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Guava viacount viability assay

Manufactured by Merck Group
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The Guava ViaCount viability assay is a laboratory instrument designed for the assessment of cell viability. It provides a quantitative analysis of live and dead cells within a sample.

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Lab products found in correlation

Countess automated cell counter, by Thermo Fisher Scientific (2 mentions) Prestoblue cell viability reagent, by Thermo Fisher Scientific (1 mentions) Purvalanol a, by Merck Group (1 mentions) Lsrii flow cytometer, by BD (1 mentions)

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Guava ViaCount (31 citations) Guava ViaCount assay (14 citations) ViaCount assay (11 citations) ViaCount (11 citations)

4 protocols using guava viacount viability assay

1

Proliferative Effects of Etomoxir and siCPT2

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To determine proliferative effects of etomoxir treatment, cells were seeded in 6-well plates at 100,000–150,000 cells per well and cultured in the presence of 0 or 200 µM etomoxir. Cells were harvested at 24, 48 and 72 h. Cell counts were determined using the Countess Automated Cell Counter (Life Technologies) according to the manufacturer’s instruction, and cell viability was assessed by performing the flow cytometry-based Guava ViaCount viability assay (Millipore) according to the manufacturer’s instruction. To determine proliferative effects of siCPT2 treatment, cells were seeded in 6-well plates at 100,000–150,000 cells per well and transfected with siNT or siCPT2 as described above. Cells were harvested at 24, 48 and 72 h and cell counts were determined using the Countess Automated Cell Counter (Life Technologies) according to the manufacturer’s instruction. Three independent biological replicates were performed for each time-point and condition.
Camarda R., Zhou Z., Kohnz R.A., Balakrishnan S., Mahieu C., Anderton B., Eyob H., Kajimura S., Tward A., Krings G., Nomura D.K, & Goga A. (2016). Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer. Nature medicine, 22(4), 427-432.
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2

Screening Spindle Genes in RPE Cells

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To screen spindle genes in RPE-NEO and RPE-MYC, cells were seeded in 12-well plates at 50,000 cells/well and transfected with 50 nM siRNA as described above or treated with 10 μM of the CDK1 inhibitor Purvalanol A (P4484, Sigma) (Figure 4A). Cells were harvested after 72 h and cell viability was assessed by performing the flow cytometry-based Guava ViaCount Viability Assay (4000–0040, Millipore) according to the manufacturer’s instructions. For further validation of the effects of siTPX2 treatment, cells were seeded in 6-well plates at 100,000 cells per well and transfected with 1.7 nM siRNA as described above. Cells were harvested at 72 hours and cell viability determined using the PrestoBlue Cell Viability Reagent (A13261, Thermo Fisher) (Figure 5E) or the Countess Automated Cell Counter and Trypan Blue Stain (0.4%) (Invitrogen) (Figure 5D) according to the manufacturer’s instructions.
Rohrberg J., Van de Mark D., Amouzgar M., Lee J.V., Taileb M., Corella A., Kilinc S., Williams J., Jokisch M.L., Camarda R., Balakrishnan S., Shankar R., Zhou A., Chang A.N., Chen B., Rugo H.S., Dumont S, & Goga A. (2020). MYC Dysregulates Mitosis, Revealing Cancer Vulnerabilities. Cell reports, 30(10), 3368-3382.e7.
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3

Cell Viability and Cell Cycle Analysis

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Cell viability was determined using a flow-cytometry-based Guava ViaCount viability assay (Millipore), performed according to the manufacturer’s instruction. For cell-cycle analysis, cells were fixed by dropwise addition of ice-cold EtOH and storage at −20C. Fixed cells were stained with propidium iodide, and samples were analyzed on a LSRII flow cytometer (BD Biosciences). Cell populations were gated to exclude doublets. Sub2N levels were determined using FlowJo (Tree Star) analysis software. Univariate cell-cycle analysis was performed by excluding dead cells and using the Watson model cell-cycle analysis program provided by FlowJo analysis software.
Huskey N.E., Guo T., Evason K.J., Momcilovic O., Pardo D., Creasman K.J., Judson R.L., Blelloch R., Oakes S.A., Hebrok M, & Goga A. (2015). CDK1 Inhibition Targets the p53-NOXA-MCL1 Axis, Selectively Kills Embryonic Stem Cells, and Prevents Teratoma Formation. Stem Cell Reports, 4(3), 374-389.
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4

Proliferative Effects of Etomoxir and siCPT2

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To determine proliferative effects of etomoxir treatment, cells were seeded in 6-well plates at 100,000–150,000 cells per well and cultured in the presence of 0 or 200 µM etomoxir. Cells were harvested at 24, 48 and 72 h. Cell counts were determined using the Countess Automated Cell Counter (Life Technologies) according to the manufacturer’s instruction, and cell viability was assessed by performing the flow cytometry-based Guava ViaCount viability assay (Millipore) according to the manufacturer’s instruction. To determine proliferative effects of siCPT2 treatment, cells were seeded in 6-well plates at 100,000–150,000 cells per well and transfected with siNT or siCPT2 as described above. Cells were harvested at 24, 48 and 72 h and cell counts were determined using the Countess Automated Cell Counter (Life Technologies) according to the manufacturer’s instruction. Three independent biological replicates were performed for each time-point and condition.
Camarda R., Zhou Z., Kohnz R.A., Balakrishnan S., Mahieu C., Anderton B., Eyob H., Kajimura S., Tward A., Krings G., Nomura D.K, & Goga A. (2016). Inhibition of fatty acid oxidation as a therapy for MYC-overexpressing triple-negative breast cancer. Nature medicine, 22(4), 427-432.
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