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antibodies against cd71  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibodies against cd71
    Antibodies Against Cd71, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 180 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against cd71/product/Cell Signaling Technology Inc
    Average 96 stars, based on 180 article reviews
    antibodies against cd71 - by Bioz Stars, 2026-03
    96/100 stars

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    Cell Signaling Technology Inc antibody against cd71
    Erastin induces the accumulation of CD63-related MVBs in resistant OVCA cells. (A) Western blot analysis of FtH, FPN, <t>CD71</t> and CD63 in OVCA cells upon administration of 8 μM erastin. GAPDH serves as loading control. (B) Representative images of morphological and ultrastructural features detected by TEM in HEY, COV318 and PEO4 cells treated with or without 8 μM erastin. Yellow arrows, multivescicular body (MVB); blue arrows, damaged mitochondria. All the experiments were carried out in triplicate.
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    Cell Signaling Technology Inc anti tfr1 antibody
    ROR1 CAR-T and RSL3 cooperatively induce tumor cell ferroptosis via PC-PUFA2. ( A ) Lipidomic profiles of NCI-H1299 cells treated with control, CAR-T, RSL3, and combination treatments ( n = 5). ( B ) Structure of PC-PUFA2. ( C ) NCI-H1299 and patient-1 cells were co-treated with 50 µM PC-PUFA2 with or without 10 µM Fer-1 for 24 h. 50 µM palmitoleic acid was added as a control lipid. CellTiter-Glo reagent was added to the culture, and the viability of tumor cells was subsequently assessed by measuring luminescence ( n = 3). Data are presented as the mean ± SEM. ( D – E ) Lipid peroxidation detected by C11-BODIPY 581/591 staining in NCI-H1299 and patient-1 cells treated with 50 µM PC-PUFA2 with or without 10 µM Fer-1 for 4 h. Relative mean fluorescence intensity (MFI) of oxidized C11-BODIPY 581/591 plotted as the mean ± SEM ( n = 3). ( F – G ) Immunofluorescence of <t>TfR1</t> expression in NCI-H1299 cells treated with vehicle, 10 µM Fer-1, or 50 µM PC (22:6_22:6) with or without 10 µM Fer-1 for 4 h. Scale bars, 10 μm. Relative intensity of TfR1 membrane staining compared with vehicle is plotted as the mean ± SEM ( n = 10). Statistical significance: n.s. ( p > 0.05); * p < 0.05; ** p < 0.01; **** p < 0.0001
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    Image Search Results


    Erastin induces the accumulation of CD63-related MVBs in resistant OVCA cells. (A) Western blot analysis of FtH, FPN, CD71 and CD63 in OVCA cells upon administration of 8 μM erastin. GAPDH serves as loading control. (B) Representative images of morphological and ultrastructural features detected by TEM in HEY, COV318 and PEO4 cells treated with or without 8 μM erastin. Yellow arrows, multivescicular body (MVB); blue arrows, damaged mitochondria. All the experiments were carried out in triplicate.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Expulsion of iron-rich ferritin via CD63-mediated exosome drives ferroptosis resistance in ovarian cancer cells

    doi: 10.3389/fcell.2025.1532097

    Figure Lengend Snippet: Erastin induces the accumulation of CD63-related MVBs in resistant OVCA cells. (A) Western blot analysis of FtH, FPN, CD71 and CD63 in OVCA cells upon administration of 8 μM erastin. GAPDH serves as loading control. (B) Representative images of morphological and ultrastructural features detected by TEM in HEY, COV318 and PEO4 cells treated with or without 8 μM erastin. Yellow arrows, multivescicular body (MVB); blue arrows, damaged mitochondria. All the experiments were carried out in triplicate.

    Article Snippet: The antibody against FtH (1:200, sc-376594) was purchased from Santa Cruz Biotechnology (Cruz Biotechnology, Dallas, Texas, United States); antibodies against CD63 (1:1000, ab231975), FPN (1:500, ab235166), Prominin2 (PROM2) (1:500, ab74977), were purchased from Abcam (Abcam, Cambridge, United Kingdom), while antibody against CD71 (1:1,000, #13208) was obtained from Cell Signaling Technology (Danvers, Massachusetts, United States).

    Techniques: Western Blot, Control

    ROR1 CAR-T and RSL3 cooperatively induce tumor cell ferroptosis via PC-PUFA2. ( A ) Lipidomic profiles of NCI-H1299 cells treated with control, CAR-T, RSL3, and combination treatments ( n = 5). ( B ) Structure of PC-PUFA2. ( C ) NCI-H1299 and patient-1 cells were co-treated with 50 µM PC-PUFA2 with or without 10 µM Fer-1 for 24 h. 50 µM palmitoleic acid was added as a control lipid. CellTiter-Glo reagent was added to the culture, and the viability of tumor cells was subsequently assessed by measuring luminescence ( n = 3). Data are presented as the mean ± SEM. ( D – E ) Lipid peroxidation detected by C11-BODIPY 581/591 staining in NCI-H1299 and patient-1 cells treated with 50 µM PC-PUFA2 with or without 10 µM Fer-1 for 4 h. Relative mean fluorescence intensity (MFI) of oxidized C11-BODIPY 581/591 plotted as the mean ± SEM ( n = 3). ( F – G ) Immunofluorescence of TfR1 expression in NCI-H1299 cells treated with vehicle, 10 µM Fer-1, or 50 µM PC (22:6_22:6) with or without 10 µM Fer-1 for 4 h. Scale bars, 10 μm. Relative intensity of TfR1 membrane staining compared with vehicle is plotted as the mean ± SEM ( n = 10). Statistical significance: n.s. ( p > 0.05); * p < 0.05; ** p < 0.01; **** p < 0.0001

    Journal: Biomarker Research

    Article Title: ROR1 CAR-T cells and ferroptosis inducers orchestrate tumor ferroptosis via PC-PUFA2

    doi: 10.1186/s40364-025-00730-0

    Figure Lengend Snippet: ROR1 CAR-T and RSL3 cooperatively induce tumor cell ferroptosis via PC-PUFA2. ( A ) Lipidomic profiles of NCI-H1299 cells treated with control, CAR-T, RSL3, and combination treatments ( n = 5). ( B ) Structure of PC-PUFA2. ( C ) NCI-H1299 and patient-1 cells were co-treated with 50 µM PC-PUFA2 with or without 10 µM Fer-1 for 24 h. 50 µM palmitoleic acid was added as a control lipid. CellTiter-Glo reagent was added to the culture, and the viability of tumor cells was subsequently assessed by measuring luminescence ( n = 3). Data are presented as the mean ± SEM. ( D – E ) Lipid peroxidation detected by C11-BODIPY 581/591 staining in NCI-H1299 and patient-1 cells treated with 50 µM PC-PUFA2 with or without 10 µM Fer-1 for 4 h. Relative mean fluorescence intensity (MFI) of oxidized C11-BODIPY 581/591 plotted as the mean ± SEM ( n = 3). ( F – G ) Immunofluorescence of TfR1 expression in NCI-H1299 cells treated with vehicle, 10 µM Fer-1, or 50 µM PC (22:6_22:6) with or without 10 µM Fer-1 for 4 h. Scale bars, 10 μm. Relative intensity of TfR1 membrane staining compared with vehicle is plotted as the mean ± SEM ( n = 10). Statistical significance: n.s. ( p > 0.05); * p < 0.05; ** p < 0.01; **** p < 0.0001

    Article Snippet: Cells were treated with 100 μΜ PC-PUFA2 for 6 h. Cells were then fixed with 4% paraformaldehyde for 20 min, blocked using 10% normal goat serum for 1 h, and stained with an anti-TfR1 antibody (CST, 13113T) at 1:100 dilution overnight.

    Techniques: Control, Staining, Fluorescence, Immunofluorescence, Expressing, Membrane