Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Frequencies of symmetrical and asymmetrical exchange aberrations induced by two inhibitors of topoisomerase II, namely, 4'-(9-acridinylamino) methanesulfon-m-anisidide (m-AMSA) and etoposide (VP16), were estimated in human peripheral blood lymphocytes. The aberrations were scored using conventional Giemsa staining and fluorescence in situ hybridization (FISH) techniques, using chromosome-specific DNA libraries. Stable aberrations (translocations) were detected using two cocktails of DNA libraries specific for three chromosomes, namely 1, 3 and X and 2, 4 and 8, representing approximately 40% of the whole human genome. The frequencies of dicentrics and translocations increased in a dose-dependent manner, however, m-AMSA was found to be a more potent inducer of chromosomal aberrations in comparison with VP16 (at concentrations at which comparable frequencies of aberrations were induced) by 20- to 30-fold. When corrected for DNA content of chromosomes in each cocktail, a higher frequency of translocations with the cocktail consisting of chromosomes 2, 4 and 8 in comparison with 1, 3 and X was evident. The genomic translocation frequency calculated from chromosome painting analysis for m-AMSA exceeded that estimated for dicentrics by approximately 2-fold. However, for VP16 almost equal frequencies of both types of chromosome exchange were found.
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PMID:Induction of chromosomal aberrations (unstable and stable) by inhibitors of topoisomerase II, m-AMSA and VP16, using conventional Giemsa staining and chromosome painting techniques. 949 92

Trypanosome mitochondrial DNA is a network containing thousands of interlocked minicircles. Silencing of a mitochondrial topoisomerase II by RNA interference (RNAi) causes progressive network shrinking, allowing assessment of the minimal network size compatible with viability. We cloned surviving cells after short-term RNAi and found, as expected, that the number of surviving clones decreased with the duration of RNAi. Unexpectedly, a clonal cell line contained heterogeneously sized networks, some being very small. Several experiments showed that cells survived network shrinkage by asymmetrical division of replicated networks, sacrificing daughters with the small progeny network. Therefore, the average network size gradually increased. During the network shrinkage and early stages of recovery, there were changes in the minicircle repertoire.
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PMID:Asymmetrical division of the kinetoplast DNA network of the trypanosome. 1223 39