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standard recombinant mult1 protein  (R&D Systems)


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    R&D Systems standard recombinant mult1 protein
    <t>MULT1</t> encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum . ( A ) Experimental design. Briefly, 6-week-old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. ( B ) RT-qPCR data and ( C ) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. ( D ) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). ( E ) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). ( F and G ) RT-qPCR showing decrease of ( F ) liver collagen I and ( G ) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of ( H and I ) collagen I, ( H and J ) α-SMA and ( H and K ) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01.
    Standard Recombinant Mult1 Protein, supplied by R&D Systems, 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/standard recombinant mult1 protein/product/R&D Systems
    Average 90 stars, based on 1 article reviews
    standard recombinant mult1 protein - by Bioz Stars, 2026-05
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    1) Product Images from "MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response"

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    Journal: Journal of Inflammation Research

    doi: 10.2147/JIR.S354224

    MULT1 encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum . ( A ) Experimental design. Briefly, 6-week-old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. ( B ) RT-qPCR data and ( C ) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. ( D ) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). ( E ) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). ( F and G ) RT-qPCR showing decrease of ( F ) liver collagen I and ( G ) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of ( H and I ) collagen I, ( H and J ) α-SMA and ( H and K ) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01.
    Figure Legend Snippet: MULT1 encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum . ( A ) Experimental design. Briefly, 6-week-old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. ( B ) RT-qPCR data and ( C ) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. ( D ) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). ( E ) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). ( F and G ) RT-qPCR showing decrease of ( F ) liver collagen I and ( G ) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of ( H and I ) collagen I, ( H and J ) α-SMA and ( H and K ) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01.

    Techniques Used: Injection, Infection, Quantitative RT-PCR, Fluorescence, Expressing, Staining, Western Blot, Protein Concentration



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    standard recombinant mult1 protein  (R&D Systems)
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    R&D Systems standard recombinant mult1 protein
    <t>MULT1</t> encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum . ( A ) Experimental design. Briefly, 6-week-old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. ( B ) RT-qPCR data and ( C ) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. ( D ) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). ( E ) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). ( F and G ) RT-qPCR showing decrease of ( F ) liver collagen I and ( G ) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of ( H and I ) collagen I, ( H and J ) α-SMA and ( H and K ) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01.
    Standard Recombinant Mult1 Protein, supplied by R&D Systems, 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/standard recombinant mult1 protein/product/R&D Systems
    Average 90 stars, based on 1 article reviews
    standard recombinant mult1 protein - by Bioz Stars, 2026-05
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    recombinant mult1 protein  (R&D Systems)
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    R&D Systems recombinant mult1 protein
    Figure 1 <t>MULT1</t> encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum. (A) Experimental design. Briefly, 6-week- old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. (B) RT-qPCR data and (C) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. (D) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). (E) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). (F and G) RT-qPCR showing decrease of (F) liver collagen I and (G) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of (H and I) collagen I, (H and J) α-SMA and (H and K) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; RT-qPCR, reverse transcription-quantitative PCR; SMA, smooth muscle actin; rMULT1, recombinant MULT1.
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    https://www.bioz.com/result/recombinant mult1 protein/product/R&D Systems
    Average 92 stars, based on 1 article reviews
    recombinant mult1 protein - by Bioz Stars, 2026-05
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    recombinant murine mult1 protein  (R&D Systems)
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    Upregulation of <t>MULT1</t> at the mRNA and protein levels in the CNS during EAE. Quantification of MULT1 expression in organs from Klrk1 −/− (black bars) and wild type ( Klrk1 +/+ ; white bars) mice either injected with CFA-PBS as control (Ctl) or subjected to active EAE and sacrificed at pre-symptomatic (presympt), onset or peak stage of disease. (A) MULT1 relative mRNA expression in the spinal cord (SC), brainstem-cerebellum (Bs-C) and forebrain (Fb). Mean ± SEM n = 4–8. Kruskal-Wallis test and Dunn's test analysis within the same genotype group; statistical differences in Klrk1 +/+ group: spinal cord and brainstem-cerebellum: peak vs. ctl, presympt, or onset; forebrain peak vs. control. Statistical differences within Klrk1 −/− group: spinal cord peak vs. control, presymptomatic or onset stage; brainstem-cerebellum peak vs. presymptomatic; forebrain peak vs. presymptomatic. * p < 0.05; * * p < 0.01. (B) MULT1 relative mRNA expression in spleen and liver. Kruskal-Wallis test and Dunn's test analysis within the same genotype group; statistical differences in spleen for both Klrk1 +/+ and Klrk1 −/− groups: peak vs. ctl. * * p < 0.01. (C–F) Western blot analysis of MULT1 and actin levels in different CNS areas from Klrk1 −/− and Klrk1 +/+ mice at different disease stages. (C) One representative western blot of spinal cord (SC), brainstem-cerebellum (Bs-C) and forebrain (Fb) from control mice and mice at EAE peak; cartoon illustrating full and cleaved forms of MULT1. (D) Quantification of 55 kDa and 25 kDa forms as relative expression compared to actin at disease peak in Klrk1 −/− (black bars) and Klrk1 +/+ (white bars) mice; levels in Klrk1 +/+ spinal cord at disease peak defined as 1. Mean ± SEM n = 4–6. (E) One representative western blot of spinal cord from Klrk1 −/− and Klrk1 +/+ mice treated as control or EAE at different disease stages. (F) Ratio of the 25kDa on 55 kDa forms in the spinal cord at peak of disease for both genotypes. Klrk1 −/− (black bars) and Klrk1 +/+ (white bars). Mean ± SEM n = 4–6.
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    MULT1 encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum . ( A ) Experimental design. Briefly, 6-week-old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. ( B ) RT-qPCR data and ( C ) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. ( D ) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). ( E ) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). ( F and G ) RT-qPCR showing decrease of ( F ) liver collagen I and ( G ) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of ( H and I ) collagen I, ( H and J ) α-SMA and ( H and K ) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/JIR.S354224

    Figure Lengend Snippet: MULT1 encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum . ( A ) Experimental design. Briefly, 6-week-old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. ( B ) RT-qPCR data and ( C ) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. ( D ) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). ( E ) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). ( F and G ) RT-qPCR showing decrease of ( F ) liver collagen I and ( G ) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of ( H and I ) collagen I, ( H and J ) α-SMA and ( H and K ) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Injection, Infection, Quantitative RT-PCR, Fluorescence, Expressing, Staining, Western Blot, Protein Concentration

    Figure 1 MULT1 encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum. (A) Experimental design. Briefly, 6-week- old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. (B) RT-qPCR data and (C) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. (D) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). (E) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). (F and G) RT-qPCR showing decrease of (F) liver collagen I and (G) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of (H and I) collagen I, (H and J) α-SMA and (H and K) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; RT-qPCR, reverse transcription-quantitative PCR; SMA, smooth muscle actin; rMULT1, recombinant MULT1.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 1 MULT1 encoding DNA injection alleviates egg granuloma and hepatic fibrosis in mice infected with Schistosoma japonicum. (A) Experimental design. Briefly, 6-week- old BALB/c female mice (n=6 per group) were artificially infected with S. japonicum by cutaneous contact with 24 cercariae on a wet cover slip. Administration of 40 μg rMULT1 DNA or vehicle DNA was carried out via hydrodynamic tail vein injection; the process was initialized at 4 weeks post infection and repeated 3 times in 1 month before the mice were anaesthetized and sacrificed at the end point. (B) RT-qPCR data and (C) sandwich fluorescence immunoassay showing elevated MULT1 expression in p-rMULT1-injected mice compared with control group mice (GFP-ctl) administered vehicle plasmids. (D) Representative H&E staining images (left panel, magnification x200) and quantification of mean (±SEM) egg-induced granuloma size in the liver (white circles). (E) Representative Masson’s trichrome staining images (left panel, magnification x200) and quantification of mean (±SEM) collagen deposition (right panel). (F and G) RT-qPCR showing decrease of (F) liver collagen I and (G) α-SMA expression. Western blotting assay demonstrating reduced protein concentration of (H and I) collagen I, (H and J) α-SMA and (H and K) TGF-β in the livers of mice administered rMULT1 DNA. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; RT-qPCR, reverse transcription-quantitative PCR; SMA, smooth muscle actin; rMULT1, recombinant MULT1.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Injection, Infection, Quantitative RT-PCR, Fluorescence, Expressing, Control, Staining, Western Blot, Protein Concentration, Binding Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Recombinant

    Figure 2 Cytokine levels in the serum and liver. (A) Cytometric bead array analysis showing similar levels of several serum cytokines between treated mice and GFP-ctl mice, including IFN-γ, IL-2, IL-17, IL-6, TNF-α and IL-4. (B) Reverse transcription-quantitative PCR showing increased IFN-γ, decreased IL-10 and similar TGF-β RNA levels in liver of the rMULT1 group relative to the GFP-ctl group. (C) Cytometric bead array analysis of liver tissue showing elevated IFN-γ, unchanged IL-2, IL-17, IL-6, TNF-α and IL-4 in treated group. Comparisons were between rMULT1 and GFP-ctl, *P<0.05. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; rMULT1, recombinant MULT1.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 2 Cytokine levels in the serum and liver. (A) Cytometric bead array analysis showing similar levels of several serum cytokines between treated mice and GFP-ctl mice, including IFN-γ, IL-2, IL-17, IL-6, TNF-α and IL-4. (B) Reverse transcription-quantitative PCR showing increased IFN-γ, decreased IL-10 and similar TGF-β RNA levels in liver of the rMULT1 group relative to the GFP-ctl group. (C) Cytometric bead array analysis of liver tissue showing elevated IFN-γ, unchanged IL-2, IL-17, IL-6, TNF-α and IL-4 in treated group. Comparisons were between rMULT1 and GFP-ctl, *P<0.05. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; rMULT1, recombinant MULT1.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Reverse Transcription, Real-time Polymerase Chain Reaction, Binding Assay, Recombinant

    Figure 3 Decreased CD4+ T, CD8+ T, NK and NKP46+ NKT cell percentages in the spleen and the liver of BALB/c mouse with chronic S. japonicum infection. BALB/c female mice aged 6 weeks were artificially infected with 24 cercariae of S. japonicum or served as the healthy control with a mock infection procedure, then without any treatment, mice were euthanized and data were collected at 8 weeks post infection. (A and C) Representative dot plot graphs and (B and D) summary data demonstrated a significantly decreased percentage of NK cells, NKP46+ NKT cells, CD8+ T cells and CD4+ T cells in (A and B) splenocytes and (C and D) liver infiltrating lymphocytes of mice. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between Infected and NC. *P<0.05 and ***P<0.001. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; rMULT1, recombinant MULT1; NK, natural killer.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 3 Decreased CD4+ T, CD8+ T, NK and NKP46+ NKT cell percentages in the spleen and the liver of BALB/c mouse with chronic S. japonicum infection. BALB/c female mice aged 6 weeks were artificially infected with 24 cercariae of S. japonicum or served as the healthy control with a mock infection procedure, then without any treatment, mice were euthanized and data were collected at 8 weeks post infection. (A and C) Representative dot plot graphs and (B and D) summary data demonstrated a significantly decreased percentage of NK cells, NKP46+ NKT cells, CD8+ T cells and CD4+ T cells in (A and B) splenocytes and (C and D) liver infiltrating lymphocytes of mice. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between Infected and NC. *P<0.05 and ***P<0.001. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; rMULT1, recombinant MULT1; NK, natural killer.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Infection, Control, Binding Assay, Recombinant

    Figure 4 rMULT1 DNA restores lymphocyte percentages in the spleens and livers of S. japonicum-infected mice. (A and C) Representative dot plot graphs and (B and D) data demonstrated a significantly increased portion of NK cells, NKP46+ NKT cells, CD8+ T cells in spleen and of NK cells, CD4+ T cells in liver but not of CD4+ T cells in spleen or NKT cell in liver, as well as a significantly decreased portion of CD8+ T in liver, of mice that received rMULT1 DNA treatment. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; rMULT1, recombinant MULT1; NK, natural killer.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 4 rMULT1 DNA restores lymphocyte percentages in the spleens and livers of S. japonicum-infected mice. (A and C) Representative dot plot graphs and (B and D) data demonstrated a significantly increased portion of NK cells, NKP46+ NKT cells, CD8+ T cells in spleen and of NK cells, CD4+ T cells in liver but not of CD4+ T cells in spleen or NKT cell in liver, as well as a significantly decreased portion of CD8+ T in liver, of mice that received rMULT1 DNA treatment. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; rMULT1, recombinant MULT1; NK, natural killer.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Infection, Binding Assay, Recombinant

    Figure 6 NK cell phenotype changes were restored by rMULT1 DNA treatment. NK cells form rMULT1 group showed increased (A and G) NKG2D, (B and H) KLRG1, (D and J) CD49b and decreased (C and I) CD69, as well as enhanced (E, F, K and L) IFN-γ secretion, compared to those from GFP-ctl group. Open red line, rMULT1 group; filled green line, GFP-ctl group in all representative histograms. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; NKG2D, natural killer group 2, member D receptor; KLRG1, killer cell lectin-like receptor G1.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 6 NK cell phenotype changes were restored by rMULT1 DNA treatment. NK cells form rMULT1 group showed increased (A and G) NKG2D, (B and H) KLRG1, (D and J) CD49b and decreased (C and I) CD69, as well as enhanced (E, F, K and L) IFN-γ secretion, compared to those from GFP-ctl group. Open red line, rMULT1 group; filled green line, GFP-ctl group in all representative histograms. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05 and **P<0.01. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; NKG2D, natural killer group 2, member D receptor; KLRG1, killer cell lectin-like receptor G1.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Binding Assay

    Figure 8 Impact of rMULT1 DNA treatment on splenic T-cell phenotype in mice with S. japonicum infection. Flow cytometry data demonstrated an elevated NKG2D expression on (A) CD8+ T cells but not on (F) CD4+ T cells from treated mice. (G) The treated group exhibited decreased CD62L expression on CD4+ T cells compared with the GFP-ctl group, while (B) CD8+ T cells exhibited similar surface level of CD62L. Both CD8+ T and CD4+ T cells exhibited increased surface expression of (C and H) KLRG1 and (D and I) CD27, as well as (E and J) enhanced IFN-γ secretion upon rMULT1 DNA treatment. (K) Combined staining of CD4+ T cells with intracellular IFN-γ and IL-4 revealed a significantly higher Th1/Th2 ratio in CD4+ T cells of the treated mice. Open red line, rMULT1 DNA; filled green line, vehicle DNA in all representative histograms. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05, **P<0.01 and ***P<0.001. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; NKG2D, natural killer group 2 member D receptor; KLRG1, killer cell lectin-like receptor G1.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 8 Impact of rMULT1 DNA treatment on splenic T-cell phenotype in mice with S. japonicum infection. Flow cytometry data demonstrated an elevated NKG2D expression on (A) CD8+ T cells but not on (F) CD4+ T cells from treated mice. (G) The treated group exhibited decreased CD62L expression on CD4+ T cells compared with the GFP-ctl group, while (B) CD8+ T cells exhibited similar surface level of CD62L. Both CD8+ T and CD4+ T cells exhibited increased surface expression of (C and H) KLRG1 and (D and I) CD27, as well as (E and J) enhanced IFN-γ secretion upon rMULT1 DNA treatment. (K) Combined staining of CD4+ T cells with intracellular IFN-γ and IL-4 revealed a significantly higher Th1/Th2 ratio in CD4+ T cells of the treated mice. Open red line, rMULT1 DNA; filled green line, vehicle DNA in all representative histograms. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05, **P<0.01 and ***P<0.001. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; NKG2D, natural killer group 2 member D receptor; KLRG1, killer cell lectin-like receptor G1.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Infection, Flow Cytometry, Expressing, Staining, Binding Assay

    Figure 9 Impact of (A, C, E, G, I, K, M) infection and (B, D, F, H, J, L, N) rMULT1 DNA treatment on liver T-cell phenotype in mice with S. japonicum infection. Flow cytometry data revealed unchanged NKG2D levels on hepatic (A and B) CD8+ T and (G and H) CD4+ T cells in response to either (A and G) infection or (B and H) consequent treatment with rMULT1 DNA. Both CD8+ T and CD4+ T cells exhibited downregulated surface expression of (C and I) KLRG1 and (E and K) IFN-γ production upon S. japonicum infection, which were reversed by rMULT1 DNA treatment (D, J, F and L). (M and N) Combined staining of CD4+ T cells with intracellular IFN-γ and IL-4 revealed (M) a significantly descent in Th1/Th2 ratio in liver CD4+ T cells due to infection and (N) a restore of that in treated mice. Open dark line, health control; filled grey line, infected; open red line, rMULT1 DNA; filled green line, vehicle DNA in all representative histograms. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05, **P<0.01 and ***P<0.001. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; NKG2D, natural killer group 2 member D receptor; KLRG1, killer cell lectin-like receptor G1.

    Journal: Journal of Inflammation Research

    Article Title: MULT1-Encoding DNA Alleviates Schistosomiasis-Associated Hepatic Fibrosis via Modulating Cellular Immune Response

    doi: 10.2147/jir.s354224

    Figure Lengend Snippet: Figure 9 Impact of (A, C, E, G, I, K, M) infection and (B, D, F, H, J, L, N) rMULT1 DNA treatment on liver T-cell phenotype in mice with S. japonicum infection. Flow cytometry data revealed unchanged NKG2D levels on hepatic (A and B) CD8+ T and (G and H) CD4+ T cells in response to either (A and G) infection or (B and H) consequent treatment with rMULT1 DNA. Both CD8+ T and CD4+ T cells exhibited downregulated surface expression of (C and I) KLRG1 and (E and K) IFN-γ production upon S. japonicum infection, which were reversed by rMULT1 DNA treatment (D, J, F and L). (M and N) Combined staining of CD4+ T cells with intracellular IFN-γ and IL-4 revealed (M) a significantly descent in Th1/Th2 ratio in liver CD4+ T cells due to infection and (N) a restore of that in treated mice. Open dark line, health control; filled grey line, infected; open red line, rMULT1 DNA; filled green line, vehicle DNA in all representative histograms. Data are representative of 4–6 animals per subgroup and 3 independent experiments. Comparisons were between rMULT1 and GFP-ctl, *P<0.05, **P<0.01 and ***P<0.001. Abbreviations: MULT1, murine UL16-binding protein-like transcript 1; NKG2D, natural killer group 2 member D receptor; KLRG1, killer cell lectin-like receptor G1.

    Article Snippet: A standard curve was drawn from the MFI of the standard recombinant MULT1 protein (R&D Systems, Inc.) and the concentration of MULT1 was calculated based on the standard curve.

    Techniques: Infection, Flow Cytometry, Expressing, Staining, Control, Binding Assay

    Upregulation of MULT1 at the mRNA and protein levels in the CNS during EAE. Quantification of MULT1 expression in organs from Klrk1 −/− (black bars) and wild type ( Klrk1 +/+ ; white bars) mice either injected with CFA-PBS as control (Ctl) or subjected to active EAE and sacrificed at pre-symptomatic (presympt), onset or peak stage of disease. (A) MULT1 relative mRNA expression in the spinal cord (SC), brainstem-cerebellum (Bs-C) and forebrain (Fb). Mean ± SEM n = 4–8. Kruskal-Wallis test and Dunn's test analysis within the same genotype group; statistical differences in Klrk1 +/+ group: spinal cord and brainstem-cerebellum: peak vs. ctl, presympt, or onset; forebrain peak vs. control. Statistical differences within Klrk1 −/− group: spinal cord peak vs. control, presymptomatic or onset stage; brainstem-cerebellum peak vs. presymptomatic; forebrain peak vs. presymptomatic. * p < 0.05; * * p < 0.01. (B) MULT1 relative mRNA expression in spleen and liver. Kruskal-Wallis test and Dunn's test analysis within the same genotype group; statistical differences in spleen for both Klrk1 +/+ and Klrk1 −/− groups: peak vs. ctl. * * p < 0.01. (C–F) Western blot analysis of MULT1 and actin levels in different CNS areas from Klrk1 −/− and Klrk1 +/+ mice at different disease stages. (C) One representative western blot of spinal cord (SC), brainstem-cerebellum (Bs-C) and forebrain (Fb) from control mice and mice at EAE peak; cartoon illustrating full and cleaved forms of MULT1. (D) Quantification of 55 kDa and 25 kDa forms as relative expression compared to actin at disease peak in Klrk1 −/− (black bars) and Klrk1 +/+ (white bars) mice; levels in Klrk1 +/+ spinal cord at disease peak defined as 1. Mean ± SEM n = 4–6. (E) One representative western blot of spinal cord from Klrk1 −/− and Klrk1 +/+ mice treated as control or EAE at different disease stages. (F) Ratio of the 25kDa on 55 kDa forms in the spinal cord at peak of disease for both genotypes. Klrk1 −/− (black bars) and Klrk1 +/+ (white bars). Mean ± SEM n = 4–6.

    Journal: Frontiers in Immunology

    Article Title: NKG2D and Its Ligand MULT1 Contribute to Disease Progression in a Mouse Model of Multiple Sclerosis

    doi: 10.3389/fimmu.2019.00154

    Figure Lengend Snippet: Upregulation of MULT1 at the mRNA and protein levels in the CNS during EAE. Quantification of MULT1 expression in organs from Klrk1 −/− (black bars) and wild type ( Klrk1 +/+ ; white bars) mice either injected with CFA-PBS as control (Ctl) or subjected to active EAE and sacrificed at pre-symptomatic (presympt), onset or peak stage of disease. (A) MULT1 relative mRNA expression in the spinal cord (SC), brainstem-cerebellum (Bs-C) and forebrain (Fb). Mean ± SEM n = 4–8. Kruskal-Wallis test and Dunn's test analysis within the same genotype group; statistical differences in Klrk1 +/+ group: spinal cord and brainstem-cerebellum: peak vs. ctl, presympt, or onset; forebrain peak vs. control. Statistical differences within Klrk1 −/− group: spinal cord peak vs. control, presymptomatic or onset stage; brainstem-cerebellum peak vs. presymptomatic; forebrain peak vs. presymptomatic. * p < 0.05; * * p < 0.01. (B) MULT1 relative mRNA expression in spleen and liver. Kruskal-Wallis test and Dunn's test analysis within the same genotype group; statistical differences in spleen for both Klrk1 +/+ and Klrk1 −/− groups: peak vs. ctl. * * p < 0.01. (C–F) Western blot analysis of MULT1 and actin levels in different CNS areas from Klrk1 −/− and Klrk1 +/+ mice at different disease stages. (C) One representative western blot of spinal cord (SC), brainstem-cerebellum (Bs-C) and forebrain (Fb) from control mice and mice at EAE peak; cartoon illustrating full and cleaved forms of MULT1. (D) Quantification of 55 kDa and 25 kDa forms as relative expression compared to actin at disease peak in Klrk1 −/− (black bars) and Klrk1 +/+ (white bars) mice; levels in Klrk1 +/+ spinal cord at disease peak defined as 1. Mean ± SEM n = 4–6. (E) One representative western blot of spinal cord from Klrk1 −/− and Klrk1 +/+ mice treated as control or EAE at different disease stages. (F) Ratio of the 25kDa on 55 kDa forms in the spinal cord at peak of disease for both genotypes. Klrk1 −/− (black bars) and Klrk1 +/+ (white bars). Mean ± SEM n = 4–6.

    Article Snippet: On day 5, recombinant murine MULT1 protein (10 μg/ml, R&D Systems) was added or not to splenocytes.

    Techniques: Expressing, Injection, Western Blot

    Increased levels of soluble MULT1 in the CSF during EAE. Quantification of soluble MULT1 in CSF from Klrk1 −/− (black bars) and wild type counterparts ( Klrk1 +/+ ; white bars) either injected with CFA-PBS as control (Ctl) or subjected to active EAE and sacrificed at pre-symptomatic (presympt), onset or peak stage of the disease. (A) One representative western blot for the detection of total protein and MULT1. (B) Quantification of 55 kDa and 25 kDa forms as relative expression compared to total protein; levels in Klrk1 +/+ at disease peak defined as 1. Mean ± SEM n = 3–4. (C) Ratio of the 25 kDa/55 kDa forms at disease peak. Mean ± SEM n = 4.

    Journal: Frontiers in Immunology

    Article Title: NKG2D and Its Ligand MULT1 Contribute to Disease Progression in a Mouse Model of Multiple Sclerosis

    doi: 10.3389/fimmu.2019.00154

    Figure Lengend Snippet: Increased levels of soluble MULT1 in the CSF during EAE. Quantification of soluble MULT1 in CSF from Klrk1 −/− (black bars) and wild type counterparts ( Klrk1 +/+ ; white bars) either injected with CFA-PBS as control (Ctl) or subjected to active EAE and sacrificed at pre-symptomatic (presympt), onset or peak stage of the disease. (A) One representative western blot for the detection of total protein and MULT1. (B) Quantification of 55 kDa and 25 kDa forms as relative expression compared to total protein; levels in Klrk1 +/+ at disease peak defined as 1. Mean ± SEM n = 3–4. (C) Ratio of the 25 kDa/55 kDa forms at disease peak. Mean ± SEM n = 4.

    Article Snippet: On day 5, recombinant murine MULT1 protein (10 μg/ml, R&D Systems) was added or not to splenocytes.

    Techniques: Injection, Western Blot, Expressing

    Soluble MULT1 augments effector functions of CD8 T lymphocytes. Splenocytes from naïve Klrk1 −/− (black bars) and wild type ( Klrk1 +/+ white bars) mice were activated with anti-CD3, anti-CD28, IL-2, and IL-15 for 5 days and then exposed or not to soluble recombinant MULT1 for an additional 2 day culture. Cells were subsequently shortly activated and analyzed by flow cytometry for the expression of CD3, CD8, NKG2D, granzyme B, and IFNγ. (A) Representative contour plots are illustrated for the detection of NKG2D or Granzyme B and IFNγ on CD3 + CD8 + T cell-gated cells from Klrk1 −/− and Klrk1 +/+ mice. Histograms showing IFNγ on CD3 + CD8 + T cell-gated cells from Klrk1 −/− and Klrk1 +/+ mice according to treatment: PBS (dotted line) or MULT1 (filled line); gray filled represents isotype control. (B) Percentage of CD8 T lymphocytes expressing NKG2D, Granzyme B or IFNγ. Mean ± SEM n = 3 individual mice of one representative experiment. (C) MFI intensity for CD8 T lymphocytes expressing NKG2D, Granzyme B or IFNγ. Mean ± SEM n = 3 individual mice of one representative experiment. Statistical differences within Klrk1 +/+ group without vs. with MULT1 * p < 0.05.

    Journal: Frontiers in Immunology

    Article Title: NKG2D and Its Ligand MULT1 Contribute to Disease Progression in a Mouse Model of Multiple Sclerosis

    doi: 10.3389/fimmu.2019.00154

    Figure Lengend Snippet: Soluble MULT1 augments effector functions of CD8 T lymphocytes. Splenocytes from naïve Klrk1 −/− (black bars) and wild type ( Klrk1 +/+ white bars) mice were activated with anti-CD3, anti-CD28, IL-2, and IL-15 for 5 days and then exposed or not to soluble recombinant MULT1 for an additional 2 day culture. Cells were subsequently shortly activated and analyzed by flow cytometry for the expression of CD3, CD8, NKG2D, granzyme B, and IFNγ. (A) Representative contour plots are illustrated for the detection of NKG2D or Granzyme B and IFNγ on CD3 + CD8 + T cell-gated cells from Klrk1 −/− and Klrk1 +/+ mice. Histograms showing IFNγ on CD3 + CD8 + T cell-gated cells from Klrk1 −/− and Klrk1 +/+ mice according to treatment: PBS (dotted line) or MULT1 (filled line); gray filled represents isotype control. (B) Percentage of CD8 T lymphocytes expressing NKG2D, Granzyme B or IFNγ. Mean ± SEM n = 3 individual mice of one representative experiment. (C) MFI intensity for CD8 T lymphocytes expressing NKG2D, Granzyme B or IFNγ. Mean ± SEM n = 3 individual mice of one representative experiment. Statistical differences within Klrk1 +/+ group without vs. with MULT1 * p < 0.05.

    Article Snippet: On day 5, recombinant murine MULT1 protein (10 μg/ml, R&D Systems) was added or not to splenocytes.

    Techniques: Recombinant, Flow Cytometry, Expressing

    Passive EAE is less severe in Klrk1 −/− than in wild type recipients. Leukocytes from MOG-immunized C57BL/6 were reactivated in vitro and then adoptively transferred to Klrk1 −/− (black) and wild type ( Klrk1 +/+ ; white) recipients. (A) Mice were followed for clinical score. Mean ± SEM, n = 9–10. 2way ANOVA Klrk1 −/− vs. Klrk1 +/+ day 22–23 * p < 0.05 for all other days from day 12 to the end: * * * p < 0.001. (B) Flow cytometry analysis of ex vivo expanded T lymphocytes from MOG-immunized donor mice. Lymph node cells were collected, labeled with CFSE, and put in culture as described in materials and methods in the absence or presence of MOG 35−55 for 72 h. PMA, ionomycin, brefeldin A and monensin were added for 4 h prior to flow cytometry staining and analysis for intracellular mediators: GM-CSF, IFNγ, IL-17 and Granzyme B (GrB) as indicated. Contour plots illustrate gated events on CD4 or CD8 T cells expanded in vitro in the absence (Nil) or presence of MOG. (C) Representative detection of demyelination using fluoromyelin and DAPI in spinal cord sections from Klrk1 −/− and Klrk1 +/+ mice. White arrows indicate zones of myelin loss. (D) Western blot detection of MULT1 and albumin in CSF from Klrk1 −/− and Klrk1 +/+ mice 50 days after the adoptive transfer of activated lymphocytes. One representative western blot is illustrated and quantification of 55 kDa and 25 kDa forms as relative expression compared to albumin Mean ± SEM n = 7. Statistical differences for relative abundance of MULT1 25kDa form Klrk1 +/+ vs. Klrk1 −/− * * p < 0.01.

    Journal: Frontiers in Immunology

    Article Title: NKG2D and Its Ligand MULT1 Contribute to Disease Progression in a Mouse Model of Multiple Sclerosis

    doi: 10.3389/fimmu.2019.00154

    Figure Lengend Snippet: Passive EAE is less severe in Klrk1 −/− than in wild type recipients. Leukocytes from MOG-immunized C57BL/6 were reactivated in vitro and then adoptively transferred to Klrk1 −/− (black) and wild type ( Klrk1 +/+ ; white) recipients. (A) Mice were followed for clinical score. Mean ± SEM, n = 9–10. 2way ANOVA Klrk1 −/− vs. Klrk1 +/+ day 22–23 * p < 0.05 for all other days from day 12 to the end: * * * p < 0.001. (B) Flow cytometry analysis of ex vivo expanded T lymphocytes from MOG-immunized donor mice. Lymph node cells were collected, labeled with CFSE, and put in culture as described in materials and methods in the absence or presence of MOG 35−55 for 72 h. PMA, ionomycin, brefeldin A and monensin were added for 4 h prior to flow cytometry staining and analysis for intracellular mediators: GM-CSF, IFNγ, IL-17 and Granzyme B (GrB) as indicated. Contour plots illustrate gated events on CD4 or CD8 T cells expanded in vitro in the absence (Nil) or presence of MOG. (C) Representative detection of demyelination using fluoromyelin and DAPI in spinal cord sections from Klrk1 −/− and Klrk1 +/+ mice. White arrows indicate zones of myelin loss. (D) Western blot detection of MULT1 and albumin in CSF from Klrk1 −/− and Klrk1 +/+ mice 50 days after the adoptive transfer of activated lymphocytes. One representative western blot is illustrated and quantification of 55 kDa and 25 kDa forms as relative expression compared to albumin Mean ± SEM n = 7. Statistical differences for relative abundance of MULT1 25kDa form Klrk1 +/+ vs. Klrk1 −/− * * p < 0.01.

    Article Snippet: On day 5, recombinant murine MULT1 protein (10 μg/ml, R&D Systems) was added or not to splenocytes.

    Techniques: In Vitro, Flow Cytometry, Ex Vivo, Labeling, Staining, Western Blot, Adoptive Transfer Assay, Expressing