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Envision multilable reader

Manufactured by PerkinElmer
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Sourced in United States

The EnVision Multilabel Reader is a high-performance, multimode microplate reader designed for a wide range of applications in life science research and drug discovery. It is capable of detecting various detection modes, including absorbance, fluorescence, luminescence, and time-resolved fluorescence.

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Lab products found in correlation

Lte4 enzyme immunoassay kit, by Cayman Chemical (2 mentions) Pgd2 mox enzyme immunoassay kit, by Cayman Chemical (2 mentions) Pde4d, by BPS Biosciences (1 mentions) Pde7a, by BPS Biosciences (1 mentions) Pde1a, by BPS Biosciences (1 mentions) Pde3a, by BPS Biosciences (1 mentions) Lance ultra camp assay kit, by PerkinElmer (1 mentions) Pde4b, by BPS Biosciences (1 mentions) Tgf β1, by Thermo Fisher Scientific (1 mentions) Collagen 1 α1, by Bio-Techne (1 mentions) Celltiter glo luminescent cell viability assay, by Promega (1 mentions) Atplite kit, by PerkinElmer (1 mentions) Caspase glo 3 7 assay, by Promega (1 mentions)

5 protocols using envision multilable reader

1

Enzyme Inhibition Assay for PDE Enzymes

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The enzyme inhibition assay was performed against human PDE enzymes (PDE1A, PDE3A, PDE4A, PDE4B, PDE4C, PDE4D, and PDE7A; BPS Biosciences, San Diego, CA, United States) according to the manufacturer’s instructions (LANCE Ultra cAMP assay kit; Perkin Elmer, United States). In each well, 5 μl of 3 nM cAMP, 2.5 μl of PDE enzyme (0.1 ng/well), and 2.5 μl of inhibitor solution were added, and incubated at 37°C for 1 h. After incubation, 5 μL each of Eu-cAMP and ULight-anti-cAMP detection reagent supplemented with 1 mM of IBMX were added. The reaction mixture was incubated at 37°C for 1 h. After incubation, emission signals were collected at 665 nm using EnVision Multilable Reader (Perkin Elmer, United States).
Purushothaman B., Arumugam P, & Song J.M. (2018). A Novel Catecholopyrimidine Based Small Molecule PDE4B Inhibitor Suppresses Inflammatory Cytokines in Atopic Mice. Frontiers in Pharmacology, 9, 485.
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2

Cytokine and Eicosanoid Quantification

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The levels of IL-4, IL-5, IL-13, and GM-CSF in the Tc2 supernatants were assayed with ELISA kits, and the concentrations of PGD2 and LTE4 in the mast cell supernatants were measured with a PGD2–MOX enzyme immunoassay kit and LTE4 enzyme immunoassay kit (Cayman Chemicals) respectively according to the manufacturer’s instructions. The results were measured in an EnVision Multilable Reader (PerkinElmer).
Hilvering B., Hinks T., Stöger L., Marchi E., Salimi M., Shrimanker R., Liu W., Chen W., Luo J., Go S., Powell T., Cane J., Thulborn S., Kurioka A., Leng T., Matthews J., Connolly C., Borg C., Bafadhel M., Willberg C., Ramasamy A., Djukanović R., Ogg G., Pavord I., Klenerman P, & Xue L. (2018). Synergistic activation of pro-inflammatory type-2 CD8+ T lymphocytes by lipid mediators in severe eosinophilic asthma. Mucosal immunology, 11(5), 1408-1419.
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3

Quantification of Inflammatory Mediators

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The levels of IL-4, IL-5, IL-13, TGF-β1 (Invitrogen) or collagen I α1 (Bio-Techne) in the supernatants after the cell treatments were assayed with ELISA kits according to the manufacturer’s instructions. The concentrations of PGD2 and LTE4 in the supernatants were measured with a PGD2–MOX enzyme immunoassay kit and LTE4 enzyme immunoassay kit (Cayman Chemicals) respectively according to the manufacturer’s instructions. The results were measured in an EnVision Multilable Reader (PerkinElmer).
Chen W., Luo J., Ye Y., Hoyle R., Liu W., Borst R., Kazani S., Shikatani E.A., Erpenbeck V.J., Pavord I.D., Klenerman P., Sandham D.A, & Xue L. (2021). The Roles of Type 2 Cytotoxic T Cells in Inflammation, Tissue Remodeling, and Prostaglandin (PG) D2 Production Are Attenuated by PGD2 Receptor 2 Antagonism. The Journal of Immunology Author Choice, 206(11), 2714-2724.
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4

Evaluating Cell Viability with CellTiter-Glo Assay

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Variations in viable cell number were assessed using the CellTiter-Glo Luminescent Cell Viability Assay (Promega). 2 × 104 cells were seeded for each well in 96-well black plates, as previously described, and treated with sunitinib 5 μM, linsitinib 5 μM and elotinib with or without growth factors (IGF1 100 nM, EGF 30 nM and VEGF 50 ng/ml) for 72 h (30 (link)). Control cells were treated with vehicle alone (DMSO). After incubation, the revealing solution was added, and the luminescent output (relative luminescence units (RLUs)) was recorded using the Envision Multilable Reader (Perkin Elmer). Results are expressed as mean value ± standard error percentage RLU vs the vehicle-treated control cells from three independent experiments in six replicates.
Bresciani G., Ditsiou A., Cilibrasi C., Vella V., Rea F., Schiavon M., Cavallesco N.G., Giamas G., Zatelli M.C, & Gagliano T. (2019). EGF and IGF1 affect sunitinib activity in BP-NEN: new putative targets beyond VEGFR?. Endocrine Connections, 8(6), 680-690.
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5

Everolimus Treatment of P-NETs

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Cell viability and caspase activation were measured as described previously (Zatelli et al. 2006 (link), Zatelli et al. 2010a,b) using the ATPlite kit (PerkinElmer Life Sciences) and the caspase-Glo 3/7 assay (Promega), respectively. Briefly, 20 P-NETs primary cultures, derived from 16 patients, were treated with or without 100 nM Everolimus for 48 h in the absence or in the presence of 100 nM IGF1. Luminescent output (relative luminescence units, RLU) was recorded after 48 h for each assessment by the Envision Multilable Reader (PerkinElmer). Results are expressed as mean value ± s.e.m. percent RLU vs untreated control cells.
According to the response to Everolimus, samples were divided into primary cultures displaying a significant reduction (P < 0.05 vs untreated cells) in cell viability under Everolimus treatment, indicated as responders (P-NET-R), and into primary cultures in which Everolimus did not reduce cell viability, indicated as nonresponders (P-NET-NR).
Falletta S., Partelli S., Rubini C., Nann D., Doria A., Marinoni I., Polenta V., Di Pasquale C., Degli Uberti E., Perren A., Falconi M, & Zatelli M.C. (2016). mTOR inhibitors response and mTOR pathway in pancreatic neuroendocrine tumors. Endocrine-related cancer, 23(11).
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