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elisa plate  (MedChemExpress)


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    MedChemExpress elisa plate
    Elisa Plate, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/elisa plate/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    elisa plate - by Bioz Stars, 2026-06
    94/100 stars

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    Integrity assessment of anti‐hCD38/⍺ECD‐ACE coupled by SA/biotin. (A) Schematic structure of anti‐hCD38/⍺ECD‐ACE coupled by SA/Biotin. Integrity analysis of anti‐hCD38/⍺ECD‐ACE confirmed by: (B ) <t>ELISA</t> via coating <t>with</t> <t>anti‐αECD</t> (D6) and anti‐βECD (B3/2) antibodies and detection with anti‐human IgG and (C) in vitro labeling of 2 × 10 5 hCD38‐D6 cells with 5 µg anti‐hCD38/⍺ECD‐ACE at a final concentration of 50 µg/mL and detection of both components of antibody (anti‐hCD38 and SA) and antigen (⍺ECD and biotin) by flow cytometry. (D) Experimental design to demonstrate the in vivo labeling of hCD38‐B3/2 (GFP + ) cells by intravenous injection of 200 µg anti‐hCD38/⍺ECD‐ACE. (E) Histogram graphs representing the in vivo labeling of cells and detection of antibody and antigen parts in both spleen and bone marrow of hCD38‐B3/2 (GFP + ) transferred into NSG‐Hc 1 mice ( n = 3 per group). anti‐hCD38/⍺ECD‐ACE, anti‐hCD38/⍺ECD‐antibody‐mediated cytotoxicity engager; hCD38‐B3/2, human CD38 transfected into mouse anti‐human AChR βECD secreting B3/2 (GFP + ) hybridoma cells.
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    Image Search Results


    Glyphosate level in serum in study groups (mean±SEM). ECLH: Low-grade and High-grade endometrial cancer (n = 32); ECL: Low-grade endometrial cancer (n = 22); EIN: Endometrial intraepithelial neoplasia (n = 4) and C: control (n = 32). Glyphosateconcentration concentration in serum, measured in ECLH, ECL, EIN and C groups. *ECLH serum level significantly differs from control serum level; GLY serum: ECLH serum 0.1829 ± 0.0272 ng/ml; ECL serum 0.2148 ± 0.0406 ng/ml; EIN serum 0.1938 ± 0.00488 ng/ml and C serum 0.1297 ± 0.0167 ng/ml.

    Journal: Toxicology Reports

    Article Title: Presence of glyphosate in endometrial cancer tissue: A cross-sectional study

    doi: 10.1016/j.toxrep.2026.102255

    Figure Lengend Snippet: Glyphosate level in serum in study groups (mean±SEM). ECLH: Low-grade and High-grade endometrial cancer (n = 32); ECL: Low-grade endometrial cancer (n = 22); EIN: Endometrial intraepithelial neoplasia (n = 4) and C: control (n = 32). Glyphosateconcentration concentration in serum, measured in ECLH, ECL, EIN and C groups. *ECLH serum level significantly differs from control serum level; GLY serum: ECLH serum 0.1829 ± 0.0272 ng/ml; ECL serum 0.2148 ± 0.0406 ng/ml; EIN serum 0.1938 ± 0.00488 ng/ml and C serum 0.1297 ± 0.0167 ng/ml.

    Article Snippet: A commercial kit (ABRAXIS Glyphosate Plate ELISA Kit, PN 500205, Gold Standard Diagnostics, Warminster, US) was used in this study.

    Techniques: Control, Concentration Assay

    Glyphosate level in endometrial tissue in study groups (mean±SEM). ECLH: Low-grade and High-grade endometrial cancer (n = 32); ECL: Low-grade endometrial cancer (n = 22); EIN: Endometrial intraepithelial neoplasia (n = 4) and C: control (n = 32). GlyphosateconcentrationGLY concentration in endometrial tissue, measured in ECLH, ECL, EIN and C groups. We adjusted the mean concentration values for the endometrium by applying a serum density value of 1.025 g/ml as a conversion factor: from pg/ml to pg/g and ng/ml to ng/g. *ECLH endometrium level shows a significant difference from the control serum level; GLY endometrium: ECLH endometrium 0.4174 ± 0.3461 ng/g; ECL endometrium 0.4073 ± 0.04162 ng/g; EIN endometrium 0.3798 ± 0.09556 ng/g and C endometrium 0.318 ± 0.0251 ng/g.

    Journal: Toxicology Reports

    Article Title: Presence of glyphosate in endometrial cancer tissue: A cross-sectional study

    doi: 10.1016/j.toxrep.2026.102255

    Figure Lengend Snippet: Glyphosate level in endometrial tissue in study groups (mean±SEM). ECLH: Low-grade and High-grade endometrial cancer (n = 32); ECL: Low-grade endometrial cancer (n = 22); EIN: Endometrial intraepithelial neoplasia (n = 4) and C: control (n = 32). GlyphosateconcentrationGLY concentration in endometrial tissue, measured in ECLH, ECL, EIN and C groups. We adjusted the mean concentration values for the endometrium by applying a serum density value of 1.025 g/ml as a conversion factor: from pg/ml to pg/g and ng/ml to ng/g. *ECLH endometrium level shows a significant difference from the control serum level; GLY endometrium: ECLH endometrium 0.4174 ± 0.3461 ng/g; ECL endometrium 0.4073 ± 0.04162 ng/g; EIN endometrium 0.3798 ± 0.09556 ng/g and C endometrium 0.318 ± 0.0251 ng/g.

    Article Snippet: A commercial kit (ABRAXIS Glyphosate Plate ELISA Kit, PN 500205, Gold Standard Diagnostics, Warminster, US) was used in this study.

    Techniques: Control, Concentration Assay

    Glyphosate level in serum and endometrial tissue in study groups (mean±SEM). ECLH: Low-grade and High-grade endometrial cancer (n = 32); ECL: Low-grade endometrial cancer (n = 22); and C: control (n = 32). Glyphosateconcentration concentration in endometrial tissue, measured in ECLH, ECL, and C groups. We converted concentration mean values in the case of endometriumendometrium using 1025 g/ml serum density value as a multiplier: pg/ml to pg/g, ng/ml to ng/g. *Endometrium level significantly differs from control serum level in all study groups. P < 0.0001; GLY levels: ECLH serum 0.1829 ± 0.0272 ng/ml; endometrium 0.4174 ± 0.3461 ng/g; ECL serum 0.2148 ± 0.0406 ng/ml; endometrium 0.4073 ± 0.04162 ng/g; and C serum 0.1297 ± 0.0167 ng/ml; endometrium 0.318 ± 0.0251 ng/g.

    Journal: Toxicology Reports

    Article Title: Presence of glyphosate in endometrial cancer tissue: A cross-sectional study

    doi: 10.1016/j.toxrep.2026.102255

    Figure Lengend Snippet: Glyphosate level in serum and endometrial tissue in study groups (mean±SEM). ECLH: Low-grade and High-grade endometrial cancer (n = 32); ECL: Low-grade endometrial cancer (n = 22); and C: control (n = 32). Glyphosateconcentration concentration in endometrial tissue, measured in ECLH, ECL, and C groups. We converted concentration mean values in the case of endometriumendometrium using 1025 g/ml serum density value as a multiplier: pg/ml to pg/g, ng/ml to ng/g. *Endometrium level significantly differs from control serum level in all study groups. P < 0.0001; GLY levels: ECLH serum 0.1829 ± 0.0272 ng/ml; endometrium 0.4174 ± 0.3461 ng/g; ECL serum 0.2148 ± 0.0406 ng/ml; endometrium 0.4073 ± 0.04162 ng/g; and C serum 0.1297 ± 0.0167 ng/ml; endometrium 0.318 ± 0.0251 ng/g.

    Article Snippet: A commercial kit (ABRAXIS Glyphosate Plate ELISA Kit, PN 500205, Gold Standard Diagnostics, Warminster, US) was used in this study.

    Techniques: Control, Concentration Assay

    ELISA quantification of biotinylated α-SFRP1 mAb levels in (A) serum and (B) brain RIPA-soluble homogenates from 4-8 month-old APP/PS1 mice. Samples were collected 6 and 24 h after a single 100 µg intraperitoneal or retro-orbital injection of α-SFRP1. “Pre-Inj.” Indicates mAb levels before the injection (expected to be zero). Data are presented as mean ± SEM. Statistical analyses were performed using (A) two-way ANOVA followed by Sidak’s post hoc test for multiple comparisons or (B) Mann-Whitney test.

    Journal: bioRxiv

    Article Title: Pharmacodynamic and stage-dependent therapeutic efficacy of SFRP1 neutralization in a mouse model of Alzheimer’s disease

    doi: 10.64898/2026.03.26.714543

    Figure Lengend Snippet: ELISA quantification of biotinylated α-SFRP1 mAb levels in (A) serum and (B) brain RIPA-soluble homogenates from 4-8 month-old APP/PS1 mice. Samples were collected 6 and 24 h after a single 100 µg intraperitoneal or retro-orbital injection of α-SFRP1. “Pre-Inj.” Indicates mAb levels before the injection (expected to be zero). Data are presented as mean ± SEM. Statistical analyses were performed using (A) two-way ANOVA followed by Sidak’s post hoc test for multiple comparisons or (B) Mann-Whitney test.

    Article Snippet: The reaction was terminated by adding 2N HCl (100 μl/well), and the resulting product was measured at 450 nm in a microtiter plate ELISA reads FLUOstar OPTIMA (BMG Lab Tech, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Injection, MANN-WHITNEY

    ( A ) Schematic of the experimental design. 4-month-old homozygous APP/PS1 mice received weekly retro-orbital injections of IgG1 or α-SFRP1.10 (100 µg) for 5 months; analyses in panels ( B–G ) were performed at 9 months of age. The time diagram indicates the expected age at which these mice initiate amyloid-β plaque accumulation. Illustration from NIAID NIH BioArt Source ( https://bioart.niaid.nih.gov/ ). ( B ) ELISA quantification of SFRP1 levels in brain RIPA-soluble homogenates. ( C ) Representative confocal images of cortices (top) and hippocampi (bottom) from IgG1-treated (left) and α-SFRP1.10-treated (right) mice stained with Thioflavin S (ThioS) to label amyloid plaque cores. Scale bar: 100 µm. Quantification of the number (top) and mean plaque area (bottom) of ( D ) ThioS+ plaques and ( E ) LAMP1-positive puncta in the cortex (left) and hippocampus (right). Quantification of (F) GFAP and (G) Iba1 fluorescence intensity in the cortex (left) and hippocampus (right), expressed as fold change relative to the mean value of the IgG1 group. Quantification analyses were performed for individual mice, averaging the results of 3-8 slices per mouse. Data are presented as mean ± SEM. Statistical analyses were performed using Student’s t test.

    Journal: bioRxiv

    Article Title: Pharmacodynamic and stage-dependent therapeutic efficacy of SFRP1 neutralization in a mouse model of Alzheimer’s disease

    doi: 10.64898/2026.03.26.714543

    Figure Lengend Snippet: ( A ) Schematic of the experimental design. 4-month-old homozygous APP/PS1 mice received weekly retro-orbital injections of IgG1 or α-SFRP1.10 (100 µg) for 5 months; analyses in panels ( B–G ) were performed at 9 months of age. The time diagram indicates the expected age at which these mice initiate amyloid-β plaque accumulation. Illustration from NIAID NIH BioArt Source ( https://bioart.niaid.nih.gov/ ). ( B ) ELISA quantification of SFRP1 levels in brain RIPA-soluble homogenates. ( C ) Representative confocal images of cortices (top) and hippocampi (bottom) from IgG1-treated (left) and α-SFRP1.10-treated (right) mice stained with Thioflavin S (ThioS) to label amyloid plaque cores. Scale bar: 100 µm. Quantification of the number (top) and mean plaque area (bottom) of ( D ) ThioS+ plaques and ( E ) LAMP1-positive puncta in the cortex (left) and hippocampus (right). Quantification of (F) GFAP and (G) Iba1 fluorescence intensity in the cortex (left) and hippocampus (right), expressed as fold change relative to the mean value of the IgG1 group. Quantification analyses were performed for individual mice, averaging the results of 3-8 slices per mouse. Data are presented as mean ± SEM. Statistical analyses were performed using Student’s t test.

    Article Snippet: The reaction was terminated by adding 2N HCl (100 μl/well), and the resulting product was measured at 450 nm in a microtiter plate ELISA reads FLUOstar OPTIMA (BMG Lab Tech, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Staining, Fluorescence

    ( A ) Schematic of the experimental design. 4-month-old homozygous APP/PS1 mice received weekly retro-orbital injections of IgG1 or α-SFRP1.10 (200 µg) for 2 months; analyses in panels ( B–H ) were performed at 6 months of age. The time diagram indicates the expected age at which these mice initiate amyloid-β plaque accumulation. Illustration from NIAID NIH BioArt Source ( https://bioart.niaid.nih.gov/ ). ( B ) Kaplan–Meier curves showing mouse survival during the treatment period; each vertical step represents a death event. ( C ) ELISA quantification of SFRP1 levels in brain RIPA-soluble homogenates. ( D ) Representative confocal images of cortices (top) and hippocampi (bottom) from IgG1-treated (left) and α-SFRP1.10-treated (right) mice stained with Thioflavin S (ThioS) to label amyloid plaque cores. Scale bar: 100 µm. Quantification of the number (top) and mean plaque area (bottom) of ( E ) ThioS+ plaques and ( F ) LAMP1+ puncta in the cortex (left) and hippocampus (right). Quantification of (G) GFAP and (H) Iba1 fluorescence intensity in the cortex (left) and hippocampus (right), expressed as fold change relative to the mean value of the IgG1 group. Quantification analyses were performed for individual mice, averaging the results of 3-8 slices per mouse. Data are presented as mean ± SEM. Statistical analyses were performed using Student’s t test.

    Journal: bioRxiv

    Article Title: Pharmacodynamic and stage-dependent therapeutic efficacy of SFRP1 neutralization in a mouse model of Alzheimer’s disease

    doi: 10.64898/2026.03.26.714543

    Figure Lengend Snippet: ( A ) Schematic of the experimental design. 4-month-old homozygous APP/PS1 mice received weekly retro-orbital injections of IgG1 or α-SFRP1.10 (200 µg) for 2 months; analyses in panels ( B–H ) were performed at 6 months of age. The time diagram indicates the expected age at which these mice initiate amyloid-β plaque accumulation. Illustration from NIAID NIH BioArt Source ( https://bioart.niaid.nih.gov/ ). ( B ) Kaplan–Meier curves showing mouse survival during the treatment period; each vertical step represents a death event. ( C ) ELISA quantification of SFRP1 levels in brain RIPA-soluble homogenates. ( D ) Representative confocal images of cortices (top) and hippocampi (bottom) from IgG1-treated (left) and α-SFRP1.10-treated (right) mice stained with Thioflavin S (ThioS) to label amyloid plaque cores. Scale bar: 100 µm. Quantification of the number (top) and mean plaque area (bottom) of ( E ) ThioS+ plaques and ( F ) LAMP1+ puncta in the cortex (left) and hippocampus (right). Quantification of (G) GFAP and (H) Iba1 fluorescence intensity in the cortex (left) and hippocampus (right), expressed as fold change relative to the mean value of the IgG1 group. Quantification analyses were performed for individual mice, averaging the results of 3-8 slices per mouse. Data are presented as mean ± SEM. Statistical analyses were performed using Student’s t test.

    Article Snippet: The reaction was terminated by adding 2N HCl (100 μl/well), and the resulting product was measured at 450 nm in a microtiter plate ELISA reads FLUOstar OPTIMA (BMG Lab Tech, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Staining, Fluorescence

    ( A ) Schematic of the experimental design. 8-month-old heterozygous APP/PS1 mice received weekly retro-orbital injections of WAY-316606 (1 µM) or vehicle (2% DMSO) for 2 months; analyses in panels ( B–D ) were performed at 10 months of age. The time diagram indicates the expected age at which these mice initiate amyloid-β plaque accumulation. Illustration from NIAID NIH BioArt Source ( https://bioart.niaid.nih.gov/ ). ( B ) ELISA quantification of SFRP1 levels in brain RIPA-soluble homogenates. ( C ) Representative confocal images of cortices (top) and hippocampi (bottom) from vehicle-treated (left), WAY-316606-treated (center) mice stained with ThioS to label amyloid plaque cores. Scale bar: 100 µm. Quantification of number (top) and mean plaque area (bottom) of ( D ) ThioS+ plaque and LAMP1+ puncta ( E ) in the cortex (left) and hippocampus (right). Quantification analyses were performed for individual mice, averaging the results of 3-8 slices per mouse. Data are presented as mean ± SEM. Statistical analyses were performed using Student’s t test.

    Journal: bioRxiv

    Article Title: Pharmacodynamic and stage-dependent therapeutic efficacy of SFRP1 neutralization in a mouse model of Alzheimer’s disease

    doi: 10.64898/2026.03.26.714543

    Figure Lengend Snippet: ( A ) Schematic of the experimental design. 8-month-old heterozygous APP/PS1 mice received weekly retro-orbital injections of WAY-316606 (1 µM) or vehicle (2% DMSO) for 2 months; analyses in panels ( B–D ) were performed at 10 months of age. The time diagram indicates the expected age at which these mice initiate amyloid-β plaque accumulation. Illustration from NIAID NIH BioArt Source ( https://bioart.niaid.nih.gov/ ). ( B ) ELISA quantification of SFRP1 levels in brain RIPA-soluble homogenates. ( C ) Representative confocal images of cortices (top) and hippocampi (bottom) from vehicle-treated (left), WAY-316606-treated (center) mice stained with ThioS to label amyloid plaque cores. Scale bar: 100 µm. Quantification of number (top) and mean plaque area (bottom) of ( D ) ThioS+ plaque and LAMP1+ puncta ( E ) in the cortex (left) and hippocampus (right). Quantification analyses were performed for individual mice, averaging the results of 3-8 slices per mouse. Data are presented as mean ± SEM. Statistical analyses were performed using Student’s t test.

    Article Snippet: The reaction was terminated by adding 2N HCl (100 μl/well), and the resulting product was measured at 450 nm in a microtiter plate ELISA reads FLUOstar OPTIMA (BMG Lab Tech, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Staining

    Integrity assessment of anti‐hCD38/⍺ECD‐ACE coupled by SA/biotin. (A) Schematic structure of anti‐hCD38/⍺ECD‐ACE coupled by SA/Biotin. Integrity analysis of anti‐hCD38/⍺ECD‐ACE confirmed by: (B ) ELISA via coating with anti‐αECD (D6) and anti‐βECD (B3/2) antibodies and detection with anti‐human IgG and (C) in vitro labeling of 2 × 10 5 hCD38‐D6 cells with 5 µg anti‐hCD38/⍺ECD‐ACE at a final concentration of 50 µg/mL and detection of both components of antibody (anti‐hCD38 and SA) and antigen (⍺ECD and biotin) by flow cytometry. (D) Experimental design to demonstrate the in vivo labeling of hCD38‐B3/2 (GFP + ) cells by intravenous injection of 200 µg anti‐hCD38/⍺ECD‐ACE. (E) Histogram graphs representing the in vivo labeling of cells and detection of antibody and antigen parts in both spleen and bone marrow of hCD38‐B3/2 (GFP + ) transferred into NSG‐Hc 1 mice ( n = 3 per group). anti‐hCD38/⍺ECD‐ACE, anti‐hCD38/⍺ECD‐antibody‐mediated cytotoxicity engager; hCD38‐B3/2, human CD38 transfected into mouse anti‐human AChR βECD secreting B3/2 (GFP + ) hybridoma cells.

    Journal: European Journal of Immunology

    Article Title: Selective Depletion of Autoreactive Plasma Cells as a Novel Strategy to Treat Acetylcholine Receptor Antibody‐Positive Myasthenia Gravis

    doi: 10.1002/eji.70166

    Figure Lengend Snippet: Integrity assessment of anti‐hCD38/⍺ECD‐ACE coupled by SA/biotin. (A) Schematic structure of anti‐hCD38/⍺ECD‐ACE coupled by SA/Biotin. Integrity analysis of anti‐hCD38/⍺ECD‐ACE confirmed by: (B ) ELISA via coating with anti‐αECD (D6) and anti‐βECD (B3/2) antibodies and detection with anti‐human IgG and (C) in vitro labeling of 2 × 10 5 hCD38‐D6 cells with 5 µg anti‐hCD38/⍺ECD‐ACE at a final concentration of 50 µg/mL and detection of both components of antibody (anti‐hCD38 and SA) and antigen (⍺ECD and biotin) by flow cytometry. (D) Experimental design to demonstrate the in vivo labeling of hCD38‐B3/2 (GFP + ) cells by intravenous injection of 200 µg anti‐hCD38/⍺ECD‐ACE. (E) Histogram graphs representing the in vivo labeling of cells and detection of antibody and antigen parts in both spleen and bone marrow of hCD38‐B3/2 (GFP + ) transferred into NSG‐Hc 1 mice ( n = 3 per group). anti‐hCD38/⍺ECD‐ACE, anti‐hCD38/⍺ECD‐antibody‐mediated cytotoxicity engager; hCD38‐B3/2, human CD38 transfected into mouse anti‐human AChR βECD secreting B3/2 (GFP + ) hybridoma cells.

    Article Snippet: ELISA plates (Sarstedt) were coated with mouse‐anti‐hAChR αECD (5 μg/mL; clone D6, DRFZ) or mouse‐anti‐hAChR βECD (5 μg/mL; clone B3/2, DRFZ), blocked with PBS/3% BSA, and incubated with the sample for 2 h at 37°C.

    Techniques: Enzyme-linked Immunosorbent Assay, In Vitro, Labeling, Concentration Assay, Flow Cytometry, In Vivo, Injection, Transfection