Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:5.99.1.2 (topoisomerase)
 9,166 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper shows that in the yeast Saccharomyces cerevisiae the levels of most mRNAs decrease, in a temporally orchestrated manner, as cells approach and enter the stationary phase. The decreased level of mRNAs is primarily due to transcriptional repression because the overall rate of in vivo transcription by RNA polymerase II is similarly reduced in the stationary phase. The reduction in mRNA levels and the general transcriptional repression are both dependent on topoisomerase I (encoded by TOP1). Specifically, these two processes are much slower in top1 mutants, as their mRNA levels and transcriptional rate remain unchanged for a longer period of time in the stationary phase before they start to decrease. In contrast, the mRNA levels in the stationary phase are not affected by perturbation of topoisomerase II activity. TOP1-dependent repression operates even on HSP26 and SSA3, which have been shown previously to be transcriptionally induced in early stationary phase. Thus, their mRNA levels are high upon the entry of the cells into the stationary phase but gradually decrease, by a TOP1-dependent mechanism, later in the stationary phase. A minor population of mRNAs is not subjected to the TOP1-dependent regulation, as their levels do not change in stationary phase. The possible role of topoisomerase I in the general transcriptional repression is discussed.
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PMID:A general topoisomerase I-dependent transcriptional repression in the stationary phase in yeast. 166 Aug 29

The performance of immunoassays for the detection of autoantibodies is of critical importance to the diagnosis and assessment of patients with systemic lupus erythematosus (SLE). Our objective was to compare 3 multiplexed assays for measurement of multiple autoantibodies and their association with global disease activity, active nephritis and cumulative organ damage in systemic lupus erythematosus (SLE). Stored sera, clinical and laboratory data from the enrollment visit of a long-term lupus registry were used. Autoantibodies were measured using the BioPlex 2200 ANA screen (Bio-Rad), QuantaPlex ENA8 (INOVA Diagnostics) and recomLine ANA/ENA (Mikrogen). The analytes included dsDNA, chromatin, ribosomal P protein, SS-A/Ro60, Ro52, SS-B/La, Sm, U1-RNP, centromere B, topoisomerase 1 and Jo-1 (histidyl tRNA synthetase). Global SLE disease activity was measured by the SLE disease activity index (SLEDAI) and cumulative organ damage by the SLICC/ACR damage index (SDI). One hundred ninety two patients (87% female; 91% Caucasian; mean disease duration 8.8years) were studied. Agreement between the 3 assays varied from 70% to 99% (Cohen's kappa: 0.04-0.88). There were significant associations between SLEDAI scores (excluding anti-dsDNA) and ANA (INOVA, Mikrogen), anti-dsDNA (Bio-Rad, Mikrogen), anti-chromatin (Bio-Rad, INOVA), anti-Ro (Mikrogen), anti-Sm and anti-U1-RNP (all 3 immunoassays) (p=0.002-0.05). Concurrent lupus nephritis was associated with anti-dsDNA (Bio-Rad (p=0.017) or Bio-Rad and Mikrogen together (p=0.015)). There was no significant association between autoantibodies and SDI scores. The overall agreement between assays for the detection of autoantibodies was reasonable. The greatest discordance (70-83%) occurred with those autoantibodies most strongly associated with global SLE disease activity (ANA, anti-dsDNA, anti-chromatin and anti-Sm). Furthermore, there were differences between assays in their associations with global SLE disease activity and lupus nephritis.
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PMID:Comparison between multiplex assays for autoantibody detection in systemic lupus erythematosus. 2043 30