Celltiter glo luminescentviability kit

Manufactured by Promega

Sourced in United States

The CellTiter Glo Luminescent Viability Kit is a cell-based assay that quantifies the amount of ATP present, which is an indicator of the presence of metabolically active cells. The kit utilizes a luciferase reaction to generate a luminescent signal proportional to the amount of ATP in the sample.

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Lab products found in correlation

Trametnib, by Selleck Chemicals (2 mentions) Wallace plate reader, by Thermo Fisher Scientific (2 mentions) Goat anti mouseig h l fitc, by Southern Biotech (2 mentions) Cd5 microbeads, by Miltenyi Biotec (2 mentions) Trametinib, by Miltenyi Biotec (2 mentions) Anti p erk, by Cell Signaling Technology (2 mentions) Macs cell separation system, by Miltenyi Biotec (2 mentions) Spectramax l microplate reader, by Molecular Devices (1 mentions) Viafect transfection reagent, by Promega (1 mentions) Epigallocatechin gallate (egcg), by Cayman Chemical (1 mentions) Pcmv6 xl5 vector, by OriGene (1 mentions) Epigallocatechin gallate (egcg), by Promega (1 mentions) 5 aza 2 deoxycytidine aza, by Merck Group (1 mentions) Snu475, by American Type Culture Collection (1 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (1 mentions) Roswell park memorial institute (rpmi), by Thermo Fisher Scientific (1 mentions) Dmem f12, by Thermo Fisher Scientific (1 mentions) Hepg2, by American Type Culture Collection (1 mentions) Topcount nxt microplate scintillation and luminescence counter, by PerkinElmer (1 mentions)

6 protocols using celltiter glo luminescentviability kit

Evaluating MEK Inhibitor Efficacy on Tumor Cells

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Selumetinib or trametnib (Sellekchem) were added to tumor cells in
96-well plates. Viability was measured using the CellTiter Glo luminescent
viability kit (Promega) after 72 hr using a Wallace plate reader (Molecular
Probe). To determine pERK after MEKis treatment, Kras mutant lung tumor cell
lines and splenocytes collected from HKP1 tumor bearing mice were treated
with selumetinib or trametinib for 2 hr at 37C. Selumetinib and trametinib
stock solutions were prepared in DMSO and diluted in media. Cells were
stimulated with 0.1 ug/ml PMA for 2 min at 37C, then immediately fixed with
4% paraformaldehyde and permeabilized using ice cold 95% methanol. pERK was
stained using anti-pERK (#9106, Cell signaling) and goat anti-mouse
Ig(H+L)–FITC (SouthernBiotech) by flow cytometry. Washout experiments
were done using CD5+ splenocytes from HKP1 tumor bearing mice. CD5+ cells
were collected using CD5 microbeads (Miltenyi MACS cell separation system),
then seeded in the presence of selumetinib or trametinib into flat bottom
96-well plates pre-coated with anti-CD3 (145–2C11, 1ug/ml) and
anti-CD28 (37N, 1ug/ml). After 24hrs, media (RIPA + 7.5% FBS + 0.1%
b-mercaptoethanol) was replaced with MEKis (continuous group) or DMSO
diluent (wash out group) and the media was changed every day with freshly
prepared MEKis. At 72hrs and 96 hr, cells were collected and analyzed by
flow cytometry.

Choi H., Deng J., Li S., Silk T., Dong L., Brea E.J., Houghton S., Redmond D., Zhong H., Boiarsky J., Akbay E.A., Smith P.D., Merghoub T., Wong K.K, & Wolchok J.D. (2019). Pulsatile MEK Inhibition Improves Anti-tumor Immunity and T Cell Function in Murine Kras Mutant Lung Cancer. Cell reports, 27(3), 806-819.e5.

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Organotypic Slice Culture Assay for 6-OHDA Toxicity

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The organotypic slice cultures were exposed to 6-OHDA at the tissue surface on DIV 8 to avoid apoptosis due to nutrients and to induce proper maturation. After treatment with 6-OHDA (100 μM) for 2 h, the slice cultures were collected from the inserts in 6-well culture plates and washed with PBS. After centrifugation at 400 x g for 5 min, the slices were resuspended in the culture medium of organotypic slices and seeded in 96-well at 5 × 10³ cells/well. Intracellular ATP was quantified using the CellTiter-Glo Luminescent Viability Kit (Promega Corporation, Madison, WI, USA), according to the manufacturer's protocol. Luminescence was measured using a SpectraMax L Microplate Reader (Molecular Devices).

, & Kim K.H. (2023). Intranasal delivery of mitochondrial protein humanin rescues cell death and promotes mitochondrial function in Parkinson's disease. Theranostics, 13(10), 3330-3345.

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Cardioprotective Effects of DYRK1A and SRSF6

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iPSC cardiomyocytes at day 6 post initial plating were transfected with 100 ng plasmid DNA using ViaFect transfection reagent (E4981, Promega) and the following human DYRK1A and SRSF6 expression constructs: DYRK1A human clone (NM_001396, SC314641, Origene), DYRK1A human tagged ORF Clone (NM_001396, RG212584, Origene), and SRSF6 cDNA ORF clone N-HA tag (HG19052-NY, Sinobiological). Control cultures were transfected with ~ 100 ng of empty PCMV6XL5 vector (Origene).
Drug treatments were initiated 24 h post-transfection with expression constructs. Daunorubicin (DAU, 14159, Cayman Chemical) and epigallocatechin gallate (EGCG, 709035, Cayman Chemical) were added to culture media for a total incubation time of 14 h. DMSO vehicle was added to controls. After treatments with DAU, iPSC cardiomyocytes were washed with PBS, and incubated in fresh culture medium, or medium supplemented with EGCG for 24 h. Cell viability was determined with the CellTiter-Glo luminescent viability kit (G7570, Promega).

Cejas R.B., Tamaño-Blanco M., Fontecha J.E, & Blanco J.G. (2022). Impact of DYRK1A Expression on TNNT2 Splicing and Daunorubicin Toxicity in Human iPSC-Derived Cardiomyocytes. Cardiovascular Toxicology, 22(8), 701-712.

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Cell Viability Assay with 5-Aza-2′-deoxycytidine

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AC16 (Millipore Sigma), HepG2 (American Type Culture Collection, ATCC), and SNU-475 (ATCC) were cultured using DMEM/F12, DMEM, and RPMI, respectively (Life Technologies), supplemented with 10% (v/v) fetal bovine serum (FBS) in standard incubation conditions at 37 °C, 5% CO₂, and 95% relative humidity.
Cells were seeded 24 h before 5-Aza-2′-deoxycytidine (Aza, Sigma-Aldrich) treatments. Aza was added to fresh culture media every 24 h for a total of 72 h. Cell viability was determined with the CellTiter-Glo Luminescent Viability Kit (Promega), according to the manufacturer’s instructions.

Cejas R.B., Ferguson D.C., Quiñones-Lombraña A., Bard J.E, & Blanco J.G. (2019). Contribution of DNA methylation to the expression of FCGRT in human liver and myocardium. Scientific Reports, 9, 8674.

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Evaluating Gemcitabine Effect on Cell Proliferation

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For evaluation of cell proliferation, KPC and PANC1 cells were seeded in 96-well plates. After overnight adhesion, 15 nM of gemcitabine was added. Cell number was imaged using phase-contrast microscopy. Images were captured using the IncuCyteTM Live-Cell Imaging System (Incucyte HD). Proliferation curves were generated based on measurement of proportion of confluence using the IncuCyte software. In addition, cells were seeded in 96-well plates, and gemcitabine was added 24 hours later at various concentrations. After 72 hours of treatment, the number of viable cells was detected using CellTiter-Glo luminescent viability kit (Promega) using TopCount NXT microplate scintillation and luminescence counter (PerkinElmer). Data are represented as a ratio of relative luminescence (RLU) following treatment with gemcitabine over RLU without treatment.

Jacoberger-Foissac C., Cousineau I., Bareche Y., Allard D., Chrobak P., Allard B., Pommey S., Messaoudi N., McNicoll Y., Soucy G., Koseoglu S., Masia R., Lake A.C., Seo H., Eeles C.B., Rohatgi N., Robson S.C., Turcotte S., Haibe-Kains B, & Stagg J. (2023). CD73 inhibits cGAS-STING and cooperates with CD39 to promote pancreatic cancer. Cancer immunology research, 11(1), 56-71.

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Evaluating MEK Inhibitor Efficacy on Tumor Cells

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