Disease relevance of Plaque Assay

• This has been achieved using a plaque assay technique to detect the same p53 mutation, present throughout a tumor specimen, in a small proportion of cells in an adjacent squamous metaplasia [1].
• Analysis of prolactin and growth hormone production in the MtT/F4 transplantable pituitary tumor by the reverse hemolytic plaque assay [2].
• We have combined a novel technique based on the display of cDNA libraries on the capsid of bacteriophage lambda and an efficient plaque assay to reveal phage displaying ligands that are enriched after only a couple of affinity purification steps [3].
• RNA transcripts from a cDNA clone of human rhinovirus 14 mutated at asparagine 68, one of the residues in the maturation cleavage site, generated normal yields of 150S particles which were noninfectious in the plaque assay because they were unable to initiate a second cycle of infection [4].
• Incubation of nontransfected cells with soluble recombinant FN2 increased IHNV infection, as measured by plaque assay [5].

High impact information on Plaque Assay

• We found that the addition of physiological concentrations of estradiol (780-2,600 pmol/liter) to PWM cultures significantly increased the accumulation of immunoglobulin M-containing and -secreting cells detected by immunofluorescence and/or by the reversed protein-A plaque assay [6].
• The present communication describes the production of rabbit antisera against culture supernates from Con A-activated spleen cells and their use in a plaque assay for mitogen-activated T cells [7].
• Renin release by isolated, single microvascular cells (with or without forskolin) was assessed using the reverse hemolytic plaque assay [8].
• A plaque assay that detects human mononuclear blood cells producing immunoglobulin (Ig)M antibody to sheep erythrocytes was investigated for its usefulness in studying B-cell activation and regulation in 24 patients with humoral immunodeficiency [9].
• Both low- and high-passage cells released the same level of murine leukemia virus, as detected by the XC plaque assay [10].

Chemical compound and disease context of Plaque Assay

• These virions were noninfectious, as judged by plaque assay and by expression of beta-galactosidase following high-multiplicity infection, but partial recovery of infectivity was achieved by using the fusogenic agent polyethylene glycol [11].
• Heterogeneity of growth hormone (GH) release by individual pituitary adenoma cells from acromegalic patients, as determined by the reverse hemolytic plaque assay: effects of SMS 201-995, GH-releasing hormone and thyrotropin-releasing hormone [12].
• The antimicrobial activities of josamycin, erythromycin, and spiramycin against Rickettsia conorii and R. rickettsii were evaluated in two tests: a dye-uptake assay and a plaque assay [13].
• A plaque assay was developed utilizing melanoma cell monolayers overlaid with nutrient medium containing carboxymethylcellulose [14].
• In vitro susceptibility of Rickettsia conorii to ciprofloxacin as determined by suppressing lethality in chicken embryos and by plaque assay [15].

Biological context of Plaque Assay

• In marked contrast, the ribonucleoside of 2,5,6-trichlorobenzimidazole (TCRB) was active against HCMV (IC50 = 2.9 microM, plaque assay; IC90 = 1.4 microM, yield assay) but only weakly active against HSV-1 (IC50 = 102 microM, plaque assay) [16].
• Monodispersed anterior pituitary cells from 1-day-old pups were cultured for 6 days with aqueous extracts of milk from early (days 2, 3, and 4) and late (days 15 and 16) lactation and then subjected to reverse hemolytic plaque assays for PRL and GH release [17].
• This was accomplished by measuring PRL release with a reverse hemolytic plaque assay and PRL gene expression with a DNA probe complementary to PRL mRNA [18].
• The modified reverse hemolytic plaque assay was shown to detect even a single CHO-K1 cell that was changed to produce mature ET-1 by transfection [19].
• Sewage-isolated, protamine-precipitated reoviruses were also used in conjunction with MDBK cells in a comparative evaluation of immunofluorescent cell count and plaque assay procedures [20].

Anatomical context of Plaque Assay

• In order to study the cellular mechanisms of anti-Sm generation, a hemolytic plaque assay to identify and enumerate lymphocytes secreting anti-Sm has been developed by using SRBC coated with purified Sm by a modified carbodiimide technique [21].
• Both TCL are capable of providing MHC-restricted polyclonal help for allogeneic B cells, as measured in the reverse hemolytic plaque assay [22].
• The secretion of lactoferrin of secondary granules and myeloperoxidase (MPO) of primary granules from single adherent human neutrophils was assayed by use of a reverse hemolytic plaque assay [23].
• The proportion of peritoneal macrophages secreting functionally active C4 or C2 was approximately 45% as measured by a hemolytic plaque assay technique [24].
• Lymph node cell preparations which were enriched in Mott cells by velocity sedimentation failed to secrete Ig in a polyclonal reverse plaque assay [25].

Associations of Plaque Assay with chemical compounds

• The antibody as well as the complementary peptide to LHRH also suppressed LHRH-stimulated luteinizing hormone release in a quantitative reverse hemolytic plaque assay, presumably by binding to the LHRH receptor and by binding LHRH, respectively [26].
• TK- recombinants could be selected by a plaque assay on TK- cells in the presence of 5-bromodeoxyuridine and distinguished from spontaneous TK- mutants by the addition of a beta-gal indicator to the agarose overlay [27].
• Similarly, as little as attograms/ml concentrations of the disulfide vitalethine stimulate immunological responses of murine splenocytes toward sheep RBC in a hemolytic plaque assay [28].
• Anti-immunoglobulin added to the plaque assay abrogated the appearance of plaques, but the addition of LPS had no effect [29].
• Insulin secretion from single beta-cells to 16.5 mmol/l glucose examined by reverse hemolytic plaque assay was nearly ablated if UCP-2 was overexpressed [30].

Gene context of Plaque Assay

• We have applied reverse hemolytic plaque assays to monitor the secretions of individual fetal human pituitary cells to determine if any of these cells secrete both hPRL and hGH [31].
• Effects of interferon and MCP-1 on HCMV replication in HRPE cells were evaluated by plaque assays [32].
• The quantity of GH released (as assessed by both RIA and reverse hemolytic plaque assay) under basal and stimulated conditions did not differ among TH-hGH and WT pituitary cell cultures [33].
• Using reverse hemolytic plaque assay (RHPA), we have compared the effects of human GHRH and GHRP-6 on GH release from the dispersed individual cells of rat anterior pituitary [34].
• The intracellular concentration of mPL-II, the number of cells that released mPL-II as assessed by reverse haemolytic plaque assay, and steady-state levels of mPL-II mRNA as assessed by Northern analysis were also reduced by hTNF-alpha treatment [35].

Analytical, diagnostic and therapeutic context of Plaque Assay

• Reverse plaque assays and quantitative reverse-transcriptase polymerase chain reaction were used to analyze the cytokine response [36].
• The latent phase of the infection in mouse tissues was analyzed by plaque assay, PCR, and explantation cocultivation in both immunocompetent and cyclophosphamide-treated mice [37].
• Cleavage-negative provirions, produced by site-directed mutagenesis of asparagine residue 363 to aspartate, threonine, or alanine, displayed no infectivity above revertant frequencies as measured by plaque assay [38].
• Pituitary cells from d 11 chicken embryos were treated with CORT and thyroid hormones, and GH-producing somatotrophs were detected by reverse hemolytic plaque assays and immunocytochemistry [39].
• To establish whether the heterogeneous secretion of glucose-stimulated beta-cells correlates with a different biosynthetic activity, we have studied the secretion and biosynthesis of the very same beta-cells by combining a hemolytic plaque assay with autoradiography [40].

References