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stem cell signaling compound library  (Selleck Chemicals)


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    Selleck Chemicals stem cell signaling compound library
    Stem Cell Signaling Compound Library, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/stem+cell+signaling+compound+library/pm41714622-259-7-12?v=Selleck+Chemicals
    Average 92 stars, based on 4 article reviews
    stem cell signaling compound library - by Bioz Stars, 2026-07
    92/100 stars

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    Selleck Chemicals kinase inhibitors
    Kinase inhibitor screening. MLS 402–91 cells were treated with 70 kinase <t>inhibitors</t> (10 µM) and compared to treatment controls (DMSO) and untreated cells. Cells from four wells using four different 96-well plates were analyzed. A Cell proliferation. The DMSO control was arbitrarily set to a value of zero. Mean ± SD is shown, n = 4. B FUS-DDIT3 and FUS mRNA expressions. The DMSO controls were arbitrarily set to a value of zero. FUS-DDIT3 (left) and FUS (right) expressions are shown pairwise for each inhibitor. Data for inhibitors 1 to 7 were excluded due to massive cell death. Mean ± SD is shown, n = 4. C FUS-DDIT3 and FUS protein expressions. The DMSO controls were arbitrarily set to a value of zero. FUS-DDIT3 (left) and FUS (right) expressions are shown pairwise for each inhibitor. Data for inhibitors 1 to 7 were excluded due to massive cell death. Mean ± SD is shown, n = 4
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    Kinase inhibitor screening. MLS 402–91 cells were treated with 70 kinase inhibitors (10 µM) and compared to treatment controls (DMSO) and untreated cells. Cells from four wells using four different 96-well plates were analyzed. A Cell proliferation. The DMSO control was arbitrarily set to a value of zero. Mean ± SD is shown, n = 4. B FUS-DDIT3 and FUS mRNA expressions. The DMSO controls were arbitrarily set to a value of zero. FUS-DDIT3 (left) and FUS (right) expressions are shown pairwise for each inhibitor. Data for inhibitors 1 to 7 were excluded due to massive cell death. Mean ± SD is shown, n = 4. C FUS-DDIT3 and FUS protein expressions. The DMSO controls were arbitrarily set to a value of zero. FUS-DDIT3 (left) and FUS (right) expressions are shown pairwise for each inhibitor. Data for inhibitors 1 to 7 were excluded due to massive cell death. Mean ± SD is shown, n = 4

    Journal: Laboratory Investigation; a Journal of Technical Methods and Pathology

    Article Title: Identification of inhibitors regulating cell proliferation and FUS-DDIT3 expression in myxoid liposarcoma using combined DNA, mRNA, and protein analyses

    doi: 10.1038/s41374-018-0046-3

    Figure Lengend Snippet: Kinase inhibitor screening. MLS 402–91 cells were treated with 70 kinase inhibitors (10 µM) and compared to treatment controls (DMSO) and untreated cells. Cells from four wells using four different 96-well plates were analyzed. A Cell proliferation. The DMSO control was arbitrarily set to a value of zero. Mean ± SD is shown, n = 4. B FUS-DDIT3 and FUS mRNA expressions. The DMSO controls were arbitrarily set to a value of zero. FUS-DDIT3 (left) and FUS (right) expressions are shown pairwise for each inhibitor. Data for inhibitors 1 to 7 were excluded due to massive cell death. Mean ± SD is shown, n = 4. C FUS-DDIT3 and FUS protein expressions. The DMSO controls were arbitrarily set to a value of zero. FUS-DDIT3 (left) and FUS (right) expressions are shown pairwise for each inhibitor. Data for inhibitors 1 to 7 were excluded due to massive cell death. Mean ± SD is shown, n = 4

    Article Snippet: To identify signaling pathways that regulate cell proliferation and FUS-DDIT3 regulation, a library of kinase inhibitors targeting stem cell signaling was applied (#L2100, Selleck chemical).

    Techniques: Control

    Kinase inhibitor validation. MLS 402–91, 2645–94 and 1765–92 cells were treated with 12 kinase inhibitors (2.5 µM) and compared to treatment controls (DMSO). Cells from three wells on the same 96-well plate were analyzed in three to four independent cell culturing experiments. A Cell proliferation. The DMSO control was arbitrarily set to a value of zero. Different gDNA assays were used for each MLS cell line based on the NormFinder algorithm (Supplementary Table ). Mean ± SEM is shown, n = 3–4. B FUS-DDIT3 and FUS mRNA expressions. The DMSO controls were arbitrarily set to a value of zero. Mean ± SEM is shown, n = 3–4. C FUS-DDIT3 and FUS protein expressions. The DMSO controls were arbitrarily set to a value of zero. Note that FUS alone cannot be quantified with our PLA in MLS 1765–92. Mean ± SEM is shown, n = 3–4

    Journal: Laboratory Investigation; a Journal of Technical Methods and Pathology

    Article Title: Identification of inhibitors regulating cell proliferation and FUS-DDIT3 expression in myxoid liposarcoma using combined DNA, mRNA, and protein analyses

    doi: 10.1038/s41374-018-0046-3

    Figure Lengend Snippet: Kinase inhibitor validation. MLS 402–91, 2645–94 and 1765–92 cells were treated with 12 kinase inhibitors (2.5 µM) and compared to treatment controls (DMSO). Cells from three wells on the same 96-well plate were analyzed in three to four independent cell culturing experiments. A Cell proliferation. The DMSO control was arbitrarily set to a value of zero. Different gDNA assays were used for each MLS cell line based on the NormFinder algorithm (Supplementary Table ). Mean ± SEM is shown, n = 3–4. B FUS-DDIT3 and FUS mRNA expressions. The DMSO controls were arbitrarily set to a value of zero. Mean ± SEM is shown, n = 3–4. C FUS-DDIT3 and FUS protein expressions. The DMSO controls were arbitrarily set to a value of zero. Note that FUS alone cannot be quantified with our PLA in MLS 1765–92. Mean ± SEM is shown, n = 3–4

    Article Snippet: To identify signaling pathways that regulate cell proliferation and FUS-DDIT3 regulation, a library of kinase inhibitors targeting stem cell signaling was applied (#L2100, Selleck chemical).

    Techniques: Biomarker Discovery, Cell Culture, Control