Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04155 (pS2)
 1,234 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the ELSA-pS2 immunoradiometric kit (CIS Bio International) for pS2 protein assay in breast cancer cytosols according to classic validation methods. In addition, we studied correlations between pS2, steroid receptors, and cathepsin-D assays. Repeatability (CV = 1.5% to 4.8%) and reproducibility (CV = 1.6% to 4.9%) were good. The results were linearly related to pS2 concentrations between 205 and 2200 ng/L; the detection limit was 40 ng/L. The accuracy of the assay was measured by assessing recovery; analytical recoveries were near 100% throughout the standard curve. The use of different compounds for cytosol preparation (Tris 10 mmol/L or phosphate 25 mmol/L, KCl 0.4 mol/L, bovine serum albumin 1 g/L) had no effect on pS2 results. pS2 was assayed in breast tumor cytosols from 197 postmenopausal and 92 premenopausal patients. The mean value was 24 micrograms/g of protein; the median and 25th and 75th percentiles were 6, 1, and 23 micrograms/g protein, respectively. We observed a relation between concentrations of pS2 and those of estrogen and progesterone receptors, but there was no relationship between the concentrations of pS2 and cathepsin-D.
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PMID:Immunoradiometric assay of pS2 protein in breast cancer cytosols. 191 81

The expression of genes subject to strict regulation can be a highly dynamic, cyclical process that sequentially achieves and then limits transcription. Kinetic investigations of the estrogen responsive pS2 (TFF1) promoter, to determine the occupancy of factors or the occurrence of covalent marks on chromatin, have provided the most comprehensive picture of the complexity of transcriptional cycling to date. Cycles are initiated by the assembly of intermediate transcription factors that in turn provoke conscription of the basal transcription machinery. These events then achieve activation of the polymerase II complex, which is subsequently followed by limitation of productivity through the action of repressive complexes. This latter phase resets the target promoter, through acting on chromatin structure, such that a subsequent cycle can be initiated. In consequence, transcription is dependent upon cis-acting elements (DNA and nucleosomes) that either interact with or are modified by trans-acting factors. Induced local structural changes to chromatin encompassing regulatory elements of gene promoters include alteration of the positional phasing of nucleosomes, substitution by variant histones, post-translational modification of nucleosomes, changes in the methylation of CpG dinucleotides and breaks in the sugar-phosphate backbone of DNA. A primary function of covalent modification of chromatin may be to drive a sequential progression of reversible interactions that achieve and regulate gene expression.
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PMID:Marking time: the dynamic role of chromatin and covalent modification in transcription. 1880 3