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ccr5 antagonist tak 779  (TargetMol)


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    TargetMol ccr5 antagonist tak 779
    Ccr5 Antagonist Tak 779, supplied by TargetMol, 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/product/ccr5+antagonist+tak+779/pm41937021-76-29-32?v=TargetMol
    Average 94 stars, based on 1 article reviews
    ccr5 antagonist tak 779 - by Bioz Stars, 2026-08
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    ccr5 antagonist tak 779  (TargetMol)
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    Ccr5 Antagonist Tak 779, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ccr5 receptor antagonist tak-779  (Millipore)
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    Interaction of G3-S16 and G2-NF16 with cellular surface markers. Notes: Activated PBMCs were treated with dendrimers, and levels of CD4, <t>CXCR4,</t> and CCR5 at the cellular surface were followed by flow cytometry. Ratio of iMFI for each surface marker in comparison to nontreated cells is shown (iMFI = % of positive cells × MFI of surface marker). X4 ANTG = CXCR4 antagonist <t>AMD3100;</t> R5 ANTG = CCR5 antagonist TAK779. Both compounds were used as controls (* P <0.05, *** P <0.001 vs control). Data represent the mean ± SD of three independent experiments. Abbreviations: PBMCs, perpipheral blood mononuclear cells; iMFI, integrated mean fluorescence intensity; SD, standard deviation; NT, nontreated.
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    Enhanced stemness of PCa cells upon direct co-culture with MSCs was independent of the <t>CCL5/CCR5</t> pathway. a–c Two different PCa cell lines (PC3, left; LNCaP, right) were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with the CCR5 antagonist Maraviroc (1 uM) for 72 h, the PCa cells were collected in each group and then flow cytometry ( a ), colony formation assay ( b ), and sphere formation assay ( c ) were performed. d PC-3 cells were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with TAK-779 (1 uM) for 72 h, the PC-3 cells were collected in each group and then colony formation (left), and sphere formation assays (right) were carried out. Data are presented as the mean ± SD; *P < 0.05, **P < 0.01; ***P < 0.001
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    Enhanced stemness of PCa cells upon direct co-culture with MSCs was independent of the <t>CCL5/CCR5</t> pathway. a–c Two different PCa cell lines (PC3, left; LNCaP, right) were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with the CCR5 antagonist Maraviroc (1 uM) for 72 h, the PCa cells were collected in each group and then flow cytometry ( a ), colony formation assay ( b ), and sphere formation assay ( c ) were performed. d PC-3 cells were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with TAK-779 (1 uM) for 72 h, the PC-3 cells were collected in each group and then colony formation (left), and sphere formation assays (right) were carried out. Data are presented as the mean ± SD; *P < 0.05, **P < 0.01; ***P < 0.001
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    Enhanced stemness of PCa cells upon direct co-culture with MSCs was independent of the <t>CCL5/CCR5</t> pathway. a–c Two different PCa cell lines (PC3, left; LNCaP, right) were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with the CCR5 antagonist Maraviroc (1 uM) for 72 h, the PCa cells were collected in each group and then flow cytometry ( a ), colony formation assay ( b ), and sphere formation assay ( c ) were performed. d PC-3 cells were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with TAK-779 (1 uM) for 72 h, the PC-3 cells were collected in each group and then colony formation (left), and sphere formation assays (right) were carried out. Data are presented as the mean ± SD; *P < 0.05, **P < 0.01; ***P < 0.001
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    Enhanced stemness of PCa cells upon direct co-culture with MSCs was independent of the <t>CCL5/CCR5</t> pathway. a–c Two different PCa cell lines (PC3, left; LNCaP, right) were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with the CCR5 antagonist Maraviroc (1 uM) for 72 h, the PCa cells were collected in each group and then flow cytometry ( a ), colony formation assay ( b ), and sphere formation assay ( c ) were performed. d PC-3 cells were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with TAK-779 (1 uM) for 72 h, the PC-3 cells were collected in each group and then colony formation (left), and sphere formation assays (right) were carried out. Data are presented as the mean ± SD; *P < 0.05, **P < 0.01; ***P < 0.001
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    Interaction of G3-S16 and G2-NF16 with cellular surface markers. Notes: Activated PBMCs were treated with dendrimers, and levels of CD4, CXCR4, and CCR5 at the cellular surface were followed by flow cytometry. Ratio of iMFI for each surface marker in comparison to nontreated cells is shown (iMFI = % of positive cells × MFI of surface marker). X4 ANTG = CXCR4 antagonist AMD3100; R5 ANTG = CCR5 antagonist TAK779. Both compounds were used as controls (* P <0.05, *** P <0.001 vs control). Data represent the mean ± SD of three independent experiments. Abbreviations: PBMCs, perpipheral blood mononuclear cells; iMFI, integrated mean fluorescence intensity; SD, standard deviation; NT, nontreated.

    Journal: International Journal of Nanomedicine

    Article Title: Antiviral mechanism of polyanionic carbosilane dendrimers against HIV-1

    doi: 10.2147/IJN.S96352

    Figure Lengend Snippet: Interaction of G3-S16 and G2-NF16 with cellular surface markers. Notes: Activated PBMCs were treated with dendrimers, and levels of CD4, CXCR4, and CCR5 at the cellular surface were followed by flow cytometry. Ratio of iMFI for each surface marker in comparison to nontreated cells is shown (iMFI = % of positive cells × MFI of surface marker). X4 ANTG = CXCR4 antagonist AMD3100; R5 ANTG = CCR5 antagonist TAK779. Both compounds were used as controls (* P <0.05, *** P <0.001 vs control). Data represent the mean ± SD of three independent experiments. Abbreviations: PBMCs, perpipheral blood mononuclear cells; iMFI, integrated mean fluorescence intensity; SD, standard deviation; NT, nontreated.

    Article Snippet: Several reagents and ARV were used as controls: zidovudine (AZT; GSK, GlaxoSmithKline plc, London, UK), enfuvirtide (T-20; Hoffman-La Roche Ltd., Basel, Switzerland), atazanavir (ATV; Bristol-Myers Squibb, New York, NY, USA), and raltegravir (RAL; Merck Millipore, Billerica, MA, USA); Suramin, a polyanionic compound that could mimic the function of dendrimers; CXCR4 chemokine receptor antagonist AMD3100, CCR5 receptor antagonist TAK-779, and colchicine, a microtubule polymerization inhibitor (all from Sigma-Aldrich Co., St Louis, MO, USA).

    Techniques: Flow Cytometry, Marker, Fluorescence, Standard Deviation

    Enhanced stemness of PCa cells upon direct co-culture with MSCs was independent of the CCL5/CCR5 pathway. a–c Two different PCa cell lines (PC3, left; LNCaP, right) were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with the CCR5 antagonist Maraviroc (1 uM) for 72 h, the PCa cells were collected in each group and then flow cytometry ( a ), colony formation assay ( b ), and sphere formation assay ( c ) were performed. d PC-3 cells were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with TAK-779 (1 uM) for 72 h, the PC-3 cells were collected in each group and then colony formation (left), and sphere formation assays (right) were carried out. Data are presented as the mean ± SD; *P < 0.05, **P < 0.01; ***P < 0.001

    Journal: Cell & Bioscience

    Article Title: Bone marrow mesenchymal stem cells promote prostate cancer cell stemness via cell–cell contact to activate the Jagged1/Notch1 pathway

    doi: 10.1186/s13578-021-00599-0

    Figure Lengend Snippet: Enhanced stemness of PCa cells upon direct co-culture with MSCs was independent of the CCL5/CCR5 pathway. a–c Two different PCa cell lines (PC3, left; LNCaP, right) were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with the CCR5 antagonist Maraviroc (1 uM) for 72 h, the PCa cells were collected in each group and then flow cytometry ( a ), colony formation assay ( b ), and sphere formation assay ( c ) were performed. d PC-3 cells were employed to establish the mono-culture, transwell-culture, and mixed co-culture with the MSCs system. After treatment with TAK-779 (1 uM) for 72 h, the PC-3 cells were collected in each group and then colony formation (left), and sphere formation assays (right) were carried out. Data are presented as the mean ± SD; *P < 0.05, **P < 0.01; ***P < 0.001

    Article Snippet: An antagonist of CCR5 (Maraviroc) was purchased from Cayman Chemicals (Ann Arbor, Michigan, USA), and another antagonist of CCR5 (TAK-779) was synthesized by Takeda Chemical Industries (Osaka).

    Techniques: Co-Culture Assay, Flow Cytometry, Colony Assay, Tube Formation Assay