmic fractionation analysis show the nuclear translocation of the ATG10 mutants without Cys 44 or/and Cys 135 . Scale bars: 15 μm. (C) The ATG10 mutants and ATG10S docking to IL28A promoter were confirmed by ChIP assay with anti-Flag, in which.a 400 bp fragment of IL28A promoter was amplified from the precipitates of the groups of ATGS and the ATG10 mutants without Cys 44 or/and Cys 135 compared with four groups of the control, the subreplicon model, and the model plus native ATG10 or plus ATG10 ΔM43 .

    Article Snippet: Anti-IL28A (sc-365834) antibody for IF and anti-Lamin B (sc-6216) for Western blotting was purchased from Santa Cruz.

    Techniques: Mutagenesis, Immunofluorescence, Fractionation, Translocation Assay, Amplification, Control