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J. Neurochem. 77(3), 849-863. CEP-1347/KT-7515, an inhibitor of SAPK/JNK pathway activation, promotes survival and blocks multiple events associated with Abeta-induced cortical neuron apoptosis. 2001

Bozyczko-Coyne, D., O'Kane, T.M., Wu, Z.L., Dobrzanski, P., Murthy, S., Vaught, J.L., Scott, RW.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay was used to assess metabolic function of neuronal cells after treatment with various concentrations of beta-amyloid. (2967)

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Biochemistry 39(14), 3972-8. A common pharmacophore for Taxol and the epothilones based on the biological activity of a taxane molecule lacking a C-13 side chain. 2000

He,L., Jagtap, P.G., Kingston, D.G., Shen, H.J., Orr, G.A., Horwitz, S.B.

Notes: The CellTiter 96® AQueous Assay (MTS/PMS) was used to analyze the IC50 of a taxol derivative. The assay was performed on taxol-sensitive and taxol-resistant cells. The SKOV3 cell line is sensitive to taxol, and SKVLB, a derivative of SKOV3, is resistant to vinblastine. The cell line A-549 as well as its taxol-resistant derivative, AT12, were tested also. (1073)

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J. Biol. Chem. 275, 565-570. A novel apoptotic pathway induced by nerve growth factor-mediated TrkA activation in medulloblastoma. 2000

Chou, T.T. , Trojanowski, J.Q., Lee, V.M.Y.

Notes: Treatment of the human medulloblastoma MED283 cells with NGF causes a reduction is cell viability over a 72-hour period as judged by the CellTiter 96® AQueous Cell Proliferation Assay. The death was due to apoptosis. Neither the PD98059 inhibitor nor the MEK Inhibitor U0126 could prevent the apoptosis. The inhibitors (50µM and 10µM, respectively) were added to the media, which was changed every 12 hours during the 72-hour period. Cells with inhibitor and no NGF were not apoptotic, nor was there any noticeable decrease in cell viability. The data for the MEK Inhibitor U0126 Inhibitor is not shown. (1296)

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J. Biol. Chem. 275(32), 24767-24775. c-Jun N-terminal kinase is essential for growth of human T98G glioblastoma cells. 2000

Potapova, O. , Gorospe, M. , Bost, F. , Dean, N. M. , Gaarde, W. A. , Mercola, D. , and Holbrook, N. J.

Notes: T98G human glioblastoma cells were transfected with antisense oligonucleotides to JNK isoforms as well as control scrambled peptides. The proliferation of the cell in the absence or presence of the oligonucleotides were analyzed and compared. Proliferation was measured with the CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS). (0035)

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FASEB J. 14, 1508-17. Carboxyl-terminal fragment of Alzheimer's APP destabilizes calcium homeostasis and renders neuronal cells vulnerable to excitotoxicity. 2000

Kim, H.S., Park, C.H., Cha, S.H., Lee, J.H., Lee, S., Kim, Y., Rah, J.C., Jeong, S.J. and Suh, Y.H.

Notes: The CytoTox® 96 Non-Radioactive Cytotoxicity Assay was used to determine the toxicity of two peptides, a C-terminal fragment of APP (CT 105), and Amyloid β protein (Aβ 1-42). Cells were treated with the peptides in the presence or absence of neuroprotective agents cholesterol, MK801, nifedipine, or verapamil. Studies were done in PC12 cells and in SK-N-SH human neuroblastoma cells. (2134)

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Nature 403, 98-103. Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta. 2000

Nakagawa, T., Zhu, H., Morishima, N., Li, E., Xu, J., Yankner, B.A., Yuan, J.

Notes: Primary mouse cortical neurons derived from caspase-12 normal and knockout mice were tested for cytotoxicity to amyloid beta peptides, staurosporine or a media component. Cytotoxicity was analyzed with the CellTiter 96® AQueous Assay (MTS/PMS). (0642)

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Pediatr. Res. 47, 136-142. Constitutive expression of placental lactogen in pancreatic beta cells: effects on cell morphology, growth, and gene expression. 2000

Fleenor, D. , Petryk, A. , Driscoll, P. , Freemark, M.

Notes: A rat islet cell line stably expressing rat placental lactogen was generated. The bioactivity of the secreted lactogen was measure with the Nb2 cell assay. The proliferation of the Nb2 cells was assayed with the CellTiter 96® AQueous Assay (MTS/PMS). (1160)

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J. Biol. Chem. 275(16), 12095-101. Cyclooxygenase-2 expression inhibits trophic withdrawal apoptosis in nerve growth factor-differentiated PC12 cells. 2000

McGinty, A., Chang, Y.W., Sorokin, A., Bokemeyer, D., Dunn, M.J.

Notes: PC12 cells were transfected to express cyclooxygenase-2 (Cox-2). Cox-2 expression was inducible with IPTG. Cox-2 expressing cells, in the presence of IPTG or without, proliferated to nearly the same levels as control, vector only transfected cells in response to EGF. The proliferation was measured with the CellTiter 96® AQueous Assay (MTS/PMS). The Cox-2 expressing cells were less prone to apoptosis when cultured with NGF and the NGF is withdrawn. Six hours after withdrawal of the NGF, the Cox-2-producing cells contain near control levels of caspase-3 activity as judged by the CaspACE™ Assay System, Fluorometric. (0712)

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Science 288, 2042-2045. Designing small-molecule switches for protein-protein interactions. 2000

Guo, Z. , Zhou, D. , and Schultz, P. G.

Notes: FDC-P1 cells transfected with a mutant human growth factor receptor were challenged with a mutant human growth hormone, termed E8, designed to bind to the mutant receptor. The proliferation of the cells under these conditions was normalized to the cell proliferation in the presence of IL-3. Proliferation was measured with the CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS). (0041)

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Brain Res. 858, 1-8. Dopamine toxicity in neuroblastoma cells: role of glutathione depletion by L-BSO and apoptosis. 2000

Stokes, A. H., Lewis, D. Y., Lash, L. H., Jerome, W. G. III, Grant, K. W., Aschner, M., Vrana, K. E.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS) was used to examine dopamine-induced toxicity. SK-N-SH human neuroblastomas were cultured for 40 hours with and without a glutathione-depleting compound prior to addition of dopamine for 24hours. Other compounds like ascorbate, pyruvate and manganese were tested in combination with the dopamine treatment. (0336)

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Am. J. Physiol. Renal Physiol. 278(1), F83-F90. Effects of chloride channel inhibitors on H(2)O(2)-induced renal epithelial cell injury. 2000

Meng, X., Reeves, W.B.

Notes: The effect of chloride channel blockers on LLC-PK1 cell viability was examined with the CellTiter 96® AQueous Assay (MTS/PMS). (0681)

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J. Biol. Chem. 275, 12090-12094. Functional analysis of the C-terminal region of recombinant human thrombopoietin. C-terminal region of thrombopoietin is a 'shuttle' peptide to help secretion. 2000

Muto, T., Feese, M.D., Shimada, Y., Kudou, Y., Okamoto, T., Ozawa, T., Tahara, T., Ohashi, H., Ogami, K., Kato, T., Miyazaki, H., Kuroki, R.

Notes: The CellTiter 96® AQueous Assay (MTS/PMS) was used in conjunction with the FDCP-hMPL5 cells as a bioassay for thrombopoietin. The FDCP-hMPL5 cells are a derivative of the FDCP-2 cells transfected with mpl-5 cDNA making it responsive to thrombopoietin. The assay was used to test over twenty mutants. (0637)

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J. Physiol.(Paris) 94(1), 71-74. Gastrin and pentagastrin enhance the tumour proliferation of human stable cultured gastric adenocarcinoma cells. 2000

Szabo, I. , Rumi, G. , Bodis, B. , Nemeth, P. , and Mozsik, G.

Notes: The proliferative response of AGS cells to gastrin and pentagastrin was measured with the CellTiter 96® AQueous Non-Radioactive Cell Prolfieration Assay (MTS/PMS). (0042)

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Proc. Natl. Acad. Sci. USA 97(14), 8027-8032. Genetically modified anthrax lethal toxin safely delivers whole HIV protein antigens into the cytosol to induce T cell immunity. 2000

Lu, Y. , Friedman, R. , Kushner, N. , Doling, A. , Thomas, L. , Touzjian, N. , Starnbach, M. /and Lieberman, J.

Notes: RAW 264.7 macrophages were challenged with wildtype and recombinant anthrax lethal factor in the presence of protective antigen. Cytotoxicity was compared to untreated cells. Viable cells were measured with the CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS). (0039)

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J. Biol. Chem. 275(28), 21241-21246. Inhibitory effects of nitric oxide and nitrosative stress on dopamine-beta-hydroxylase. 2000

Zhou, X. , Espey, M. G. , Chen, J. X. , Hofseth, L. J. , Miranda, K. M. , Hussain, S. P. , Wink, D. A. , and Harris, C. C.

Notes: The SK-N-MC human neuroblastoma cell line was treated with a nitric oxide donor, DEA/NO, and a enzyme secreted into the media was measured. To insure that the DEA/NO treatment did not harm the cells, the cell viability was examined with the CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS). (0037)

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J. Immunol. 164, 4868-4877. Ley/H: an endothelial-selective, cytokine-inducible, angiogenic mediator. 2000

Halloran, M.M., Carley, W.W., Polverini, P.J., Haskell, C.J., Phan, S., Anderson, B.J., Woods, J.M., Campbell, P.L., Volin, M.V., Backer, A.E., Koch, A.E.

Notes: The CellTiter 96® AQueous Assay (MTS/PMS) was used to measure the proliferation of HMVEC, human dermal microvascular endothelial cells, in respone to glucose analogs or bFGF. (1096)

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Biochemistry 39, 5977-5987. Monomeric midkine induces tumor cell proliferation in the absence of cell-surface proteoglycan binding 2000

Qiu, L., Escalante, C.R., Aggarwal, A.K., Wilson, P.D., Burrow, C.R.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS) was used to analyze the proliferation of G401 cells in response to midkine, a retinoic acid-inducible heparin binding protein. Proliferation was measured in the presence of various compounds including heparin and heparinase. (2491)

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J. Immunol. 165(3), 1491-1497. Purification and cloning of an apoptosis-inducing protein derived from fish infected with Anisakis simplex, a causative nematode of human anisakiasis. 2000

Jung, S. K. , Mai, A. , Iwamoto, M. , Arizono, N. , Fujimoto, D. , Sakamaki, K. , and Yonehara, S.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS) was used to assess the cytotoxicity of the fish apoptosis-inducing protein to human HL-60 myeloblasts. (0036)

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J. Immunol. 165(5), 2755-2763. Reduction of inflammatory cytokines and prostaglandin E2 by IL-13 gene therapy in rheumatoid arthritis synovium. 2000

Woods, J. M. , Katschke, K. J. , Jr, Tokuhira, M. , Kurata, H. , Arai, K. I. , Campbell, P. L. , and Koch, A. E.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS) was used to determine the proliferation rate of human TF-1 pre-leukemic B cells. The cells were tested with conditioned media of cells infected with an IL-13-producing adenovirus. Preincubation of the media with a neutralizing anti-IL-13 antibody prevented the proliferation. (0034)

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J. Immunol. 164, 345-349. Rescue of defective T cell development and function in Atm–/– mice by a functional TCRalpha-beta transgene. 2000

Chao, C., Yang, E.M., Xu, Y.

Notes: Mouse spleen cells containing 4 x 104 CD4+ T cells/well were cultured in 96-well plates in triplicate and assayed for proliferation in response to a synthetic peptide after 60 hours in culture. The CellTiter 96® AQueous Cell Proliferation Assay was used to monitor proliferation. (1362)

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Mol. Cell. Biol. 20, 5381-5391. Role of the IkappaB kinase complex in oncogenic ras- and raf-mediated transformation of rat liver epithelial cells. 2000

Arsura, M., Mercurio, F., Oliver, A.L., Thorgeirsson, S.S. and Sonenshein, G.E.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay was used in Rat Liver Epithelial cells (RLEs). Response to treatment with TGF-β1 was compared between normal RLE cell lines and RLEs transformed with Ha-ras (F22-ras cell line), or with v-Raf (F3611-T2 and F3611-TH cell lines). TGF-β1 treatment dramatically inhibited growth of the wild type RLEs, but two of the three transformed lines showed only a modest decrease in proliferation. Cells were plated in 96 well dishes at 2x105 cells per well in 100 µl total volume. (2133)

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J. Biol. Chem. 275, 288-296. Sphingosine 1-Phosphate-induced cell proliferation 2000

An, S., Zheng, Y., Bleu, T.

Notes: The authors investigated the mechanism by which sphingosine 1-phosphate-induced cell proliferation occurs. Human hepatoma cells, HTC4, were plated in 96-well plates, serum-starved for 4 hours and treated with or without sphingosine 1-phosphate in serum-free medium. Cell proliferation was assayed using the CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay. (2509)

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Proc. Natl. Acad. Sci. USA 97(13), 7124-7129. Structure-based discovery of an organic compound that binds Bcl-2 protein and induces apoptosis of tumor cells. 2000

Wang, J. L. , Liu, D. , Zhang, Z. J. , Shan, S. , Han, X. , Srinivasula, S. M. , Croce, C. M. , Alnemri, E. S. , and Huang, Z.

Notes: The response of HL-60 cells to a Bcl-2 binding molecule, HA14-1, was examined with the CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS). The compound strongly induced cytotoxicity via apoptosis. (0040)

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Toxicol. Sci. 54, 500-508. Studies on the mechanisms of arsenic-induced self tolerance developed in liver epithelial cells through continuous low-level arsenite exposure 2000

Romach, E.H., Zhao, C.Q., Del Razo, L.M., Cebrian, M.E., Waalkes, M.P.

Notes: A culture of TRL 1215 cells was grown for 18-20 weeks in the presence of low levels (500nM) of arsenic to generate a chronic exposed cell line. These cells were tested versus the original cell line for cytotoxicity due to arsenic. The chronically exposed cells were at least a log less sensitive to the chemical. the cytotoxicity was determined with the CellTiter 96® AQueous Cell Proliferation Assay. (2546)

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J. Biol. Chem. 275(27), 20315-20323. The transcription factor EGR-1 directly transactivates the fibronectin gene and enhances attachment of human glioblastoma cell line U251. 2000

Liu, C. , Yao, J. , Mercola, D. , and Adamson, E.

Notes: The CellTiter 96® AQueous Non-Radioactive Cell Proliferation Assay (MTS/PMS) was used to determine the adherence of normal and transfected U251 human glioblastoma cells to fibronectin. The U251 cells were transfected with an EGR-1 transcription factor-expressing construct. The EGR-1 expressing cells adhered to the matrix better than the normal cells or vector only cells. The binding was blocked by RGD-containing peptides. (0038)

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