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h398  (Hycult Biotech)


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    Structured Review

    Hycult Biotech h398
    Binding activities of ATROSAB and <t> H398. </t>
    H398, supplied by Hycult Biotech, 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/h398/product/Hycult Biotech
    Average 90 stars, based on 1 article reviews
    h398 - by Bioz Stars, 2025-02
    90/100 stars

    Images

    1) Product Images from "Monovalent TNF receptor 1-selective antibody with improved affinity and neutralizing activity"

    Article Title: Monovalent TNF receptor 1-selective antibody with improved affinity and neutralizing activity

    Journal: mAbs

    doi: 10.1080/19420862.2018.1524664

    Binding activities of ATROSAB and  H398.
    Figure Legend Snippet: Binding activities of ATROSAB and H398.

    Techniques Used: Binding Assay, Enzyme-linked Immunosorbent Assay



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    Image Search Results


    Binding activities of ATROSAB and  H398.

    Journal: mAbs

    Article Title: Monovalent TNF receptor 1-selective antibody with improved affinity and neutralizing activity

    doi: 10.1080/19420862.2018.1524664

    Figure Lengend Snippet: Binding activities of ATROSAB and H398.

    Article Snippet: H398 (HM2020SP-b) was purchased from Hycult biotech (Plymouth Meeting, PA, USA).

    Techniques: Binding Assay, Enzyme-linked Immunosorbent Assay

    KEY RESOURCES TABLE

    Journal: Cancer cell

    Article Title: Vitamin B6 addiction in acute myeloid leukemia

    doi: 10.1016/j.ccell.2019.12.002

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Anti-GFP , Hypromatrix , HM2020.

    Techniques: Plasmid Preparation, Recombinant, Mutagenesis, RNA Extraction, Gel Extraction, Clone Assay, Purification, Flow Cytometry, Sequencing, CRISPR, Functional Assay, shRNA, Software

    Expression of transgenic hu/mTNFR1-k/i and hu/mTNFR2-k/i in homozygous mice. Splenocytes or thymocytes were isolated from C57BL/6J wild-type (A and B), hu/mTNFR1-k/i (A), or hu/mTNFR2-k/i (B) mice. Then mouse TNFR1 (HP8002) and human TNFR1 (HP9002) (A) or mouse TNFR2 (HP8003) and human TNFR2 (HP9003) (B) expression was analyzed by flow cytometry using subgates for CD45R+ B cells, CD68+ macrophages (splenocytes), and CD8+ thymocytes. Gray histograms show the isotype controls; black lines indicate signals measured for TNFR1 or TNFR2 expression. Data are presented as normalized to unit area.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Essential protective role of tumor necrosis factor receptor 2 in neurodegeneration

    doi: 10.1073/pnas.1605195113

    Figure Lengend Snippet: Expression of transgenic hu/mTNFR1-k/i and hu/mTNFR2-k/i in homozygous mice. Splenocytes or thymocytes were isolated from C57BL/6J wild-type (A and B), hu/mTNFR1-k/i (A), or hu/mTNFR2-k/i (B) mice. Then mouse TNFR1 (HP8002) and human TNFR1 (HP9002) (A) or mouse TNFR2 (HP8003) and human TNFR2 (HP9003) (B) expression was analyzed by flow cytometry using subgates for CD45R+ B cells, CD68+ macrophages (splenocytes), and CD8+ thymocytes. Gray histograms show the isotype controls; black lines indicate signals measured for TNFR1 or TNFR2 expression. Data are presented as normalized to unit area.

    Article Snippet: Antibodies against mouse (HP8002, HP8003) and human TNFRs (HM2020, HP9002 and HM2023, HP9003) were from Hycult Biotec.

    Techniques: Expressing, Transgenic Assay, Isolation, Flow Cytometry

    Expression of transgenic hu/mTNFR1-k/i and hu/mTNFR2-k/i in primary cells isolated from homozygous mice. Primary MEFs were isolated from wild-type (A and B), hu/mTNFR1-k/i (A), or hu/mTNFR2-k/i (B) C57BL/6 mice. Expression of mouse TNFR1 (HP8002) and human TNFR1 (HP9002) (A) or mouse TNFR2 (HP8003) and human TNFR2 (HP9003) (B) was analyzed by flow cytometry. Data are presented as normalized to unit area. (C and D) Brain tissue isolated from wild-type (C and D), hu/mTNFR1-k/I (C), or hu/mTNFR2-k/i (D) C57BL/6 mice. Tissue was lyzed and expression of huTNFR1 (wild-type, hu/mTNFR1-k/i, H398) or huTNFR2 (wild-type, hu/mTNFR2-k/i, MR2-1) was analyzed by Western blot.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Essential protective role of tumor necrosis factor receptor 2 in neurodegeneration

    doi: 10.1073/pnas.1605195113

    Figure Lengend Snippet: Expression of transgenic hu/mTNFR1-k/i and hu/mTNFR2-k/i in primary cells isolated from homozygous mice. Primary MEFs were isolated from wild-type (A and B), hu/mTNFR1-k/i (A), or hu/mTNFR2-k/i (B) C57BL/6 mice. Expression of mouse TNFR1 (HP8002) and human TNFR1 (HP9002) (A) or mouse TNFR2 (HP8003) and human TNFR2 (HP9003) (B) was analyzed by flow cytometry. Data are presented as normalized to unit area. (C and D) Brain tissue isolated from wild-type (C and D), hu/mTNFR1-k/I (C), or hu/mTNFR2-k/i (D) C57BL/6 mice. Tissue was lyzed and expression of huTNFR1 (wild-type, hu/mTNFR1-k/i, H398) or huTNFR2 (wild-type, hu/mTNFR2-k/i, MR2-1) was analyzed by Western blot.

    Article Snippet: Antibodies against mouse (HP8002, HP8003) and human TNFRs (HM2020, HP9002 and HM2023, HP9003) were from Hycult Biotec.

    Techniques: Expressing, Transgenic Assay, Isolation, Flow Cytometry, Western Blot

    TNF-α accentuates TGF-β1–driven EMT via TNFR1. A: Flow cytometry analysis demonstrates that PBECs express TNFR1 on their cell surface, but express little to no TNFR2. B: Stimulation of PBECs (n = 6) with soluble TNF-α (TNFsol), membrane-bound TNF-α (TNFcys), TNFR1-specific mutant (Cys-TNF32W/86T) membrane-bound TNF (TNFcysR1), or TNFR2-specific mutant (Cys-TNF143N/145R) membrane-bound TNF (TNFcysR2) (all 20 ng/mL) for 72 hours alone has no effect on the expression of E-cadherin, vimentin, or fibronectin. Stimulation, however, with TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, increases pro-MMP-9 secretion. TGF-β1 (10 ng/mL) down-regulates the expression of E-cadherin, increases the expression of vimentin and fibronectin, and increases the secretion of pro-MMP-9. Co-stimulation of the cells with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates the changes in EMT marker expression compared to TGF-β1 alone. C: Co-stimulation of PBECs with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates changes in cell morphology and EMT marker expression compared to TGF-β1 alone. FL1-H, height of fluorescence intensity; FSC-H, height of forward scatter; SSC-H, height of side scatter.

    Journal: The American Journal of Pathology

    Article Title: The Critical Role of TAK1 in Accentuated Epithelial to Mesenchymal Transition in Obliterative Bronchiolitis after Lung Transplantation

    doi: 10.1016/j.ajpath.2012.02.022

    Figure Lengend Snippet: TNF-α accentuates TGF-β1–driven EMT via TNFR1. A: Flow cytometry analysis demonstrates that PBECs express TNFR1 on their cell surface, but express little to no TNFR2. B: Stimulation of PBECs (n = 6) with soluble TNF-α (TNFsol), membrane-bound TNF-α (TNFcys), TNFR1-specific mutant (Cys-TNF32W/86T) membrane-bound TNF (TNFcysR1), or TNFR2-specific mutant (Cys-TNF143N/145R) membrane-bound TNF (TNFcysR2) (all 20 ng/mL) for 72 hours alone has no effect on the expression of E-cadherin, vimentin, or fibronectin. Stimulation, however, with TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, increases pro-MMP-9 secretion. TGF-β1 (10 ng/mL) down-regulates the expression of E-cadherin, increases the expression of vimentin and fibronectin, and increases the secretion of pro-MMP-9. Co-stimulation of the cells with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates the changes in EMT marker expression compared to TGF-β1 alone. C: Co-stimulation of PBECs with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates changes in cell morphology and EMT marker expression compared to TGF-β1 alone. FL1-H, height of fluorescence intensity; FSC-H, height of forward scatter; SSC-H, height of side scatter.

    Article Snippet: TNFR1 (HM2020; Hycult, Uden, The Netherlands) and TNFR2 (HM2007; Hycult) 21 primary antibodies were used to detect receptor expression by flow cytometry.

    Techniques: Flow Cytometry, Mutagenesis, Expressing, Marker, Fluorescence

    TNF-α accentuates TGF-β1–driven EMT via TNFR1. A: Flow cytometry analysis demonstrates that PBECs express TNFR1 on their cell surface, but express little to no TNFR2. B: Stimulation of PBECs (n = 6) with soluble TNF-α (TNFsol), membrane-bound TNF-α (TNFcys), TNFR1-specific mutant (Cys-TNF32W/86T) membrane-bound TNF (TNFcysR1), or TNFR2-specific mutant (Cys-TNF143N/145R) membrane-bound TNF (TNFcysR2) (all 20 ng/mL) for 72 hours alone has no effect on the expression of E-cadherin, vimentin, or fibronectin. Stimulation, however, with TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, increases pro-MMP-9 secretion. TGF-β1 (10 ng/mL) down-regulates the expression of E-cadherin, increases the expression of vimentin and fibronectin, and increases the secretion of pro-MMP-9. Co-stimulation of the cells with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates the changes in EMT marker expression compared to TGF-β1 alone. C: Co-stimulation of PBECs with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates changes in cell morphology and EMT marker expression compared to TGF-β1 alone. FL1-H, height of fluorescence intensity; FSC-H, height of forward scatter; SSC-H, height of side scatter.

    Journal: The American Journal of Pathology

    Article Title: The Critical Role of TAK1 in Accentuated Epithelial to Mesenchymal Transition in Obliterative Bronchiolitis after Lung Transplantation

    doi: 10.1016/j.ajpath.2012.02.022

    Figure Lengend Snippet: TNF-α accentuates TGF-β1–driven EMT via TNFR1. A: Flow cytometry analysis demonstrates that PBECs express TNFR1 on their cell surface, but express little to no TNFR2. B: Stimulation of PBECs (n = 6) with soluble TNF-α (TNFsol), membrane-bound TNF-α (TNFcys), TNFR1-specific mutant (Cys-TNF32W/86T) membrane-bound TNF (TNFcysR1), or TNFR2-specific mutant (Cys-TNF143N/145R) membrane-bound TNF (TNFcysR2) (all 20 ng/mL) for 72 hours alone has no effect on the expression of E-cadherin, vimentin, or fibronectin. Stimulation, however, with TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, increases pro-MMP-9 secretion. TGF-β1 (10 ng/mL) down-regulates the expression of E-cadherin, increases the expression of vimentin and fibronectin, and increases the secretion of pro-MMP-9. Co-stimulation of the cells with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates the changes in EMT marker expression compared to TGF-β1 alone. C: Co-stimulation of PBECs with TGF-β1 and TNFsol, TNFcys, or TNFcysR1, but not TNFcysR2, accentuates changes in cell morphology and EMT marker expression compared to TGF-β1 alone. FL1-H, height of fluorescence intensity; FSC-H, height of forward scatter; SSC-H, height of side scatter.

    Article Snippet: Antibodies TNFR1 (HM2020; Hycult, Uden, The Netherlands) and TNFR2 (HM2007; Hycult) 21 primary antibodies were used to detect receptor expression by flow cytometry.

    Techniques: Flow Cytometry, Mutagenesis, Expressing, Marker, Fluorescence