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ATCC
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Santa Cruz Biotechnology
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AcceGen Biotechnology
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Japan SLC inc
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JCRB Cell Bank
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Verlag GmbH
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Image Search Results
Journal: iScience
Article Title: RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia
doi: 10.1016/j.isci.2023.106795
Figure Lengend Snippet: RUNX1-KD is associated with a genome-wide reduction in H3K27ac (A) Experimental strategy of NOTCH1 inhibition (NOTCH1-INB) and RUNX1 knockdown (RUNX1-KD). NSC means non-silencing control and GSI means gamma secretase inhibitor. The number of replicates is indicated in brackets. (B) Anti-RUNX1 Western blot of protein levels following knockdown by shRUNX1-58 and shRUNX1-59. Numbers below the RUNX1 panel indicate their relative expression level after normalization to β-actin loading control. (C) Growth competition assays showing the fraction of GFP+ cells following transduction with GFP-tagged lentiviruses expressing shRUNX1s and normalized to a scrambled shRNA control (RUNX1-CTL). (D) Normalized read densities of H3K27ac and H3K4me1 peaks following RUNX1-KD (red ≥ 2-fold loss; black ≥2-fold gain; and gray unchanged). Read densities were normalized by sequencing depth. (E) Mean RUNX1 ChIP-seq read densities at gained, lost, and stable H3K27ac regions following RUNX1-KD. RUNX1 ChIP-seq data was derived from CUTLL1 and p values were calculated using KS-test. (F) Western blot of histone H3, H3K27ac, and H3K4me1 levels in control (RUNX1-WT) and RUNX1-KOs (KO1 and KO2) using two CRISPR guides in KOPTK1. (G) Ratio of H3K27ac and H3K4me1 relative to the H3 control was quantified from the protein bands shown in (F). Three independent experiments were performed to calculate p values using unpaired two-tailed t-test where ∗ indicates p value ≤ 0.05 and ∗∗ for p value ≤ 0.01. Data are mean ± s.e.m. of H3K27ac/H3. (H) Western blot analysis of K3K27ac and RUNX1 in control (RUNX1-WT) and RUNX1-KOs (KO1 and KO2) in Jurkat, HL60, and DU145 cell lines. Where shown, percent reduction was calculated by comparing control (RUNX1-WT) to the knockout samples.
Article Snippet: Prostate adenocarcinoma ,
Techniques: Genome Wide, Inhibition, Knockdown, Control, Western Blot, Expressing, Transduction, shRNA, Sequencing, ChIP-sequencing, Derivative Assay, CRISPR, Two Tailed Test, Knock-Out
Journal: iScience
Article Title: RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia
doi: 10.1016/j.isci.2023.106795
Figure Lengend Snippet:
Article Snippet: Prostate adenocarcinoma ,
Techniques: Recombinant, Expressing, Plasmid Preparation, Software
Journal: Pharmacological research
Article Title: A selective alpha1D-adrenoreceptor antagonist inhibits human prostate cancer cell proliferation and motility "in vitro".
doi: 10.1016/j.phrs.2015.11.017
Figure Lengend Snippet: Figure 4: Cell cycle analysis and p27 and p21 levels in PC3 and DU145 cells exposed to A175.
Article Snippet: Human androgen independent prostate cancer PC3 and
Techniques: Cell Cycle Assay
Journal: Pharmacological research
Article Title: A selective alpha1D-adrenoreceptor antagonist inhibits human prostate cancer cell proliferation and motility "in vitro".
doi: 10.1016/j.phrs.2015.11.017
Figure Lengend Snippet: Figure 5: Effect of A175 on PC3 and DU145 cell motility.
Article Snippet: Human androgen independent prostate cancer PC3 and
Techniques:
Journal: Oncotarget
Article Title: Development of an orally-administrative MELK-targeting inhibitor that suppresses the growth of various types of human cancer
doi:
Figure Lengend Snippet: The graphs indicate growth inhibition curves of OTSSP167 for various types of human cancel cell line; (A) A549 (lung cancer), (B) T47D (breast cancer), (C) DU4475 (breast cancer), and (D) 22Rv1 (prostate cancer) cells, in which MELK is highly expressed, as well as (E) HT1197 (bladder cancer) cell line, in which MELK expression is hardly detectable.
Article Snippet:
Techniques: Inhibition, Expressing
Journal: Oncotarget
Article Title: Development of an orally-administrative MELK-targeting inhibitor that suppresses the growth of various types of human cancer
doi:
Figure Lengend Snippet: Nude mice bearing (A,B) MDA-MB-231 (triple-negative breast cancer), (C,D) A549 (lung cancer), (E) DU145 (prostate cancer), or (F) MIAPaCa-2 (pancreatic cancer) were treated with either vehicle control or OTSSP167 of given concentrations for 14 days. The administration doses were (A) 20 mg/kg intravenously once every two days or (B) 10 mg/kg orally once a day for MDA-MB-231; (C) 1, 5, or 10 mg/kg intravenously once a day or (D) 5 or 10 mg/kg orally once a day for A549; (E) 10 mg/kg orally once a day for DU145; and (F) 10 mg/kg orally once a day for MIAPaCa-2. Mean tumor volumes ± SD (n = 6 for each treatment group) are shown. (G) Lysates of tumor samples taken from A549 and PC-14 xenograft mice were immunoblotted with anti-MELK and anti-ACTB antibodies. (H) OTSSP167 was administered to nude mice bearing PC-14 (MELK-negative bladder cancer cells) at a dose of 10 mg/kg orally once a day. Mean tumor volumes ± SD (n = 3 per group) are shown. i.v. q.2d; intravenously once every two days, i.v. q.d.; intravenously once a day, p.o. q.d.; orally once a day.
Article Snippet:
Techniques: