Notes: Antisense fluorophore octaarginine peptide nucleic acid (PNA) conjugates are investigated cellular activity using a photochemical internalization (PCI) drug delivery method. PCI utilizes light to generate reactive oxygen species that can damage the endosomal membrane and lead to drug release. Specifically, cellular localization and antisense activity was monitored for two conjugates, tetramethylrhodamine and Alexa Fluor 555. Luminescence and cell viability were measured using the Bright-Glo™ Assay and CellTiter-Glo® Assay, respectively. (5172)

Notes: The authors investigated the role of the liver kinase B1 (LKB1)-adenosine monophosphate-activated kinase (AMPK) signaling pathway in cancer cell survival and metabolic adaptation. The CellTiter-Glo® 2.0, ROS-Glo™ and CellTiter® 96 AQueous One Solution Assays were used to monitor ATP content, reactive oxygen species and cell proliferation in LKB1 and AMPK knockdown cells. Additionally, the pGL3 Vector and Dual-Luciferase® Assay System were used to monitor matrix metalloproteinase-9 (MMP-9) promoter activity. (5162)

Notes: miR-195 overexpression is shown to repress non-small cell lung cancer (NSCLC) tumor growth through a high-throughput screen using the CellTiter-Glo® Assay. To determine miR-195 targets, regulatory regions of prospective targets were cloned into a luciferase fusion construct and monitored using the Dual-Glo® Luciferase Assay System. miRNA was shown to regulate cyclin D3 and survivin, leading the regulation of cell cycle arrest and apoptosis. (5171)

Notes: Coiled-coil-helix-coiled-coil-helix domain-containing 10 (CHCHD10) protein mutations are associated with multiple neurodegenerative diseases. Here, the cellular role of CHCHD10 in oxidative phosphorylation in the nucleus and mitochondria is investigated. CHCHD10 is shown to be a regulator of genes containing the oxygen response element (ORE) using the Dual-Luciferase® Reporter Assay. Interestingly, two disease variants are shown to lead to reduced respiration and increased reactive oxygen species (ROS). (5090)

Notes: DUX4 is dysregulated in Facioscapulohumeral dystrophy (FSHD) leading to cellular apoptosis and disease. The genes and pathways involved in DUX4-mediated apoptosis are uncharacterized. Here, an siRNA screen to identify involved components is performed, and cell survival was measured using CellTiter-Glo. A counter screen to identify false positives which inhibited DUX4 induction by doxycycline was done using the ONE-Glo EX Luciferase Assay System. (5135)

Notes: Cell viability results were used to evaluate the effectiveness of agents against schwannoma and meningioma cell systems. (5028)

Notes: In this study, the CellTiter-Glo® 2.0 Assay was used to determine viability after treatment of cells with various compounds, and the GSH/GSSG-Glo™ Assay used to measure glutathione levels. The pGL3 Vectors and Dual-Luciferase® Assay were used in Reporter Assays. (5006)

Notes: These authors investigated Gas6-mediated Axl signaling in Clear Cell Renal Cell Carcinoma (CCRCC), a cancer that is associated with development of chemoresistance and recurrence. They report that Axl signaling was enhanced in the presence of Sunitinib, possibly contributing to acquired chemoresistance. As part of the study the CellTox™ Green and CellTiter-Glo® 2.0 Assays were used to assess late apoptosis and cell viability, respectively. (5037)

Notes: Both A549 and H460 cells were treated with the glutaminase inhibitor, BPTES. ATP content or viability was reduced about 30% in A549 cells and 60% in H460 cells. A549 and H460 cell ATP levels were mostly recovered by co-treatment with GSHE, a bioavailable form of glutathione. Despite a 60% decrease in ATP, H460 cells only demonstrated 5% cytotoxicity and A549 cells about 2.5% cytotoxicity. Co-treatment with GSHE reduced cytotoxicity to at or near background—no treatment levels. ATP content was assessed with the CellTiter-Glo® 2.0 Assay, and cytotoxicity was judged with the CellTox™ Green Cytotoxicity Assay. (4710)

Notes: The BRD9 subunit of the SWI-SNF chromatin-remodeling complex is investigated in the context of aberrant cell proliferation in acute myeloid leukemia. Specifically, the NanoBRET system was used to measure the interactions of BRD9 and Histone H3.3. A small molecule inhibitor of the BRB9 bromodomain function, BI-7273, was further assessed in HEK293T cells. Disruption of BRB9 interaction with Histone H3.3 was confirmed at sub-micromolar concentrations of BI-7273. Cell viability in the presence of inhibitor was determined using the CellTiter-Glo System. (5079)

Notes: The authors demonstrated that CellTiter-Glo® Cell Viability Assay could be used for anthelminthic drug discovery.  The pilot study identified hits previously reported to have some anti-parasite activity.  To demonstrate that the CellTiter-Glo® Reagent was able to penetrate the schistosomula, the reagent was mixed with the CellTox™ Green Cytotoxicity Assay and visualized by fluorescent confocal microscopy.  (4648)

Notes: Imaging oxygen in neural cell and tissue models by means of anionic cell-permeable phosphorescent nanoparticles. aCell permeable phosphorescent nanoparticle probes designed to enable the study of cell and tissue oxygenation were assessed for cytotoxicity in monolayer culture and rat brain slices.  The probe demonstrated no significant cytotoxicity on cultured PC12, mouse endothelial fibroblasts, primary cortical or cerebellar granule neurons in concentrations and exposure time tested as judged with the CellTiter-Glo® Cell Viability Assay.  Rat brain slices (400µm) were incubated with and without the nano probes and cytotoxicity visualized by fluorescent microscopy following 3 hour incubation with 0.05% CellTox™ Green Dye.  The probe had no effect on cell viability in the 3 to 24 hour time frame.  (4645)

Notes: PC12 cells were plated and deprived of oxygen and glucose for 5-7 hours. Parallel samples were assessed for viability with the CellTiter-Glo® Cell Viability Assay and cytotoxicity with CellTox™ Green Cytotoxicity Assay (end-point method).  Deprived cells were also analyzed by RT-PCR following RNA extraction with the SV Total RNA Isolation System and converted to cDNA with the ImProm-II™ Reverse Transcriptase in the presence of RNasin® Ribonuclease Inhibitor and PCR performed with the PCR Master Mix for a limited number of cycles.  (4647)