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ifnar1  (Proteintech)


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    Proteintech ifnar1
    Ifnar1, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+ifnar1/IRF7+Antibody/pm41831815-101-59-60
    Average 95 stars, based on 55 article reviews
    ifnar1 - by Bioz Stars, 2026-09
    95/100 stars

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    other:

    Article Title: Pretreatment of UC-MSCs with IFN-α2 improves treatment of liver fibrosis by recruiting neutrophils.
    Article Snippet: The primary antibodies were anti-IFNAR1 (1:500; Proteintech, USA), β-actin (1:1000; Servicebio, China), anti-STAT1 (1:2000; Proteintech, USA), phospho-STAT1 (Tyr701; 1:1000; Proteintech, USA), anti-STAT2 (1:500; Proteintech, USA), phospho-STAT2 (Tyr690; 1:1000; SAB, USA), anti-STAT3 (1:500; SAB, USA), and phosphoSTAT3 (Try705; (1:500; SAB, USA).

    Article Title: The oncoprotein BCL6 enables solid tumor cells to evade genotoxic stress
    Article Snippet: The antibodies used are listed as follows: anti- BCL6 (1;1000, Cell Signaling Technology Cat# 14895, RRID: AB_2798638), anti- phospho- mTORS2448 (1;1000, Cell Signaling Technology Cat# 2971, RRID: AB_330970), anti- mTOR (1;1000, Cell Signaling Technology Cat# 2972, RRID: AB_330978), antiphospho- p70S6KT389 (1;1000, Cell Signaling Technology Cat# 9206, RRID: AB_2285392), anti- p70S6K (1;1000, Cell Signaling Technology Cat# 9202, RRID: AB_331676), anti- phospho- S6S235/S236 (1;1000, Cell Signaling Technology Cat# 2211, RRID: AB_331679), anti- S6 (1;1000, Cell Signaling Technology Cat# 2217, RRID: AB_331355), anti- phospho- H2AXS139 (1;1000, Cell Signaling Technology Cat# 9718, RRID: AB_2118009), anti- PTEN (1;1000, Cell Signaling Technology Cat# 9559, RRID: AB_390810), anti- GAPDH (1;10000, Abcam Cat# ab181602, RRID: AB_2630358), anti- STAT1 (1;1000, Abclonal Cat# A19563, RRID: AB_2862669), and anti- IFNAR1 (1;1000, Proteintech Cat# 13083–1- AP, RRID: AB_2122626).

    Article Title: Pseudorabies virus manipulates mitochondrial tryptophanyl-tRNA synthetase 2 for viral replication
    Article Snippet: Anti-ACACA (#3676), anti-p-ACACA (#11818) and anti-p-eIF2α (#3398) antibodies were purchased from Cell Signaling Technology (MA, USA); anti-WARS2 (13944-1-AP), anti-cGAS (26416-1-AP), anti-STING (19851-1-AP), anti-TBK1 (28397-1-AP), anti-IFR3 (11312-1-AP), anti-IFNAR1 (13083-1-AP), anti-eIF2α (11170-1-AP) and anti-β-actin (20536-1-AP), anti-NDUFA9 (20312-1-AP), anti-SDHA (14865-1-AP) and anti-COXI (13393-1-AP) were purchased from Proteintech (Wuhan, China); anti-FASN (ab22759) was purchased from Abcam (MA, USA); anti-FLAG (F3165), anti-puromycin (MABE343) and anti-HMGCR (MABS1233) was purchased from Sigma-Aldrich (MO, USA); anti-p-HMGCR (bs-4063R) was purchased from Bioss (MA, USA); horseradish peroxidase (HRP)-conjugated donkey anti-mouse IgG (715-035-150) and anti-rabbit IgG (711-035-152) were purchased from Jackson Immuno Research Laboratories (PA, USA).

    Article Title: Pseudorabies virus manipulates mitochondrial tryptophanyl-tRNA synthetase 2 for viral replication.
    Article Snippet: 102 103 2.2 Antibodies 104 Anti-ACACA (#3676), anti-p-ACACA (#11818) and anti-p-eIF2α (#3398) antibodies 105 were purchased from Cell Signaling Technology (MA, USA); anti-WARS2 (13944-1-AP), 106 anti-cGAS (26416-1-AP), anti-STING (19851-1-AP), anti-TBK1 (28397-1-AP), anti-IFR3 107 (11312-1-AP), anti-IFNAR1 (13083-1-AP), anti-eIF2α (11170-1-AP) and anti-β-actin 108 (20536-1-AP), anti-NDUFA9 (20312-1-AP), anti-SDHA (14865-1-AP) and anti-COXI 109 (13393-1-AP) were purchased from Proteintech (Wuhan, China); anti-FASN (ab22759) was 110 Jo urn al Pr e-p roo f purchased from Abcam (MA, USA); anti-FLAG (F3165), anti-puromicin (MABE343) and 111 anti-HMGCR (MABS1233) was purchased from Sigma-Aldrich (MO, USA); anti-p-HMGCR 112 (bs-4063R) was purchased from Bioss (MA, USA); horseradish peroxidase (HRP)-conjugated 113 donkey anti-mouse IgG (715-035-150) and anti-rabbit IgG (711-035-152) were purchased 114 from Jackson Immuno Research Laboratories (PA, USA).

    Article Title: The oncoprotein BCL6 enables solid tumor cells to evade genotoxic stress
    Article Snippet: The antibodies used are listed as follows: anti-BCL6 (1;1000, Cell Signaling Technology Cat# 14895, RRID: AB_2798638 ), anti-phospho-mTOR S2448 (1;1000, Cell Signaling Technology Cat# 2971, RRID: AB_330970 ), anti-mTOR (1;1000, Cell Signaling Technology Cat# 2972, RRID: AB_330978 ), anti-phospho-p70S6K T389 (1;1000, Cell Signaling Technology Cat# 9206, RRID: AB_2285392 ), anti-p70S6K (1;1000, Cell Signaling Technology Cat# 9202, RRID: AB_331676 ), anti-phospho-S6 S235/S236 (1;1000, Cell Signaling Technology Cat# 2211, RRID: AB_331679 ), anti-S6 (1;1000, Cell Signaling Technology Cat# 2217, RRID: AB_331355 ), anti-phospho-H2AX S139 (1;1000, Cell Signaling Technology Cat# 9718, RRID: AB_2118009 ), anti-PTEN (1;1000, Cell Signaling Technology Cat# 9559, RRID: AB_390810 ), anti-GAPDH (1;10000, Abcam Cat# ab181602, RRID: AB_2630358 ), anti-STAT1 (1;1000, Abclonal Cat# A19563, RRID: AB_2862669 ), and anti-IFNAR1 (1;1000, Proteintech Cat# 13083–1-AP, RRID: AB_2122626 ).

    Article Title: Pretreatment of UC-MSCs with IFN-α2 improves treatment of liver fibrosis by recruiting neutrophils
    Article Snippet: The primary antibodies were anti-IFNAR1 (1:500; Proteintech, USA), β-actin (1:1000; Servicebio, China), anti-STAT1 (1:2000; Proteintech, USA), phospho-STAT1 (Tyr701; 1:1000; Proteintech, USA), anti-STAT2 (1:500; Proteintech, USA), phospho-STAT2 (Tyr690; 1:1000; SAB, USA), anti-STAT3 (1:500; SAB, USA), and phospho-STAT3 (Try705; (1:500; SAB, USA).

    Membrane:

    Article Title: STING activation induces polarized cytokine secretion of IFN-β and IL-17A promoting photoreceptor death and choroidal disruption in age-related macular degeneration.
    Article Snippet: .. The following primary antibodies were used to probe the membrane; anti-CRYBA1 (1:1000, Invitrogen, Cat. #PA5-28954), anti-STING (1:1000, Novus Biologicals, Cat. # NBP2-24683), anti-IL17A (1:1000, Abcam, Cat. #ab79056), anti-IFNAR1 (1:1000, Proteintech, cat83002-4-RR), anti-phospho STAT1 (1:1000, Abcam, cat#109461), STAT1 (1:1000, Cell Signaling Technology, Cat. #14994), anti-phospho STAT3 (Tyr705) (1:1000, Cell Signaling Technology, Cat. #9131), anti-STAT3 (1:1000, Cell Signaling Technology, Cat. #4904), anti-cleaved caspase 1 (1:1000, Cell Signaling Technology, Cat. #4199), anti-H3 (1:2000, Cell Signaling Technology, Cat. #4499, Cell Signaling Technology), anti--Actin (1:2000, Cat. #4970, Cell signaling technology) and anti-Vinculin (1:2000, Cell Signaling Technology, Cat. #13901). .. After primary incubation, membranes were washed three times in TBST for 10 minutes each and incubated with HRP-conjugated anti-rabbit IgG secondary antibody (1:3000, Cell Signaling Technology, Cat. #7074) for 1 h at RT with gentle shaking.

    Article Title: STING activation induces polarized cytokine secretion of IFN-β and IL-17A promoting photoreceptor death and choroidal disruption in age-related macular degeneration
    Article Snippet: .. The following primary antibodies were used to probe the membrane; anti-CRYBA1 (1:1000, Invitrogen, Cat. #PA5-28954), anti-STING (1:1000, Novus Biologicals, Cat. #NBP2-24683), anti-IL17A (1:1000, Abcam, Cat. #ab79056), anti-IFNAR1 (1:1000, Proteintech, Cat. #83002-4-RR), anti-phospho STAT1 (1:1000, Abcam, Cat. #109461), STAT1 (1:1000, Cell Signaling Technology, Cat. #14994), anti-phospho STAT3 (Tyr705) (1:1000, Cell Signaling Technology, Cat. #9131), anti-STAT3 (1:1000, Cell Signaling Technology, Cat. #4904), anti-cleaved caspase 1 (1:1000, Cell Signaling Technology, Cat. #4199), anti-H3 (1:2000, Cell Signaling Technology, Cat. #4499, Cell Signaling Technology), anti-β-Actin (1:2000, Cat. #4970, Cell Signaling Technology) and anti-Vinculin (1:2000, Cell Signaling Technology, Cat. #13901). .. After primary incubation, membranes were washed three times in TBST for 10 min each and incubated with HRP-conjugated anti-rabbit IgG secondary antibody (1:3000, Cell Signaling Technology, Cat. #7074) for 1 h at RT with gentle shaking.



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    ( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human <t>IFNAR1</t> (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].
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    (A) Feature plots of IFN receptors, including IFN-I receptor ( <t>IFNAR1/IFNAR2</t> ), IFN-II receptor ( IFNGR1/IFNGR2 ), IFN-III receptor ( IFNLR1/IL10RB ), in epithelial cells and CD14 + myeloid cells, from the scRNA-seq analysis of human colonic biopsies in . (B) Feature plots of IFN receptors, from the scRNA-seq analysis of DSS-induced colitis in . (C) Flow cytometry analysis of IFNAR1 + cells in mouse colon with or without DSS exposure, gated by immune cell marker CD45 and epithelial cell marker EpCAM. (D) Proportions of IFNAR1 + cells classified as immune cells (CD45 + /EpCAM - ) or epithelial cells (CD45 - /EpCAM + ) in mouse colon with or without DSS exposure. n=5 per group. (E-F) Flow cytometry analysis and quantification of median fluorescence intensity (MFI) of IFNAR1 expression in immune cells (CD45 + /EpCAM - ) and epithelial cells (CD45 - /EpCAM + ) from DSS-treated mouse colon.
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    Image Search Results


    ( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

    Journal: Science Advances

    Article Title: Inflammatory arthritis irAE may represent a unique autoimmune disease primarily driven by T cells but likely not autoantibodies

    doi: 10.1126/sciadv.aea4262

    Figure Lengend Snippet: ( A to G ) PBMCs from the patients with irAE were cultured in the plate coated with anti-CD3 and anti-CD28 (10 μg/ml) in the presence of IgG1 isotype control or anti–human IL-6R (50 μg/ml), anti–human IL-12p40 (50 μg/ml), and anti–human IFNAR1 (50 μg/ml) for 3 days; n = 9. (A) Expression of CD38 and CD127 on CD8 + T cells. Right: Percentage of CD38 + CD127 − CD8 + T cells. (B and C) CD8 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (B) Expression of granzyme B and IFN-γ. Right: Percentage of granzyme B + IFN-γ + CD8 + T cells. (C) Expression of perforin and IFN-γ. Right: Percentage of perforin + IFN-γ + CD8 + T cells. [(D) and (E)] MFIs of GluCy5 (D), TMRM, and MTDR (E) in CD8 + T cells were presented. [(F) and (G)] CD4 + T cells activated for 5 days were restimulated with PMA, ionomycin, and monensin for 5 hours. (F) Expression of IL-21 and IL-2. Right: Percentage of IL-21 + IL-2 + CD4 + T cells. (G) Expression of CD38 and CXCR5 on CD4 + T cells. Right: Percentage of CD38 + CXCR5 − CD4 + T cells. Data in graphs represent mean ± SEM. Significance was tested paired Student’s t test [(A) to (G)].

    Article Snippet: PBMCs from patients with irAE were thawed and rested in a complete medium for 1 hour and then activated with plate-coated anti–human CD3 and anti–human CD28 (10 μg/ml) with IgG1 isotype control (Bio X Cell, catalog no. CP174) or a combination of anti–human IL-6R 50 μg/ml; Bio X Cell, catalog no. SIM0014), anti–human IL-12p40 (50 μg/ml; Bio X Cell, catalog no. SIM0020), and anti–human IFNAR1 (50 μg/ml; Bio X Cell, catalog no. SIM0022) for 3 days.

    Techniques: Cell Culture, Control, Expressing

    (A) Feature plots of IFN receptors, including IFN-I receptor ( IFNAR1/IFNAR2 ), IFN-II receptor ( IFNGR1/IFNGR2 ), IFN-III receptor ( IFNLR1/IL10RB ), in epithelial cells and CD14 + myeloid cells, from the scRNA-seq analysis of human colonic biopsies in . (B) Feature plots of IFN receptors, from the scRNA-seq analysis of DSS-induced colitis in . (C) Flow cytometry analysis of IFNAR1 + cells in mouse colon with or without DSS exposure, gated by immune cell marker CD45 and epithelial cell marker EpCAM. (D) Proportions of IFNAR1 + cells classified as immune cells (CD45 + /EpCAM - ) or epithelial cells (CD45 - /EpCAM + ) in mouse colon with or without DSS exposure. n=5 per group. (E-F) Flow cytometry analysis and quantification of median fluorescence intensity (MFI) of IFNAR1 expression in immune cells (CD45 + /EpCAM - ) and epithelial cells (CD45 - /EpCAM + ) from DSS-treated mouse colon.

    Journal: bioRxiv

    Article Title: Type I interferon signaling promotes mucosal inflammation in murine models of colitis

    doi: 10.64898/2026.03.02.709022

    Figure Lengend Snippet: (A) Feature plots of IFN receptors, including IFN-I receptor ( IFNAR1/IFNAR2 ), IFN-II receptor ( IFNGR1/IFNGR2 ), IFN-III receptor ( IFNLR1/IL10RB ), in epithelial cells and CD14 + myeloid cells, from the scRNA-seq analysis of human colonic biopsies in . (B) Feature plots of IFN receptors, from the scRNA-seq analysis of DSS-induced colitis in . (C) Flow cytometry analysis of IFNAR1 + cells in mouse colon with or without DSS exposure, gated by immune cell marker CD45 and epithelial cell marker EpCAM. (D) Proportions of IFNAR1 + cells classified as immune cells (CD45 + /EpCAM - ) or epithelial cells (CD45 - /EpCAM + ) in mouse colon with or without DSS exposure. n=5 per group. (E-F) Flow cytometry analysis and quantification of median fluorescence intensity (MFI) of IFNAR1 expression in immune cells (CD45 + /EpCAM - ) and epithelial cells (CD45 - /EpCAM + ) from DSS-treated mouse colon.

    Article Snippet: For pharmacologic inhibition of IFNAR1, mice were intraperitoneally injected with 0.5 mg anti-mouse IFNAR1 antibody (BioXcell, BE0241) or mouse IgG1 isotype control (BioXcell, BE0083) on day 2 and day 5 after DSS exposure.

    Techniques: Flow Cytometry, Marker, Fluorescence, Expressing

    (A) Schematic illustrating how the serine-to-alanine substitution at position 535 of murine IFNAR1 protein affects phosphorylation and ubiquitination-dependent degradation. (B) qRT-PCR analysis of selected IFN-I signature genes in spleen and colon from WT and SA mice at baseline. Data were normalized to the mean of WT mice (set as 1). n=5-10 per group. (C) qRT-PCR analysis of selected IFN-I signature genes in bone marrow-derived macrophages (BMDMs) from WT and SA mice, at baseline (untreated) and after stimulation by interferon-β (IFNβ, 200 IU/mL x 8 hours) or lipopolysaccharides (LPS, 1 µg/mL x 8 hours). Data were normalized to the mean of WT BMDMs at baseline (set as 1). n=5-10 per group. (D-E) Mass cytometry (CyTOF) analysis of colon from WT (n=4) and SA (n=6) mice at baseline. (D) UMAP plots with cells colored by identity. (E) Proportions of immune cells (CD45 + /EpCAM - ), epithelial cells (CD45 - /EpCAM + ), and stromal cells (CD45 - /EpCAM - ). ns: not significant. (F) Heatmap showing the mean expression of target proteins in the antibody panel (Supplemental Table 4), with those having p <0.05 by SAM (Significance Analysis of Microarrays) for their median expression indicated by red asterisks.

    Journal: bioRxiv

    Article Title: Type I interferon signaling promotes mucosal inflammation in murine models of colitis

    doi: 10.64898/2026.03.02.709022

    Figure Lengend Snippet: (A) Schematic illustrating how the serine-to-alanine substitution at position 535 of murine IFNAR1 protein affects phosphorylation and ubiquitination-dependent degradation. (B) qRT-PCR analysis of selected IFN-I signature genes in spleen and colon from WT and SA mice at baseline. Data were normalized to the mean of WT mice (set as 1). n=5-10 per group. (C) qRT-PCR analysis of selected IFN-I signature genes in bone marrow-derived macrophages (BMDMs) from WT and SA mice, at baseline (untreated) and after stimulation by interferon-β (IFNβ, 200 IU/mL x 8 hours) or lipopolysaccharides (LPS, 1 µg/mL x 8 hours). Data were normalized to the mean of WT BMDMs at baseline (set as 1). n=5-10 per group. (D-E) Mass cytometry (CyTOF) analysis of colon from WT (n=4) and SA (n=6) mice at baseline. (D) UMAP plots with cells colored by identity. (E) Proportions of immune cells (CD45 + /EpCAM - ), epithelial cells (CD45 - /EpCAM + ), and stromal cells (CD45 - /EpCAM - ). ns: not significant. (F) Heatmap showing the mean expression of target proteins in the antibody panel (Supplemental Table 4), with those having p <0.05 by SAM (Significance Analysis of Microarrays) for their median expression indicated by red asterisks.

    Article Snippet: For pharmacologic inhibition of IFNAR1, mice were intraperitoneally injected with 0.5 mg anti-mouse IFNAR1 antibody (BioXcell, BE0241) or mouse IgG1 isotype control (BioXcell, BE0083) on day 2 and day 5 after DSS exposure.

    Techniques: Phospho-proteomics, Ubiquitin Proteomics, Quantitative RT-PCR, Derivative Assay, Mass Cytometry, Expressing

    Weight change (A and E) , clinical disease activity index (CDAI) (B and F) , colon length (C and G) , and qRT-PCR analysis of selected inflammatory cytokines and IFN-I signature genes (D and H) in colon in DSS-induced colitis (A-D) and piroxicam-accelerated enterocolitis (E-H) . (I-P) Schematics of experimental design (I and M) , clinical disease activity index (CDAI) (J and N) , colon length (K and O) , and qRT-PCR analysis of selected inflammatory cytokines and IFN-I signature genes (L and P) to assess the effect of tamoxifen-induced knockout of IFNAR1 (I-L) and administration of blocking anti-IFNAR1 antibody (M-P) on DSS-induced colitis.

    Journal: bioRxiv

    Article Title: Type I interferon signaling promotes mucosal inflammation in murine models of colitis

    doi: 10.64898/2026.03.02.709022

    Figure Lengend Snippet: Weight change (A and E) , clinical disease activity index (CDAI) (B and F) , colon length (C and G) , and qRT-PCR analysis of selected inflammatory cytokines and IFN-I signature genes (D and H) in colon in DSS-induced colitis (A-D) and piroxicam-accelerated enterocolitis (E-H) . (I-P) Schematics of experimental design (I and M) , clinical disease activity index (CDAI) (J and N) , colon length (K and O) , and qRT-PCR analysis of selected inflammatory cytokines and IFN-I signature genes (L and P) to assess the effect of tamoxifen-induced knockout of IFNAR1 (I-L) and administration of blocking anti-IFNAR1 antibody (M-P) on DSS-induced colitis.

    Article Snippet: For pharmacologic inhibition of IFNAR1, mice were intraperitoneally injected with 0.5 mg anti-mouse IFNAR1 antibody (BioXcell, BE0241) or mouse IgG1 isotype control (BioXcell, BE0083) on day 2 and day 5 after DSS exposure.

    Techniques: Activity Assay, Quantitative RT-PCR, Knock-Out, Blocking Assay