NBP1-84381 Search Results


antibodies against ifnlr1  (Novus Biologicals)
91
Novus Biologicals antibodies against ifnlr1
Differentially expressed genes (DEGs, P-FDR < 0.05) were identified by RNA-seq analysis in IFN-λ3-GFP, IFN-λ4-GFP and <t>IFN-λ4-GFP-IFNLR1</t> KO HepG2 cells after 72 hrs of induction by dox, comparing to controls (dox-conditions). Cutoff threshold (fold change > +/-1.5) is indicated by dotted lines. (A) Analysis of all DEGs (n=3251) detected for IFN-λ4-GFP or IFN-λ4-GFP-IFNLR1 KO cells. In blue - DEGs (n=2,735) specific to IFN-λ4-GFP and considered IFNLR1-dependent. In black - DEGs (n=145) shared between both groups and considered IFNLR1-independent. In orange - DEGs (n=371) specific to IFN-λ4-GFP-IFNLR1 KO . (B) DEGs of IFN-λ4-GFP analyzed in IFN-λ3-GFP transcriptome. In black - DEGs (n=1,506) shared in IFN-λ4-GFP and IFN-λ3-GFP and in blue - IFN-λ4-signature DEGs (n=1,229) detected in IFN-λ4-GFP but not in IFN-λ3-GFP producing cells. Additional details are provided in Fig. S3 and Table S6. (C , D) Cell cycle analysis of cells synchronized by 24 hrs of serum starvation, treated with or without dox (0.5 µg/ml) for 72 hrs and analyzed by flow cytometry after PI staining. The plot shows a representative picture and the percentage of cells in each phase of the cell cycle. All data are shown as mean± SEM from triplicate experiments. *, P < 0.05. (E , F) Bromodeoxyuridine (BRDU, %) incorporation indicating cell proliferation in HepG2 cells expressing IFN-λ3-GFP, IFN-λ4-GFP and IFN-λ4-GFP-IFNLR1KO. Cells were cocultured with HepG2 cells labeled with Far Red proliferation dye, dox-induced for 72 hrs and treated with BRDU for 3 hrs before analysis. Gates show HepG2 cells exposed to IFN-λs (IFN-λ treated cells) and HepG2 expressing IFN-λs. P-values compare corresponding dox+ vs. dox-HepG2 cells, ** p<0.01, Student’s T-test. Graphs represent one of three independent experiments, each in biological triplicates.
Antibodies Against Ifnlr1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/antibodies against ifnlr1/product/Novus Biologicals
Average 91 stars, based on 1 article reviews
antibodies against ifnlr1 - by Bioz Stars, 2026-02
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ifn λr1 il 28ra  (Novus Biologicals)
90
Novus Biologicals ifn λr1 il 28ra
Expression of type III interferons (IFNs) (IFN‐λ1/interleukin (IL)−29, IFN‐λ2/IL‐28A and IFN‐λ3/IL‐28B) and their signalling receptor <t>(IFN‐λR1/IL‐28Rα)</t> (a) in minor salivary gland (MSG) tissues that belong to the three Sjögren's syndrome (SS) subgroups, as these classified by the grade of the inflammatory lesion (SS‐I: mild, n = 16; SS‐II: intermediate, n = 14; and SS‐III: severe, n = 16 MSG lesions. Sicca controls CT, n = 17), (b) in non‐malignant parotid glands of patients undergoing parotidectomy due to mixed tumours. Original magnification ×200.
Ifn λr1 Il 28ra, supplied by Novus Biologicals, 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/ifn λr1 il 28ra/product/Novus Biologicals
Average 90 stars, based on 1 article reviews
ifn λr1 il 28ra - by Bioz Stars, 2026-02
90/100 stars
  Buy from Supplier

Image Search Results


Differentially expressed genes (DEGs, P-FDR < 0.05) were identified by RNA-seq analysis in IFN-λ3-GFP, IFN-λ4-GFP and IFN-λ4-GFP-IFNLR1 KO HepG2 cells after 72 hrs of induction by dox, comparing to controls (dox-conditions). Cutoff threshold (fold change > +/-1.5) is indicated by dotted lines. (A) Analysis of all DEGs (n=3251) detected for IFN-λ4-GFP or IFN-λ4-GFP-IFNLR1 KO cells. In blue - DEGs (n=2,735) specific to IFN-λ4-GFP and considered IFNLR1-dependent. In black - DEGs (n=145) shared between both groups and considered IFNLR1-independent. In orange - DEGs (n=371) specific to IFN-λ4-GFP-IFNLR1 KO . (B) DEGs of IFN-λ4-GFP analyzed in IFN-λ3-GFP transcriptome. In black - DEGs (n=1,506) shared in IFN-λ4-GFP and IFN-λ3-GFP and in blue - IFN-λ4-signature DEGs (n=1,229) detected in IFN-λ4-GFP but not in IFN-λ3-GFP producing cells. Additional details are provided in Fig. S3 and Table S6. (C , D) Cell cycle analysis of cells synchronized by 24 hrs of serum starvation, treated with or without dox (0.5 µg/ml) for 72 hrs and analyzed by flow cytometry after PI staining. The plot shows a representative picture and the percentage of cells in each phase of the cell cycle. All data are shown as mean± SEM from triplicate experiments. *, P < 0.05. (E , F) Bromodeoxyuridine (BRDU, %) incorporation indicating cell proliferation in HepG2 cells expressing IFN-λ3-GFP, IFN-λ4-GFP and IFN-λ4-GFP-IFNLR1KO. Cells were cocultured with HepG2 cells labeled with Far Red proliferation dye, dox-induced for 72 hrs and treated with BRDU for 3 hrs before analysis. Gates show HepG2 cells exposed to IFN-λs (IFN-λ treated cells) and HepG2 expressing IFN-λs. P-values compare corresponding dox+ vs. dox-HepG2 cells, ** p<0.01, Student’s T-test. Graphs represent one of three independent experiments, each in biological triplicates.

Journal: bioRxiv

Article Title: IFN-λ4 may contribute to HCV persistence by increasing ER stress and enhancing IRF1 signaling

doi: 10.1101/2020.10.28.359398

Figure Lengend Snippet: Differentially expressed genes (DEGs, P-FDR < 0.05) were identified by RNA-seq analysis in IFN-λ3-GFP, IFN-λ4-GFP and IFN-λ4-GFP-IFNLR1 KO HepG2 cells after 72 hrs of induction by dox, comparing to controls (dox-conditions). Cutoff threshold (fold change > +/-1.5) is indicated by dotted lines. (A) Analysis of all DEGs (n=3251) detected for IFN-λ4-GFP or IFN-λ4-GFP-IFNLR1 KO cells. In blue - DEGs (n=2,735) specific to IFN-λ4-GFP and considered IFNLR1-dependent. In black - DEGs (n=145) shared between both groups and considered IFNLR1-independent. In orange - DEGs (n=371) specific to IFN-λ4-GFP-IFNLR1 KO . (B) DEGs of IFN-λ4-GFP analyzed in IFN-λ3-GFP transcriptome. In black - DEGs (n=1,506) shared in IFN-λ4-GFP and IFN-λ3-GFP and in blue - IFN-λ4-signature DEGs (n=1,229) detected in IFN-λ4-GFP but not in IFN-λ3-GFP producing cells. Additional details are provided in Fig. S3 and Table S6. (C , D) Cell cycle analysis of cells synchronized by 24 hrs of serum starvation, treated with or without dox (0.5 µg/ml) for 72 hrs and analyzed by flow cytometry after PI staining. The plot shows a representative picture and the percentage of cells in each phase of the cell cycle. All data are shown as mean± SEM from triplicate experiments. *, P < 0.05. (E , F) Bromodeoxyuridine (BRDU, %) incorporation indicating cell proliferation in HepG2 cells expressing IFN-λ3-GFP, IFN-λ4-GFP and IFN-λ4-GFP-IFNLR1KO. Cells were cocultured with HepG2 cells labeled with Far Red proliferation dye, dox-induced for 72 hrs and treated with BRDU for 3 hrs before analysis. Gates show HepG2 cells exposed to IFN-λs (IFN-λ treated cells) and HepG2 expressing IFN-λs. P-values compare corresponding dox+ vs. dox-HepG2 cells, ** p<0.01, Student’s T-test. Graphs represent one of three independent experiments, each in biological triplicates.

Article Snippet: The membranes were probed with primary antibodies against IFNLR1 (#NBP1-84381, Novus Biologicals), STAT1 (#9172, Cell Signaling Technology), phospho-STAT1 (Tyr701, #58D6, Cell Signaling Technology), IFN-λ4 (ab196984; Abcam), GAPDH (ab37168, Abcam) and HRP-linked secondary antibody, goat anti-rabbit IgG (#7074; Cell Signaling Technology) or goat anti-mouse IgG (San Cruz, sc-2031).

Techniques: RNA Sequencing, Cell Cycle Assay, Flow Cytometry, Staining, BrdU Incorporation Assay, Expressing, Labeling

(A) Unsupervised clustering of activities of 54 regulons that were significantly and directionally enriched with HepG2-DEGs in the set of 885 of TCGA-LIHC regulons. The heatmap shows differences in activity scores (dES) for the IFN-λ4-enriched regulons organized by GSEA-2T results for the IFN-λ4-GFP, IFN-λ3-GFP and IFN-λ4-GFP-IFNLR1 KO DEG signatures. Cluster I: regulons with dES > 0 in IFN-λ4-GFP; cluster II: regulons with dES < 0 in IFN-λ4-GFP. Table S7 provides the regulon activity scores presented in Figure 2A. (B-G) GSEA-2T plots for IRF1 and IRF2, respectively, in DEG signatures for (B-C) IFN-λ3-GFP, ( D-E ) IFN-λ4-GFP, and ( F-G ) IFN-λ4-GFP-IFNLR1 KO . (H) Inhibition of proliferation in IFN-λ4-GFP HepG2 cells, for one of three independent experiments. Cells were treated with IRF1 siRNA for 24 hrs, labeled with Far Red proliferation dye and dox-induced at indicated concentrations for 72 hrs. Proliferation was assessed by flow cytometry with a graph representing the geometric mean expression of Far Red proliferation dye with higher values indicating reduced cell proliferation. P-values compare dox-treated control siRNA with dox-treated IRF1 siRNA. ** p<0.01, Student’s T-test. Below: Western blots showing IRF1 protein levels following siRNA knockdown.

Journal: bioRxiv

Article Title: IFN-λ4 may contribute to HCV persistence by increasing ER stress and enhancing IRF1 signaling

doi: 10.1101/2020.10.28.359398

Figure Lengend Snippet: (A) Unsupervised clustering of activities of 54 regulons that were significantly and directionally enriched with HepG2-DEGs in the set of 885 of TCGA-LIHC regulons. The heatmap shows differences in activity scores (dES) for the IFN-λ4-enriched regulons organized by GSEA-2T results for the IFN-λ4-GFP, IFN-λ3-GFP and IFN-λ4-GFP-IFNLR1 KO DEG signatures. Cluster I: regulons with dES > 0 in IFN-λ4-GFP; cluster II: regulons with dES < 0 in IFN-λ4-GFP. Table S7 provides the regulon activity scores presented in Figure 2A. (B-G) GSEA-2T plots for IRF1 and IRF2, respectively, in DEG signatures for (B-C) IFN-λ3-GFP, ( D-E ) IFN-λ4-GFP, and ( F-G ) IFN-λ4-GFP-IFNLR1 KO . (H) Inhibition of proliferation in IFN-λ4-GFP HepG2 cells, for one of three independent experiments. Cells were treated with IRF1 siRNA for 24 hrs, labeled with Far Red proliferation dye and dox-induced at indicated concentrations for 72 hrs. Proliferation was assessed by flow cytometry with a graph representing the geometric mean expression of Far Red proliferation dye with higher values indicating reduced cell proliferation. P-values compare dox-treated control siRNA with dox-treated IRF1 siRNA. ** p<0.01, Student’s T-test. Below: Western blots showing IRF1 protein levels following siRNA knockdown.

Article Snippet: The membranes were probed with primary antibodies against IFNLR1 (#NBP1-84381, Novus Biologicals), STAT1 (#9172, Cell Signaling Technology), phospho-STAT1 (Tyr701, #58D6, Cell Signaling Technology), IFN-λ4 (ab196984; Abcam), GAPDH (ab37168, Abcam) and HRP-linked secondary antibody, goat anti-rabbit IgG (#7074; Cell Signaling Technology) or goat anti-mouse IgG (San Cruz, sc-2031).

Techniques: Activity Assay, Inhibition, Labeling, Flow Cytometry, Expressing, Control, Western Blot, Knockdown

Representative confocal images of HepG2 cells transduced with a mammalian baculovirus delivery system (BacMam) of GFP-tagged proteins targeting specific organelles - lysosomes, Golgi, early and late endosomes. After transduction for 6 hrs, cells were transiently transfected with Halo-tagged constructs for IFN-λ4 or control for indicated times, stained with cell-permeant Halo-tag ligand TMR (red), and imaged. (A) Confocal images showing IFN-λ4 accumulation in lysosomes but not in early endosomes. (B) Late endosomal trafficking of IFN-λ4, with the inset showing larger magnification. (C) Unfolded protein response (UPR) is represented by lysosomal enlargement after protein accumulation. (D) Live images of IFN-λ4-expressing HepG2 cells undergoing apoptosis, characterized by membrane blebbing and cell death. Images were scanned every minute for 12 hrs. Scale bars – 10 um. (E) Apoptosis detection with ApoTox-Glo assays in corresponding untreated and dox-induced cells for indicated time points. RLU, relative luminescence units. (F) Graph showing counts from colony formation assay for HepG2 cells expressing IFN-λ4 or IFNLR1 KO grown in 6-well plates with or without dox for 13 days. Cell colonies were stained with crystal violet and manually counted. The graph represents the number of colonies as a percentage of initial plated counts. (G,H) mRNA (G) and protein levels ( H ) of DDIT3 after siRNA knockdown tested by qRT-PCR and Western blot assays, respectively. (I-J) Apoptosis (I) and cell viability (J) assays were performed after siRNA knockdown of DDIT3 in dox-induced IFN-λ4-GFP cells. * p<0.05, ** p< 0.01, *** p<0.001.

Journal: bioRxiv

Article Title: IFN-λ4 may contribute to HCV persistence by increasing ER stress and enhancing IRF1 signaling

doi: 10.1101/2020.10.28.359398

Figure Lengend Snippet: Representative confocal images of HepG2 cells transduced with a mammalian baculovirus delivery system (BacMam) of GFP-tagged proteins targeting specific organelles - lysosomes, Golgi, early and late endosomes. After transduction for 6 hrs, cells were transiently transfected with Halo-tagged constructs for IFN-λ4 or control for indicated times, stained with cell-permeant Halo-tag ligand TMR (red), and imaged. (A) Confocal images showing IFN-λ4 accumulation in lysosomes but not in early endosomes. (B) Late endosomal trafficking of IFN-λ4, with the inset showing larger magnification. (C) Unfolded protein response (UPR) is represented by lysosomal enlargement after protein accumulation. (D) Live images of IFN-λ4-expressing HepG2 cells undergoing apoptosis, characterized by membrane blebbing and cell death. Images were scanned every minute for 12 hrs. Scale bars – 10 um. (E) Apoptosis detection with ApoTox-Glo assays in corresponding untreated and dox-induced cells for indicated time points. RLU, relative luminescence units. (F) Graph showing counts from colony formation assay for HepG2 cells expressing IFN-λ4 or IFNLR1 KO grown in 6-well plates with or without dox for 13 days. Cell colonies were stained with crystal violet and manually counted. The graph represents the number of colonies as a percentage of initial plated counts. (G,H) mRNA (G) and protein levels ( H ) of DDIT3 after siRNA knockdown tested by qRT-PCR and Western blot assays, respectively. (I-J) Apoptosis (I) and cell viability (J) assays were performed after siRNA knockdown of DDIT3 in dox-induced IFN-λ4-GFP cells. * p<0.05, ** p< 0.01, *** p<0.001.

Article Snippet: The membranes were probed with primary antibodies against IFNLR1 (#NBP1-84381, Novus Biologicals), STAT1 (#9172, Cell Signaling Technology), phospho-STAT1 (Tyr701, #58D6, Cell Signaling Technology), IFN-λ4 (ab196984; Abcam), GAPDH (ab37168, Abcam) and HRP-linked secondary antibody, goat anti-rabbit IgG (#7074; Cell Signaling Technology) or goat anti-mouse IgG (San Cruz, sc-2031).

Techniques: Transduction, Transfection, Construct, Control, Staining, Expressing, Membrane, Colony Assay, Knockdown, Quantitative RT-PCR, Western Blot

Expression of type III interferons (IFNs) (IFN‐λ1/interleukin (IL)−29, IFN‐λ2/IL‐28A and IFN‐λ3/IL‐28B) and their signalling receptor (IFN‐λR1/IL‐28Rα) (a) in minor salivary gland (MSG) tissues that belong to the three Sjögren's syndrome (SS) subgroups, as these classified by the grade of the inflammatory lesion (SS‐I: mild, n = 16; SS‐II: intermediate, n = 14; and SS‐III: severe, n = 16 MSG lesions. Sicca controls CT, n = 17), (b) in non‐malignant parotid glands of patients undergoing parotidectomy due to mixed tumours. Original magnification ×200.

Journal: Clinical and Experimental Immunology

Article Title: Expression of type III interferons (IFNλs) and their receptor in Sjögren's syndrome

doi: 10.1111/cei.12865

Figure Lengend Snippet: Expression of type III interferons (IFNs) (IFN‐λ1/interleukin (IL)−29, IFN‐λ2/IL‐28A and IFN‐λ3/IL‐28B) and their signalling receptor (IFN‐λR1/IL‐28Rα) (a) in minor salivary gland (MSG) tissues that belong to the three Sjögren's syndrome (SS) subgroups, as these classified by the grade of the inflammatory lesion (SS‐I: mild, n = 16; SS‐II: intermediate, n = 14; and SS‐III: severe, n = 16 MSG lesions. Sicca controls CT, n = 17), (b) in non‐malignant parotid glands of patients undergoing parotidectomy due to mixed tumours. Original magnification ×200.

Article Snippet: Rabbit polyclonal antibodies to human IFN‐λ1/IL‐29 (Santa Cruz, Dallas, Texas, USA), IFN‐λ2/IL‐28A (Antibodies‐online, Atlanta, GA, USA), IFN‐λ/IL‐28B (Bioss, Woburn, MA, USA), IFN‐λR1/IL‐28Ra (Novus Biologicals, Littleton, CO, USA) and CD3 (Dako, Glostrup, Denmark) were used.

Techniques: Expressing

Representative double immunofluorescent staining for the common type III interferon (IFN) signalling receptor [IFN‐λR1/interleukin (IL)−28Rα] and markers of inflammatory cells [plasmatocytoid dendritic cells (pDCs): CD303 and CD123, macrophages: CD68, T lymphocytes: CD3 and B lymphocytes: CD20] in a minor salivary gland (MSG) tissue from a Sjögren's syndrome (SS) patient. Co‐localization is indicated with yellow arrows. Original magnification ×1000.

Journal: Clinical and Experimental Immunology

Article Title: Expression of type III interferons (IFNλs) and their receptor in Sjögren's syndrome

doi: 10.1111/cei.12865

Figure Lengend Snippet: Representative double immunofluorescent staining for the common type III interferon (IFN) signalling receptor [IFN‐λR1/interleukin (IL)−28Rα] and markers of inflammatory cells [plasmatocytoid dendritic cells (pDCs): CD303 and CD123, macrophages: CD68, T lymphocytes: CD3 and B lymphocytes: CD20] in a minor salivary gland (MSG) tissue from a Sjögren's syndrome (SS) patient. Co‐localization is indicated with yellow arrows. Original magnification ×1000.

Article Snippet: Rabbit polyclonal antibodies to human IFN‐λ1/IL‐29 (Santa Cruz, Dallas, Texas, USA), IFN‐λ2/IL‐28A (Antibodies‐online, Atlanta, GA, USA), IFN‐λ/IL‐28B (Bioss, Woburn, MA, USA), IFN‐λR1/IL‐28Ra (Novus Biologicals, Littleton, CO, USA) and CD3 (Dako, Glostrup, Denmark) were used.

Techniques: Staining