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3154001b  (fluidigm)


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    fluidigm 3154001b
    3154001b, supplied by fluidigm, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/3154001b/Anti-Human+CD45+(HI30)-154Sm/pm41916320-679-188-186
    Average 94 stars, based on 7 article reviews
    3154001b - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Recombinase Polymerase Amplification:

    Article Title: High-fat diet causes rapid loss of intestinal group 3 innate lymphoid cells through microbiota-driven inflammation and mitochondrial stress.
    Article Snippet: Article High-fat diet causes rapid loss of intestinal group 3 innate lymphoid cells through microbiota-driven inflammation and mitochondrial stress

    other:

    Article Title: HLA-DR cancer cells expression correlates with T cell infiltration and is enriched in lung adenocarcinoma with indolent behavior
    Article Snippet: CD45 , 154-Sm , Surface , HI30 , Fluidigm , 3154001B.

    Article Title: Unsupervised machine learning reveals risk stratifying glioblastoma tumor cells
    Article Snippet: Antibody , Anti-CD45 (mouse-monoclonal) , Fluidigm , RRID: AB_2810854 Cat# 3154001B Clone: HI30 , MC (1:400).

    Article Title: Mass Cytometry Assessment of Cell Phenotypes and Signaling States in Human Whole Blood
    Article Snippet: 154 Sm , CD45 , HI30 , Fluidigm 3154001B.




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    Image Search Results


    Fig. 5. MDM2/XPO1 inhibition leaves alive p21high/Ki-67low AML cells and triple inhibition of MDM2, XPO1 and BCL2 exhibits superior anti-leukemia effects in Ven-R AML cells. (A) Uniform manifold approximation and projection (UMAP) data of target protein levels determined in OCI-AML3 cells with indicated treatments (160 nM of Mil and/or Sel, 48 hours). Top: Two major populations of live (left) and dead (right) cells under each treatment condition. Bottom: Protein levels on a color scale with residual AML cells after Mil + Sel highlighted in connected red rectangles. (B) Schematic of the in vivo PDX AML model. (C) Percentages of live human AML cell numbers in PB specimens from mice treated with the indicated drugs. (D) OS of mice with indicated treatments (N = 8, 8, 8, 5, 7, 7, 8, and 8 for vehicle, Ven, Mil, Sel, Mil + Sel, Mil + Ven, Sel + Ven. and Mil + Sel + Ven groups, respectively). (E) Murine platelet counts in PB specimens in each treatment group at week of 7. (F) Murine CD45+ cell numbers in PB specimens collected from indicated treatment groups over the entire treatment courses (N = 6). Data represent means ± SEM values in (C), (E), and (F). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: Science advances

    Article Title: Enhanced TP53 reactivation disrupts MYC transcriptional program and overcomes venetoclax resistance in acute myeloid leukemias.

    doi: 10.1126/sciadv.adh1436

    Figure Lengend Snippet: Fig. 5. MDM2/XPO1 inhibition leaves alive p21high/Ki-67low AML cells and triple inhibition of MDM2, XPO1 and BCL2 exhibits superior anti-leukemia effects in Ven-R AML cells. (A) Uniform manifold approximation and projection (UMAP) data of target protein levels determined in OCI-AML3 cells with indicated treatments (160 nM of Mil and/or Sel, 48 hours). Top: Two major populations of live (left) and dead (right) cells under each treatment condition. Bottom: Protein levels on a color scale with residual AML cells after Mil + Sel highlighted in connected red rectangles. (B) Schematic of the in vivo PDX AML model. (C) Percentages of live human AML cell numbers in PB specimens from mice treated with the indicated drugs. (D) OS of mice with indicated treatments (N = 8, 8, 8, 5, 7, 7, 8, and 8 for vehicle, Ven, Mil, Sel, Mil + Sel, Mil + Ven, Sel + Ven. and Mil + Sel + Ven groups, respectively). (E) Murine platelet counts in PB specimens in each treatment group at week of 7. (F) Murine CD45+ cell numbers in PB specimens collected from indicated treatment groups over the entire treatment courses (N = 6). Data represent means ± SEM values in (C), (E), and (F). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: We used the following antibodies: BCL-XL (141 Pr, clone 54H6; CST, 2764BF), cleaved caspase-3 (142 Nd, clone D3E9;Standard BioTools, 3142004A), BCL2 (144 Nd, clone 100; BioLegend, 658702), CD123 (145 Nd, clone 7G3; BD Biosciences, 554527), CD34 (148 Nd, clone 581; BD Biosciences, 555820); LC3B (150 Nd, clone D11; CST 3868 custom), p21 (153 Eu, 12D1; CST 2947BF), CD45 (154 Sm, clone HI30; Standard BioTools 3154001B), CD33 (158 Gd, clone WM53; Standard BioTools, 3158001B), ATF4 (160 Gd, polyclonal; ProteinTech 10835-1-AP), p53 (165 Ho, clone 184721; R&D, MAB1355), CD44 (166 Er, clone BJ18; Standard BioTools, 3166001B), CD38 (168 Er, HIT2; BioLegend, 303502), CXCR4 (172 Yb, clone 12G5; BioLegend, 306502), BAX (173 Yb, clone 2D2; BioLegend, 633602), Ki-67 (175 Lu, clone Ki-67; BioLegend, 350502), and MCL1 (176 Yb, clone D2W9E; CST, 94296BF).

    Techniques: Inhibition, In Vivo