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Luminescent cell viability assay

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The Luminescent Cell Viability Assay is a laboratory tool that measures the number of viable cells in a sample. It uses a luminescent signal to quantify the metabolic activity of cells, providing an indication of cell health and proliferation.

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Lab products found in correlation

Glomax multi detection system, by Promega (3 mentions) Baf3 cells, by American Type Culture Collection (1 mentions) Prism 5, by GraphPad (1 mentions) Prism 9, by GraphPad (1 mentions) Mojosort mouse neutrophil isolation kit, by BioLegend (1 mentions) Human holo transferrin, by Merck Group (1 mentions) Vivoglo luciferin, by Promega (1 mentions) Cyanine5 amine cy5, by Lumiprobe (1 mentions) Milli q advantage a10 water purification system, by Merck Group (1 mentions) Triethylamine tea, by Merck Group (1 mentions) Hydrofluoric acid, by Avantor (1 mentions) Sulforhodamine b, by Merck Group (1 mentions) Envision multilabel reader, by PerkinElmer (1 mentions) Infinite m1000 pro, by Tecan (1 mentions) Celltiter glo, by Promega (1 mentions) 96 well opaque culture plate, by BD (1 mentions) Glomax 96 microplate luminometer, by Promega (1 mentions) Synergy h1, by Agilent Technologies (1 mentions) Caspase glo 3 7 assay, by Promega (1 mentions) Xcelligence rtca s16, by Agilent Technologies (1 mentions)

Close spelling variants of this product

Luminescent assays (2 citations) CellTiter-Glo Luminescent Cell Viability Assays kit (2 citations)

18 protocols using luminescent cell viability assay

1

ERK1/2-deficient Jak2V617F cell proliferation

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Ba/F3 cells (ATCC) stably expressing Jak2V617F along with erythropoietin receptor (EPOR) were cultured in RPMI1640/10%FCS, supplemented with 10 U/ml EPO if expressing Jak2WT. ERK1/2-deficient Jak2V617F cells were generated by transducing ERK1/2-specific shRNA in pLKO-Tet-On vector, puromycin selection and doxycycline induction (Supplementary Table 2). Proliferation was assessed upon ERK1/2 knockdown and/or exposure to inhibitors for 48 h using Cell viability luminescent assay (Promega). Experiments were repeated independently three times. IC50 was determined with Prism 9.0.
Brkic S., Stivala S., Santopolo A., Szybinski J., Jungius S., Passweg J.R., Tsakiris D., Dirnhofer S., Hutter G., Leonards K., Lischer H.E., Dettmer M.S., Neel B.G., Levine R.L, & Meyer S.C. (2021). Dual targeting of JAK2 and ERK interferes with the myeloproliferative neoplasm clone and enhances therapeutic efficacy. Leukemia, 35(10), 2875-2884.
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2

Assessing Anti-Proliferative Inhibitor Effects

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To assess anti-proliferative effects of inhibitors, all cell lines were cultured at 10.000 cells/200 μl with increasing inhibitor concentrations in triplicate. Proliferation was assessed at 48 hr using the Cell viability luminescent assay (Promega) and normalized to cell growth in media with an equivalent volume of DMSO (Koppikar et al., 2010 (link)). The concentration inhibiting proliferation by 50% (IC50) was determined with Graph Pad Prism 5.0. Anti-proliferative activity of inhibitors in SET2, CMK and K562 cells was also determined by incubation for 72 hr and proliferation measured by colorimetric WST-1 cell viability readout (Roche). Of each triplicate the mean was calculated and data were plotted in XLfit 4 (ID Business Solutions Ltd) to determine half-maximal growth inhibition (GI50).
Meyer S.C., Keller M.D., Chiu S., Koppikar P., Guryanova O.A., Rapaport F., Xu K., Manova K., Pankov D., O’Reilly R.J., Kleppe M., McKenney A.S., Shih A.H., Shank K., Ahn J., Papalexi E., Spitzer B., Socci N., Viale A., Mandon E., Ebel N., Andraos R., Rubert J., Dammassa E., Romanet V., Dölemeyer A., Zender M., Heinlein M., Rampal R., Weinberg R.S., Hoffman R., Sellers W.R., Hofmann F., Murakami M., Baffert F., Gaul C., Radimerski T, & Levine R.L. (2015). CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms. Cancer cell, 28(1), 15-28.
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3

Generation of JAK2 Inhibitor-Resistant Cell Lines

Cited 3 times
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SET2 cells cultured in RPMI1640/20%FCS were exposed to increasing concentrations of type II JAK2 inhibitor CHZ868 to generate JAK2 inhibitor resistant SET2 cells with gradually increased IC50. JAKi-r SET2 cells were then kept at 0.3 μmol/L CHZ868 and JAKi-R SET2 cells at 0.5 μmol/L of CHZ868 as maintenance concentrations. Ba/F3 cells stably expressing Jak2V617F along with erythropoietin receptor (EPOR) cultured in RPMI1640/10%FCS (20, 23 (link)) were analogously exposed to CHZ868 and kept at 0.5 μmol/L CHZ868 maintenance concentration. AXL-deficient JAKi-R SET2 cells were generated by transduction with AXL-specific short hairpin RNAs (shRNA; Supplementary Table S1) in pLKO-Tet-On vector and puromycin selection followed by doxycycline induction. Cell proliferation was assessed upon AXL knockdown or inhibitor exposure for 48 hours using Cell Viability Luminescent Assay (Promega) in JAK inhibitor resistant (JAKi-r, JAKi-R) vs. sensitive (JAKi-S) cells. IC50 was determined with Prism 9.0 (GraphPad). Effects of inhibitor combinations were assessed in R-Studio with SynergyFinder package and Zero Interaction Potency (ZIP) model as described (24, 25 (link)). JAKi-R SET2 cells for intravenous engraftment in NOD/SCID gamma (NSG) mice stably expressed firefly luciferase upon transduction with GFP/luciferase as described before (26 (link)).
Codilupi T., Szybinski J., Arunasalam S., Jungius S., Dunbar A.C., Stivala S., Brkic S., Albrecht C., Vokalova L., Yang J.L., Buczak K., Ghosh N., Passweg J.R., Rovo A., Angelillo-Scherrer A., Pankov D., Dirnhofer S., Levine R.L., Koche R, & Meyer S.C. (2023). Development of Resistance to Type II JAK2 Inhibitors in MPN Depends on AXL Kinase and Is Targetable. Clinical Cancer Research, 30(3), 586-599.
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4

Luminescent Cell Viability Assay

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To detect cell proliferation and cell viability, a luminescent readout assay was performed according to the manufacturer’s instructions. In brief, glioma cells (LN229 and U118) with or without GSC-EV treatments were washed twice with PBS, incubated with luciferase reporter assay 1X buffer (Luminescent Cell Viability Assay, Promega, Madison, WI, USA) at room temperature for 15 min and read using a luminometer. Data were normalised to the non-treatment group and presented as a change in ratio.
Ma C., Nguyen H.P., Jones J.J., Stylli S.S., Whitehead C.A., Paradiso L., Luwor R.B., Areeb Z., Hanssen E., Cho E., Putz U., Kaye A.H, & Morokoff A.P. (2022). Extracellular Vesicles Secreted by Glioma Stem Cells Are Involved in Radiation Resistance and Glioma Progression. International Journal of Molecular Sciences, 23(5), 2770.
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5

Neutrophil-Mediated Tumor Cell Cytotoxicity

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The neutrophil cytotoxic assay was performed following the protocol described previously.[39] Neutrophils were isolated using the MojoSort Mouse Neutrophil Isolation Kit (BioLegend, 480057) from the mouse peripheral blood collected by cardiac punch. Five thousand tumor cells carrying luciferase were seeded into the 96‐well plate four hours before coculture. Then, isolated neutrophils were co‐cultured with tumor cells (100:1) for 12 h. At endpoint, the live cells were measured by the Luminescent Cell Viability Assay (Promega, G7570). During the coculture, live imaging was taken by the ImageXpress Pico System to monitor the process of neutrophil migration.
Wang L., Wang E., Prado Balcazar J., Wu Z., Xiang K., Wang Y., Huang Q., Negrete M., Chen K., Li W., Fu Y., Dohlman A., Mines R., Zhang L., Kobayashi Y., Chen T., Shi G., Shen J.P., Kopetz S., Tata P.R., Moreno V., Gersbach C., Crawford G., Hsu D., Huang E., Bu P, & Shen X. (2021). Chromatin Remodeling of Colorectal Cancer Liver Metastasis is Mediated by an HGF‐PU.1‐DPP4 Axis. Advanced Science, 8(19), 2004673.
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6

CBDA Cell Viability Assay

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The effect
of CNBDA on cell viability
was determined using a luminescent cell viability assay (Promega)
that measures growth based on ATP levels. We followed the manufacturer’s
protocol in growing cells, preparation of the reagents, and measurement
of luminescence. Cells were treated with a vehicle or CBDA concentrations
ranging from 100 nM to 1.6 μM in a 2× serial dilution for
24 h. Cell viability was measured in a Synergen H3 (Biotech) plate
reader and the data were analyzed with the IGEN-5 software.
Hartman Z., Geldenhuys W.J, & Agazie Y.M. (2020). Novel Small-Molecule Inhibitor for the Oncogenic Tyrosine Phosphatase SHP2 with Anti-Breast Cancer Cell Effects. ACS Omega, 5(39), 25113-25124.
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7

Functionalized Nanoparticle Synthesis Protocol

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Silicon wafers used for the manufacturing of the nanoparticles were purchased from Siltronix (Archamps, France). Luminescent cell viability assay and VivoGloTM Luciferin were purchased from Promega. Cyanine5 amine (Cy5) was purchased from Lumiprobe. Hydrofluoric acid (HF, 49%) was purchased from J. T. Baker (Center Valley, PA, USA). Human holo-transferrin, undecylenic acid (UA), 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC) hydrochloride, N-hydroxysulfosuccinimide (NHS), 2-(N-morpholino)ethanesulfonic acid (MES) hydrate, ethanol (EtOH), dimethylformamide (DMF), dichloromethane (DCM), and triethylamine (TEA) were purchased from Merck (Macquarie Park, Australia). All solvents were of analytical grade. Water (HPLC grade) was obtained with a Milli-Q Advantage A10 water purification system (Merck Millipore, Bayswater, Australia). α-Carboxyl-ω-amino poly(ethylene glycol) 10 kDa (NH2-PEG-COOH) and methoxy poly-(ethylene glycol)-amine 10 kDa (mPEG-NH2) were purchased from Advanced BioChemicals (Lawrenceville, GA, USA). All other chemicals were purchased from Sigma-Aldrich (Macquarie Park, Australia) unless stated otherwise.
Zhang W., Zhu D., Tong Z., Peng B., Cheng X., Esser L, & Voelcker N.H. (2023). Influence of Surface Ligand Density and Particle Size on the Penetration of the Blood–Brain Barrier by Porous Silicon Nanoparticles. Pharmaceutics, 15(9), 2271.
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8

Quantifying Cell Viability by ATP Assay

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Proliferation of the control and CCM1-BOECs was measured following the “Luminescent Cell Viability Assay” (Promega, Madison, WI, USA) instructions. This is a homogeneous quantitative method to determine the number of viable cells in culture based on quantitation of ATP, which indicates metabolically active cells. Briefly, 5000 cells per well were seeded in quadruplicate in a collagen-coated P-96 plate. Cell Titer-Glo reagent (lysis buffer, Ultra-Glo Recombinant Luciferase, luciferine, and Mg2+) was added to wells to a final proportion of 1:1 and gently mixed for 30 min at room temperature (RT). Next, luminescence was measured in three independent measurements using a Glomax Multidetection System (www.promega.com/tbs/, 26 March 2024; Promega).
Lorente-Herraiz L., Cuesta A.M., Granado J., Recio-Poveda L., Botella L.M, & Albiñana V. (2024). Molecular and Cellular Characterization of Primary Endothelial Cells from a Familial Cavernomatosis Patient. International Journal of Molecular Sciences, 25(7), 3952.
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9

Cytotoxicity Evaluation of Antineoplastic Drugs

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The MDA-MB-231 and MDA-MB-468 cells were seeded into 96-well plates with viable cell density of 1 × 105 cells/mL and viability of >95%. At 4 h post-seeding, the solution of free drugs (mertansine, gemcitabine, paclitaxel, or doxorubicin) was added to cells to reach a series of final concentration of 200, 100, 50, 20, 10, 5, 2, 1, 0 nM (DM1, GC, PTX, DM1 + GC, PTX + AC) and 0–1.5 µM (AC). At 5 days post-treatment, the viable cells were measured by Luminescent Cell Viability Assay (Promega, Madison, WI, USA). The relative viability was calculated as (viable cells in treatment group/control group) × 100%.
Si Y., Zhang Y., Ngo H.G., Guan J.S., Chen K., Wang Q., Singh A.P., Xu Y., Zhou L., Yang E.S, & Liu X.(. (2021). Targeted Liposomal Chemotherapies to Treat Triple-Negative Breast Cancer. Cancers, 13(15), 3749.
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10

Measuring IC50 of Agents in Cells

Cited 1 time
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The IC50 values of different agents in adherent and suspension cells were measured by the sulforhodamine B (SRB; Sigma, MO) assay and luminescent cell viability assay (Promega, Madison, WI) respectively, as reported previously [42 (link), 45 (link)]. Cells were seeded into 96-well plates, cultured overnight and treated with gradient concentrations of the tested agents for 72 h. Optic density for both assays was read with an EnVision Multilabel Reader (PerkinElmer, Waltham, MA). The averaged IC50 values were determined with the Logit method from three independent experiments.
Yi J.M., Zhang X.F., Huan X.J., Song S.S., Wang W., Tian Q.T., Sun Y.M., Chen Y., Ding J., Wang Y.Q., Yang C.H, & Miao Z.H. (2015). Dual targeting of microtubule and topoisomerase II by α-carboline derivative YCH337 for tumor proliferation and growth inhibition. Oncotarget, 6(11), 8960-8973.
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