Detail of "21416-88-6"

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DNA strand breaks induced by the anti-topoisomerase II bis-dioxopiperazine ICRF-193

DNA strand breaks induced by the anti-topoisomerase II bis-dioxopiperazine ICRF-193. Hajji, N.; Pastor, N.; Mateos, S.; Dominguez, I.; Cortes, F. (Faculty of Biology, Department of Cell Biology, University of Seville, Seville 41012, Spain). Mutation Research, 530(1,2), 35-46 (English) 2003 Elsevier Science B.V. CODEN: MUREAV. ISSN: 0027-5107. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The bis-dioxopiperazine ICRF-193 has long time been considered as a pure topoisomerase II catalytic inhibitor able to exert its inhibitory effect on the enzyme without stabilization of the so-called cleavable complex formed by DNA covalently bound to topoisomerase II. In recent years, however, this concept has been challenged, as a no.There are some commonly used reagents with their cas registry numbers 142805-56-9 and 21416-88-6 in this article. of reports have shown that ICRF-193 really "poisons" the enzyme, most likely through a different mechanism from that shown by the classical topoisomerase II poisons used in cancer chemotherapy. In the present investigation, we have carried out a study of the capacity of ICRF-193 to induce DNA strand breaks, as classical poisons do, in cultured V79 and irs-2 Chinese hamster lung fibroblasts using the comet assay and pulsed-field gel electrophoresis (PFGE). Our results clearly show that ICRF-193 readily induces breakage in DNA through a mechanism as yet poorly understood. .

DNA topoisomerase II inhibitors enhance random integration of transfected vectors into human chromosomes

DNA topoisomerase II inhibitors enhance random integration of transfected vectors into human chromosomes. Fujimaki, Katsumichi; Aratani, Yasuaki; Fujisawa, Shin; Motomura, Shigeki; Okubo, Takao; Koyama, Hideki (Kihara Inst. Biological Res., Yokohama City Univ., Yokohama 244, Japan). Somatic Cell and Molecular Genetics, 22(4), 279-290 (English) 1996 Plenum. CODEN: SCMGDN. ISSN: 0740-7750. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Genetics) Section cross-reference(s): 13 To study the involvement of DNA topoisomerase (topo) II on nonhomologous (illegitimate) recombination, we examd. the effect of topo II inhibitors on random integration of exogenous vectors into human chromosomes. We transfected human cell lines PA1, HeLa and EJ-1 with linearized plasmid pSV2neo by electroporation, treated with topo II inhibitors and detd. the frequency of Geneticin-resistant (G418r) colonies. We found that three topo II inhibitors, etoposide (VP-16), ICRF-193 and amsacrine (m-AMSA), greatly enhanced the frequency of G418r colonies. These effects were maximally expressed by as little as 12 h treatment with the drugs. Similar enhancements were found with different vectors (closed-circular and linear), different cell types, or by different transfection methods (calcium pptn. 142805-56-9 and 21416-88-6 are also in the experiment. and lipofection). In contrast, the inhibitor treatments did not affect the transient expression of chloramphenicol acetyltransferase and b-galactosidase activity following transfection with pSV2CAT and pCH110, resp. Southern blot anal. revealed that the integration pattern of transfected pSV2neo into PA1 chromosomes was random and not characteristic for each inhibitor. These results suggest that topo II inhibitors directly act at a nonhomologous recombination reaction, promoting the integration process of transfected vectors into human chromosomes. We discuss the enhancement mechanism with a special emphasis on DNA strand breaks induced by the inhibitors. .