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microbeads ultrapure  (Miltenyi Biotec)


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    Miltenyi Biotec microbeads ultrapure
    Microbeads Ultrapure, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 98/100, based on 234 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/microbeads ultrapure/product/Miltenyi Biotec
    Average 98 stars, based on 234 article reviews
    microbeads ultrapure - by Bioz Stars, 2026-03
    98/100 stars

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    MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, <t>10058-F4,</t> and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.
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    MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, <t>10058-F4,</t> and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.
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    A) Experimental scheme for B16-OVA transplantation in nude mice followed by RMC-6236 oral gavage (10 mg/kg, daily) ; B) C omparison of tumor size between vehicle and RMC-6236–treated nude mice ; C) Tumor growth curves ; D,E) Flow-cytometry analysis of TAM CD206 (D) and CD86 (E) with vehicle or RMC-6236 ; F) Immunofluorescence showing macrophages <t>(F4/80,</t> green) and MHC-I (red) with DAPI (blue) ; G–I) Flow-cytometry quantification in TAMs of MHC-I (H-2K b ) (G) , OVA-specific presentation (SIINFEKL) (H) , and MHC-II (I-A/I-E) (I); J) Schematic of anti-CSF1R– mediated monocyte/macrophage depletion during RMC-6236 treatment; K) Tumor growth with RMC-6236 plus IgG or anti-CSF1R ; L, M) Intratumoral CD8 + T-cell frequency after monocyte depletion ; N,O) Granzyme B (N) and perforin (O) in tumor CD8 + T-cells. Data are shown as mean ± SEM. *p < 0.05, **p< 0.01, ***p < 0.001 and ****p < 0.0001 using unpaired two-tailed t-tests and Two-way ANOVA followed by Sidak’s multiple comparisons test (n≥6).
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    A) Experimental scheme for B16-OVA transplantation in nude mice followed by RMC-6236 oral gavage (10 mg/kg, daily) ; B) C omparison of tumor size between vehicle and RMC-6236–treated nude mice ; C) Tumor growth curves ; D,E) Flow-cytometry analysis of TAM CD206 (D) and CD86 (E) with vehicle or RMC-6236 ; F) Immunofluorescence showing macrophages <t>(F4/80,</t> green) and MHC-I (red) with DAPI (blue) ; G–I) Flow-cytometry quantification in TAMs of MHC-I (H-2K b ) (G) , OVA-specific presentation (SIINFEKL) (H) , and MHC-II (I-A/I-E) (I); J) Schematic of anti-CSF1R– mediated monocyte/macrophage depletion during RMC-6236 treatment; K) Tumor growth with RMC-6236 plus IgG or anti-CSF1R ; L, M) Intratumoral CD8 + T-cell frequency after monocyte depletion ; N,O) Granzyme B (N) and perforin (O) in tumor CD8 + T-cells. Data are shown as mean ± SEM. *p < 0.05, **p< 0.01, ***p < 0.001 and ****p < 0.0001 using unpaired two-tailed t-tests and Two-way ANOVA followed by Sidak’s multiple comparisons test (n≥6).
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    A) Experimental scheme for B16-OVA transplantation in nude mice followed by RMC-6236 oral gavage (10 mg/kg, daily) ; B) C omparison of tumor size between vehicle and RMC-6236–treated nude mice ; C) Tumor growth curves ; D,E) Flow-cytometry analysis of TAM CD206 (D) and CD86 (E) with vehicle or RMC-6236 ; F) Immunofluorescence showing macrophages <t>(F4/80,</t> green) and MHC-I (red) with DAPI (blue) ; G–I) Flow-cytometry quantification in TAMs of MHC-I (H-2K b ) (G) , OVA-specific presentation (SIINFEKL) (H) , and MHC-II (I-A/I-E) (I); J) Schematic of anti-CSF1R– mediated monocyte/macrophage depletion during RMC-6236 treatment; K) Tumor growth with RMC-6236 plus IgG or anti-CSF1R ; L, M) Intratumoral CD8 + T-cell frequency after monocyte depletion ; N,O) Granzyme B (N) and perforin (O) in tumor CD8 + T-cells. Data are shown as mean ± SEM. *p < 0.05, **p< 0.01, ***p < 0.001 and ****p < 0.0001 using unpaired two-tailed t-tests and Two-way ANOVA followed by Sidak’s multiple comparisons test (n≥6).
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    A) Experimental scheme for B16-OVA transplantation in nude mice followed by RMC-6236 oral gavage (10 mg/kg, daily) ; B) C omparison of tumor size between vehicle and RMC-6236–treated nude mice ; C) Tumor growth curves ; D,E) Flow-cytometry analysis of TAM CD206 (D) and CD86 (E) with vehicle or RMC-6236 ; F) Immunofluorescence showing macrophages <t>(F4/80,</t> green) and MHC-I (red) with DAPI (blue) ; G–I) Flow-cytometry quantification in TAMs of MHC-I (H-2K b ) (G) , OVA-specific presentation (SIINFEKL) (H) , and MHC-II (I-A/I-E) (I); J) Schematic of anti-CSF1R– mediated monocyte/macrophage depletion during RMC-6236 treatment; K) Tumor growth with RMC-6236 plus IgG or anti-CSF1R ; L, M) Intratumoral CD8 + T-cell frequency after monocyte depletion ; N,O) Granzyme B (N) and perforin (O) in tumor CD8 + T-cells. Data are shown as mean ± SEM. *p < 0.05, **p< 0.01, ***p < 0.001 and ****p < 0.0001 using unpaired two-tailed t-tests and Two-way ANOVA followed by Sidak’s multiple comparisons test (n≥6).
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    Image Search Results


    MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, 10058-F4, and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: Combining anti-gene γPNA with small molecules and RNA inhibitors: A strategy to enhance anti-tumor efficacy

    doi: 10.1016/j.omtn.2025.102804

    Figure Lengend Snippet: MYC/MAX inhibitors in combination with anti-transcription γPNA1 Cell viability of (A) U2932 and (B) Raji cells treated with increasing doses of MYC/MAX inhibitors (Myci975, EN4, 10058-F4, and sAJM589) alone and in combination with γPNA1 and ScR-γPNA2 (8 μM) for 72 h. Results are presented as mean ± SEM. The IC 50 (95% CI) values of MYC/MAX inhibitors alone and combination treatment of MYC/MAX with γPNA1 in (C) U2932 and (D) Raji cells. (E) Cell viability of γPNA1-treated U2932 and Raji cells at 8 μM concentration. Western blot analysis representing the change in c-MYC protein 72 h after treatment with γPNA1 and ScR-γPNA2 in combination with (F) Myci975, (G) EN4, (H) 10058-F4, and (I) sAJM589. ∗∗(F–I) Cyclophilin B was used as an endogenous control, and the same blots are presented in A–S7D. c-MYC, EZH2, and cyclophilin B were probed from the same blot. Results are presented as mean ± SEM, p value for one-way ANOVA.

    Article Snippet: Cells were cotreated with 1:2 dilutions of MYC/MAX inhibitors (Myci975 [Selleckchem, #S8906]), EN4 (MedChemExpress, #HY-134761), 10058-F4 (MedChemExpress, #HY-12702), SAJM589 (MedChemExpress, #HY-122683), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. Cells were cotreated with 1:10 dilutions of small molecule inhibitors (JQ1 [MedChemExpress, #HY-13030]), sapanisertid (MedChemExpress, #HY-13328), and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB 231 cells were cotreated with dinaciclid (MedChemExpress, #HY-10492) and γPNA1 and ScR-γPNA2 at 8 μM for 72 h. MDA-MB-231 and HeLa cells were cotreated with c-Myc siRNA (50 nM) and γPNA1 and ScR-γPNA2 for 48 h. At 0 μM concentration, cells were treated only with PBS and not treated with MYC/MAX inhibitors, HDAC inhibitors, small molecule inhibitors, or γPNA1.

    Techniques: Concentration Assay, Western Blot, Control

    A) Experimental scheme for B16-OVA transplantation in nude mice followed by RMC-6236 oral gavage (10 mg/kg, daily) ; B) C omparison of tumor size between vehicle and RMC-6236–treated nude mice ; C) Tumor growth curves ; D,E) Flow-cytometry analysis of TAM CD206 (D) and CD86 (E) with vehicle or RMC-6236 ; F) Immunofluorescence showing macrophages (F4/80, green) and MHC-I (red) with DAPI (blue) ; G–I) Flow-cytometry quantification in TAMs of MHC-I (H-2K b ) (G) , OVA-specific presentation (SIINFEKL) (H) , and MHC-II (I-A/I-E) (I); J) Schematic of anti-CSF1R– mediated monocyte/macrophage depletion during RMC-6236 treatment; K) Tumor growth with RMC-6236 plus IgG or anti-CSF1R ; L, M) Intratumoral CD8 + T-cell frequency after monocyte depletion ; N,O) Granzyme B (N) and perforin (O) in tumor CD8 + T-cells. Data are shown as mean ± SEM. *p < 0.05, **p< 0.01, ***p < 0.001 and ****p < 0.0001 using unpaired two-tailed t-tests and Two-way ANOVA followed by Sidak’s multiple comparisons test (n≥6).

    Journal: bioRxiv

    Article Title: Macrophage Antigen Presentation Is Unleashed by Pan-RAS Inhibition to Promote Antitumor Immunity

    doi: 10.64898/2026.01.30.702886

    Figure Lengend Snippet: A) Experimental scheme for B16-OVA transplantation in nude mice followed by RMC-6236 oral gavage (10 mg/kg, daily) ; B) C omparison of tumor size between vehicle and RMC-6236–treated nude mice ; C) Tumor growth curves ; D,E) Flow-cytometry analysis of TAM CD206 (D) and CD86 (E) with vehicle or RMC-6236 ; F) Immunofluorescence showing macrophages (F4/80, green) and MHC-I (red) with DAPI (blue) ; G–I) Flow-cytometry quantification in TAMs of MHC-I (H-2K b ) (G) , OVA-specific presentation (SIINFEKL) (H) , and MHC-II (I-A/I-E) (I); J) Schematic of anti-CSF1R– mediated monocyte/macrophage depletion during RMC-6236 treatment; K) Tumor growth with RMC-6236 plus IgG or anti-CSF1R ; L, M) Intratumoral CD8 + T-cell frequency after monocyte depletion ; N,O) Granzyme B (N) and perforin (O) in tumor CD8 + T-cells. Data are shown as mean ± SEM. *p < 0.05, **p< 0.01, ***p < 0.001 and ****p < 0.0001 using unpaired two-tailed t-tests and Two-way ANOVA followed by Sidak’s multiple comparisons test (n≥6).

    Article Snippet: Macrophages were purified using anti-mouse F4/80 MicroBeads (Miltenyi Biotec) according to the manufacturer’s protocol.

    Techniques: Transplantation Assay, Flow Cytometry, Immunofluorescence, Two Tailed Test