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enzyme linked immunosorbent assay elisa kit  (R&D Systems)


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    R&D Systems enzyme linked immunosorbent assay elisa kit
    Enzyme Linked Immunosorbent Assay Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 157 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/enzyme linked immunosorbent assay elisa kit/product/R&D Systems
    Average 96 stars, based on 157 article reviews
    enzyme linked immunosorbent assay elisa kit - by Bioz Stars, 2026-06
    96/100 stars

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    G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered <t>CXCL10</t> production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.
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    ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, <t>CXCL10,</t> IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.
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    Image Search Results


    G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered CXCL10 production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.

    Journal: Cell Reports Medicine

    Article Title: Histone methyl-transferase G9a inhibition boosts the efficacy of immune checkpoint inhibitors in experimental hepatocellular carcinoma

    doi: 10.1016/j.xcrm.2026.102717

    Figure Lengend Snippet: G9a inhibition potentiates the immunogenic effects of IFN-γ in HCC cells (A) Effect of CM272 and EZM8266 on IFN-γ-triggered CXCL10 production in murine (PM299L) and human (HuH7) HCC cells. Cells were treated with CM272 for 48 h or with CM272 for 24 h and then with IFN-γ (75 U/mL) for another 24 h or with IFN-γ alone for 24 h. PM299L were treated with 400 nM, and HuH7 received 1 μM of CM272 ( n = 3). For EZM8266, cells were pretreated for 48 h with EZM8266 (5 mM) and then with IFN-γ (75 U/mL) for another 24 h, as indicated. CXCL10 protein levels were measured by ELISA in cells’ conditioned media ( n = 3). (B) Effect of G9a inhibition with CM272 or EZM8266 on the expression of MHC class I complex protein (MHC-I) on the surface of PM299L cells. Cells were treated with IFN-γ and CM272 or EZM8266 as indicated in (A), and MHC-I levels were determined by FACS analysis ( n = 3). (C) ChIP analyses of H3K9me2 levels in the proximal promoter regions of CXCL10 and HLA-A genes in HuH7 cells treated with IFN-γ (75 U/mL) and CM272 (400 nM), as indicated in (A) ( n = 3). (D) Evaluation of the expression of transposable elements (TEs) and endogenous retroviral sequences (ERVs) by RNA-seq in NM53 murine HCC cells treated with IFN-γ, CM272, and their combination as indicated in (A). (E) Immunofluorescence analyses of dsRNA in PM299L HCC cells treated with CM272 (24 h) or EZM8266 (48 h). Representative images are shown. Scale bars, 10 μm. Right panel shows a control without primary antibody ( n = 3). Data are represented as mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. All the replicates represent biological replicates.

    Article Snippet: CXCL9 and CXCL10 concentrations were measured in culture supernatants collected at the end of the incubation periods using commercial ELISA kits for mouse CXCL9 (DY492) and CXCL10 (DY466), both from R&D Systems, and an ELISA kit for human CXCL10 (550926) from BD Biosciences (Franklin Lanes, NJ, USA).

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Expressing, Retroviral, RNA Sequencing, Immunofluorescence, Control

    ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.

    Journal: Science Advances

    Article Title: Sympathetic nerve aggravates autoimmune skin disease via NE–adrenergic receptor axis: Neuroimmune cross-talk insights from vitiligo

    doi: 10.1126/sciadv.aea7017

    Figure Lengend Snippet: ( A and B ) Flow cytometry and statistical analysis of CD8 + CD45 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( C and D ) Flow cytometry and statistical analysis of IFN-γ + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( E and F ) Flow cytometry and statistical analysis of Granzyme B + CD8 + T cells in the mouse tail epidermis and dermis of vehicle, 6-OHDA, and 6-OHDA + NE groups ( n =3 per group). ( G ) The secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in the tail skin of mice in the vehicle, 6-OHDA, and 6-OHDA + NE groups were detected by ELISA ( n =4 per group). All vehicle mice were only treated with 0.1% ascorbic acid in 0.9% sterile NaCl. Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001.

    Article Snippet: ELISA analysis on serum samples, skin samples, and cell culture supernatants were performed using the NE ELISA Kit (E-EL-0047c, Elabscience, Wuhan, China), Human CXCL9 ELISA Kit (EHC114.96, Neobioscience Technology Co, Ltd., China), Human CXCL10 ELISA Kit (EHC157.96, Neobioscience Technology Co, Ltd., China), Human IL-6 ELISA Kit (EHC007.96, Neobioscience Technology Co, Ltd., China), Human IL-15 ELISA Kit (EHC013.96, Neobioscience Technology Co, Ltd., China), Mouse CXCL9 ELISA Kit (E-EL-M3077, Elabscience, Wuhan, China), Mouse CXCL10 ELISA Kit (E-EL-M0021, Elabscience, Wuhan, China), Mouse IL-6 ELISA Kit (EMC004.96, Neobioscience Technology Co, Ltd., China), and Mouse IL-15 ELISA Kit (EMC126.96, Neobioscience Technology Co, Ltd., China) following the manufacturer’s instructions.

    Techniques: Flow Cytometry, Enzyme-linked Immunosorbent Assay, Sterility

    ( A ) Volcano plots illustrated the expression of adrenergic receptors on fibroblasts in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRA2A expression on fibroblasts in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of fibroblasts, ADRA2A, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRA2A (red) expression in BJ cells after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells were detected by ELISA with treatment with aposcopolamine (Apos) or NE ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells with ADRA2A siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Journal: Science Advances

    Article Title: Sympathetic nerve aggravates autoimmune skin disease via NE–adrenergic receptor axis: Neuroimmune cross-talk insights from vitiligo

    doi: 10.1126/sciadv.aea7017

    Figure Lengend Snippet: ( A ) Volcano plots illustrated the expression of adrenergic receptors on fibroblasts in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRA2A expression on fibroblasts in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of fibroblasts, ADRA2A, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRA2A (red) expression in BJ cells after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells were detected by ELISA with treatment with aposcopolamine (Apos) or NE ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in BJ cells with ADRA2A siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Article Snippet: ELISA analysis on serum samples, skin samples, and cell culture supernatants were performed using the NE ELISA Kit (E-EL-0047c, Elabscience, Wuhan, China), Human CXCL9 ELISA Kit (EHC114.96, Neobioscience Technology Co, Ltd., China), Human CXCL10 ELISA Kit (EHC157.96, Neobioscience Technology Co, Ltd., China), Human IL-6 ELISA Kit (EHC007.96, Neobioscience Technology Co, Ltd., China), Human IL-15 ELISA Kit (EHC013.96, Neobioscience Technology Co, Ltd., China), Mouse CXCL9 ELISA Kit (E-EL-M3077, Elabscience, Wuhan, China), Mouse CXCL10 ELISA Kit (E-EL-M0021, Elabscience, Wuhan, China), Mouse IL-6 ELISA Kit (EMC004.96, Neobioscience Technology Co, Ltd., China), and Mouse IL-15 ELISA Kit (EMC126.96, Neobioscience Technology Co, Ltd., China) following the manufacturer’s instructions.

    Techniques: Expressing, Immunofluorescence, Control, Staining, Enzyme-linked Immunosorbent Assay

    ( A ) Volcano plots illustrated the expression of adrenergic receptors on keratinocytes in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRB2 expression on keratinocytes in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of keratinocytes, ADRB2, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRB2 (red) expression in keratinocytes after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes were detected by ELISA with treatment with NE or ICI ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes with ADRB2 siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Journal: Science Advances

    Article Title: Sympathetic nerve aggravates autoimmune skin disease via NE–adrenergic receptor axis: Neuroimmune cross-talk insights from vitiligo

    doi: 10.1126/sciadv.aea7017

    Figure Lengend Snippet: ( A ) Volcano plots illustrated the expression of adrenergic receptors on keratinocytes in human skin, including ADRA1A, ADRA1B, ADRA1D, ADRA2A, ADRA2B, ADRA2C, ADRB1, ADRB2, and ADRB3. ( B ) Bubble map illustrated the up-regulation of ADRB2 expression on keratinocytes in the lesional skin of patients with vitiligo and the normal skin of healthy controls. ( C ) Representative immunofluorescence images of keratinocytes, ADRB2, CXCL9, CXCL10, and CD8 + T cells from the normal skin of the healthy control and the lesional skin of the patient with vitiligo ( n =3 per group). Nuclei were counterstained with DAPI (blue). Scale bars, 50 μm. ( D ) Immunofluorescence analysis of ADRB2 (red) expression in keratinocytes after treatment with 5 μM NE for 48 hours. Cell nuclei were stained with DAPI (blue). Scale bar, 50 μm. ( E ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes were detected by ELISA with treatment with NE or ICI ( n =3 per group). ( F ) Secretion levels of CXCL9, CXCL10, IL-6, and IL-15 in keratinocytes with ADRB2 siRNA or control siRNA were detected by ELISA ( n =3 per group). Error bars represent mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, not significant.

    Article Snippet: ELISA analysis on serum samples, skin samples, and cell culture supernatants were performed using the NE ELISA Kit (E-EL-0047c, Elabscience, Wuhan, China), Human CXCL9 ELISA Kit (EHC114.96, Neobioscience Technology Co, Ltd., China), Human CXCL10 ELISA Kit (EHC157.96, Neobioscience Technology Co, Ltd., China), Human IL-6 ELISA Kit (EHC007.96, Neobioscience Technology Co, Ltd., China), Human IL-15 ELISA Kit (EHC013.96, Neobioscience Technology Co, Ltd., China), Mouse CXCL9 ELISA Kit (E-EL-M3077, Elabscience, Wuhan, China), Mouse CXCL10 ELISA Kit (E-EL-M0021, Elabscience, Wuhan, China), Mouse IL-6 ELISA Kit (EMC004.96, Neobioscience Technology Co, Ltd., China), and Mouse IL-15 ELISA Kit (EMC126.96, Neobioscience Technology Co, Ltd., China) following the manufacturer’s instructions.

    Techniques: Expressing, Immunofluorescence, Control, Staining, Enzyme-linked Immunosorbent Assay