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mouse anti human antibody  (R&D Systems)


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    Structured Review

    R&D Systems mouse anti human antibody
    Mouse Anti Human Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse anti human antibody/product/R&D Systems
    Average 93 stars, based on 24 article reviews
    mouse anti human antibody - by Bioz Stars, 2026-02
    93/100 stars

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    Fig. 1. Working scheme of tracking EMT-like phenotype switching during MAPKi therapy. (A) Melanoma cells undergo EMT-like phenotype switching in response to MAPKi therapy and secret EVs into blood circulation. (B) Serum EVs are captured by <t>anti-MCSP</t> and anti-MCAM antibodies immobilized on an electrode and subsequently labeled with SERS nanotags against EMT-associated biomarkers N-cadherin, E-cadherin, THBS1 and ABCB5 under the applied ac-EHD field. (C) EV phenotypes are characterized by SERS mapping. Under the laser excitation, SERS nanotags with MBA, TFMBA, DTNB, and MPY molecules generate characteristic peaks at 1075, 1375, 1335, and 1005 cm−1, respectively. The false-color SERS spectral images are established based on the characteristic Raman signals of four SERS nanotags, indicating the expression of four biomarkers (N-cadherin-MBA, red; E-cadherin-TFMBA, blue; THBS1-DTNB, green; ABCB5-MPY, yellow). The expression levels of four target biomarkers are determined by calculating the average signal spectra of false-color SERS spectral images. (D) EMT-associated EV phenotypic evolution in response to MAPKi treatment.
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    Fig. 1. Working scheme of tracking EMT-like phenotype switching during MAPKi therapy. (A) Melanoma cells undergo EMT-like phenotype switching in response to MAPKi therapy and secret EVs into blood circulation. (B) Serum EVs are captured by <t>anti-MCSP</t> and anti-MCAM antibodies immobilized on an electrode and subsequently labeled with SERS nanotags against EMT-associated biomarkers N-cadherin, E-cadherin, THBS1 and ABCB5 under the applied ac-EHD field. (C) EV phenotypes are characterized by SERS mapping. Under the laser excitation, SERS nanotags with MBA, TFMBA, DTNB, and MPY molecules generate characteristic peaks at 1075, 1375, 1335, and 1005 cm−1, respectively. The false-color SERS spectral images are established based on the characteristic Raman signals of four SERS nanotags, indicating the expression of four biomarkers (N-cadherin-MBA, red; E-cadherin-TFMBA, blue; THBS1-DTNB, green; ABCB5-MPY, yellow). The expression levels of four target biomarkers are determined by calculating the average signal spectra of false-color SERS spectral images. (D) EMT-associated EV phenotypic evolution in response to MAPKi treatment.
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    Culture and identification of hOPCs. The transplanted cells were identified based on their morphology and main markers. (A) Identification of the bright field morphology of hOPCs. Scale bar is 200 μm, inset 100 μm. (B) Flow cytometry to detect PDGFR-α, A2B5, <t>NG2,</t> and Ki67 of hOPCs. (C) Tissue immunofluorescence staining to detect PDGFR-α, A2B5, NG2, and Ki67 of transplanted hOPCs. Scale bar is 100 μm. A2B5, ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1; hOPCs, human–derived oligodendrocyte precursor cells; PDGFR-α, platelet-derived growth factor receptor alpha; NG2, chondroitin sulfate proteoglycan 4.
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    Culture and identification of hOPCs. The transplanted cells were identified based on their morphology and main markers. (A) Identification of the bright field morphology of hOPCs. Scale bar is 200 μm, inset 100 μm. (B) Flow cytometry to detect PDGFR-α, A2B5, <t>NG2,</t> and Ki67 of hOPCs. (C) Tissue immunofluorescence staining to detect PDGFR-α, A2B5, NG2, and Ki67 of transplanted hOPCs. Scale bar is 100 μm. A2B5, ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1; hOPCs, human–derived oligodendrocyte precursor cells; PDGFR-α, platelet-derived growth factor receptor alpha; NG2, chondroitin sulfate proteoglycan 4.
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    R&D Systems monoclonal mouse apc conjugated anti ng2
    Culture and identification of hOPCs. The transplanted cells were identified based on their morphology and main markers. (A) Identification of the bright field morphology of hOPCs. Scale bar is 200 μm, inset 100 μm. (B) Flow cytometry to detect PDGFR-α, A2B5, <t>NG2,</t> and Ki67 of hOPCs. (C) Tissue immunofluorescence staining to detect PDGFR-α, A2B5, NG2, and Ki67 of transplanted hOPCs. Scale bar is 100 μm. A2B5, ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1; hOPCs, human–derived oligodendrocyte precursor cells; PDGFR-α, platelet-derived growth factor receptor alpha; NG2, chondroitin sulfate proteoglycan 4.
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    Image Search Results


    Fig. 1. Working scheme of tracking EMT-like phenotype switching during MAPKi therapy. (A) Melanoma cells undergo EMT-like phenotype switching in response to MAPKi therapy and secret EVs into blood circulation. (B) Serum EVs are captured by anti-MCSP and anti-MCAM antibodies immobilized on an electrode and subsequently labeled with SERS nanotags against EMT-associated biomarkers N-cadherin, E-cadherin, THBS1 and ABCB5 under the applied ac-EHD field. (C) EV phenotypes are characterized by SERS mapping. Under the laser excitation, SERS nanotags with MBA, TFMBA, DTNB, and MPY molecules generate characteristic peaks at 1075, 1375, 1335, and 1005 cm−1, respectively. The false-color SERS spectral images are established based on the characteristic Raman signals of four SERS nanotags, indicating the expression of four biomarkers (N-cadherin-MBA, red; E-cadherin-TFMBA, blue; THBS1-DTNB, green; ABCB5-MPY, yellow). The expression levels of four target biomarkers are determined by calculating the average signal spectra of false-color SERS spectral images. (D) EMT-associated EV phenotypic evolution in response to MAPKi treatment.

    Journal: Biosensors & bioelectronics

    Article Title: Tracking the EMT-like phenotype switching during targeted therapy in melanoma by analyzing extracellular vesicle phenotypes.

    doi: 10.1016/j.bios.2023.115819

    Figure Lengend Snippet: Fig. 1. Working scheme of tracking EMT-like phenotype switching during MAPKi therapy. (A) Melanoma cells undergo EMT-like phenotype switching in response to MAPKi therapy and secret EVs into blood circulation. (B) Serum EVs are captured by anti-MCSP and anti-MCAM antibodies immobilized on an electrode and subsequently labeled with SERS nanotags against EMT-associated biomarkers N-cadherin, E-cadherin, THBS1 and ABCB5 under the applied ac-EHD field. (C) EV phenotypes are characterized by SERS mapping. Under the laser excitation, SERS nanotags with MBA, TFMBA, DTNB, and MPY molecules generate characteristic peaks at 1075, 1375, 1335, and 1005 cm−1, respectively. The false-color SERS spectral images are established based on the characteristic Raman signals of four SERS nanotags, indicating the expression of four biomarkers (N-cadherin-MBA, red; E-cadherin-TFMBA, blue; THBS1-DTNB, green; ABCB5-MPY, yellow). The expression levels of four target biomarkers are determined by calculating the average signal spectra of false-color SERS spectral images. (D) EMT-associated EV phenotypic evolution in response to MAPKi treatment.

    Article Snippet: The primary antibodies were mouse anti-human MCSP (R&D Systems, MAB2585) and MCAM (R&D Systems, MAB932) antibodies.

    Techniques: Labeling, Expressing

    Fig. 3. Specificity of the SERS-based microfluidic biosensor. Representative SERS false-color spectral images and average SERS intensities of EVs derived from SK-MEL-28 (high expression of MCSP and MCAM) and MCF7 (low expression of MCSP and MCAM) cell lines, and control experiments including (++) PBS, (-+) without capture antibodies and (+-) with nontarget IgG antibody on SERS nanotags. EV biomarkers are represented by red (N-cadherin), blue (E-cadherin), green (THBS1) and yellow (ABCB5). Average SERS intensities were generated at 1075 cm−1 (N-cadherin), 1375 cm−1 (E-cadherin), 1335 cm−1 (THBS1), and 1005 cm−1

    Journal: Biosensors & bioelectronics

    Article Title: Tracking the EMT-like phenotype switching during targeted therapy in melanoma by analyzing extracellular vesicle phenotypes.

    doi: 10.1016/j.bios.2023.115819

    Figure Lengend Snippet: Fig. 3. Specificity of the SERS-based microfluidic biosensor. Representative SERS false-color spectral images and average SERS intensities of EVs derived from SK-MEL-28 (high expression of MCSP and MCAM) and MCF7 (low expression of MCSP and MCAM) cell lines, and control experiments including (++) PBS, (-+) without capture antibodies and (+-) with nontarget IgG antibody on SERS nanotags. EV biomarkers are represented by red (N-cadherin), blue (E-cadherin), green (THBS1) and yellow (ABCB5). Average SERS intensities were generated at 1075 cm−1 (N-cadherin), 1375 cm−1 (E-cadherin), 1335 cm−1 (THBS1), and 1005 cm−1

    Article Snippet: The primary antibodies were mouse anti-human MCSP (R&D Systems, MAB2585) and MCAM (R&D Systems, MAB932) antibodies.

    Techniques: Derivative Assay, Expressing, Control, Generated

    Fig. 2. Characterization of EVs derived from melanoma (SK-MEL-28) and breast cancer (MCF7) cell lines. (A) The expression of canonical tetraspanin CD63 and (B) size distributions of SK-MEL-28 and MCF7 EVs using nanoflow cytometry. (C) The expression of melanoma-specific biomarkers MCSP and MCAM on SK-MEL- 28 and MCF7 EVs, measured by western blot.

    Journal: Biosensors & bioelectronics

    Article Title: Tracking the EMT-like phenotype switching during targeted therapy in melanoma by analyzing extracellular vesicle phenotypes.

    doi: 10.1016/j.bios.2023.115819

    Figure Lengend Snippet: Fig. 2. Characterization of EVs derived from melanoma (SK-MEL-28) and breast cancer (MCF7) cell lines. (A) The expression of canonical tetraspanin CD63 and (B) size distributions of SK-MEL-28 and MCF7 EVs using nanoflow cytometry. (C) The expression of melanoma-specific biomarkers MCSP and MCAM on SK-MEL- 28 and MCF7 EVs, measured by western blot.

    Article Snippet: The primary antibodies were mouse anti-human MCSP (R&D Systems, MAB2585) and MCAM (R&D Systems, MAB932) antibodies.

    Techniques: Derivative Assay, Expressing, Cytometry, Western Blot

    Culture and identification of hOPCs. The transplanted cells were identified based on their morphology and main markers. (A) Identification of the bright field morphology of hOPCs. Scale bar is 200 μm, inset 100 μm. (B) Flow cytometry to detect PDGFR-α, A2B5, NG2, and Ki67 of hOPCs. (C) Tissue immunofluorescence staining to detect PDGFR-α, A2B5, NG2, and Ki67 of transplanted hOPCs. Scale bar is 100 μm. A2B5, ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1; hOPCs, human–derived oligodendrocyte precursor cells; PDGFR-α, platelet-derived growth factor receptor alpha; NG2, chondroitin sulfate proteoglycan 4.

    Journal: Stem Cells and Development

    Article Title: Study on the Safety of Human Oligodendrocyte Precursor Cell Transplantation in Young Animals and Its Efficacy on Myelination

    doi: 10.1089/scd.2021.0012

    Figure Lengend Snippet: Culture and identification of hOPCs. The transplanted cells were identified based on their morphology and main markers. (A) Identification of the bright field morphology of hOPCs. Scale bar is 200 μm, inset 100 μm. (B) Flow cytometry to detect PDGFR-α, A2B5, NG2, and Ki67 of hOPCs. (C) Tissue immunofluorescence staining to detect PDGFR-α, A2B5, NG2, and Ki67 of transplanted hOPCs. Scale bar is 100 μm. A2B5, ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 1; hOPCs, human–derived oligodendrocyte precursor cells; PDGFR-α, platelet-derived growth factor receptor alpha; NG2, chondroitin sulfate proteoglycan 4.

    Article Snippet: HOPCs were surface stained with PDGFR-α BV421 mouse anti-human (Cat. #562799; BD Biosciences, Franklin Lake, NJ), A2B5 PE mouse anti-human (Cat. #130-093-581; Miltenyi Biotec, Bergisch-Gladbach, Germany), NG2 APC mouse anti-human (Cat. #FAB2585A; R&D Systems, Minnesota), and Ki67 PE mouse anti-human (Cat. # ab270650; Abcam, Cambridge, UK) antibodies for flow cytometry (FACSanto II; BD Biosciences).

    Techniques: Flow Cytometry, Immunofluorescence, Staining, Derivative Assay