Detail of "28718-90-3"

Reference

Interaction of 4',6-diamidino-2-phenylindole to nucleic acids, and its implication to their template activity in RNA-polymerase reaction of E

Interaction of 4',6-diamidino-2-phenylindole to nucleic acids, and its implication to their template activity in RNA-polymerase reaction of E. coli bacteria and of Friend-virus infected mouse spleen. Mildner, Boris; Metz, Angelika; Chandra, Prakash (Gustav-Embden-Zent. Biol. Chem., Univ. Frankfurt, Frankfurt/Main, Ger.). Cancer Lett., 4(2), 89-98 (English) 1978. CODEN: CALEDQ. ISSN: 0304-3835. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) The interaction between 4',6-diamidino-2-phenylindole-2HCl (I) [28718-90-3] and a variety of DNAs and synthetic polydeoxynucleotides was investigated in order to delineate the nucleic acid structural features necessary for binding. Apparently, I interacts preferentially to dAT-rich sites of DNA. The drug exhibits a very high affinity towards the hybrid polymer, poly (rA)×poly (dT) [27156-07-6]. The preferential binding of I to dAT-rich sites of DNA was also obsd. in enzymic studies. The inhibitory effect of I on the RNA-polymerase [9014-24-8] reaction of bacterial cells was strictly dependent on the base compn. of the template used. This inhibition was of the competitive type, as evidenced by the Lineweaver-Burk plots of the kinetic data. Studies with RNA-polymerase I and II of the nuclei from FLV-infected mouse spleen revealed that the inhibitory effect of I in both of the systems was similar. The drug-to-DNA ratio required to inhibit 50% of the enzyme activity was identical for both of the systems.

Effect of drug-DNA interactions upon transcription initiation at the lac promoter

Effect of drug-DNA interactions upon transcription initiation at the lac promoter. Straney, David C.; Crothers, Donald M. (Dep. Mol. Biophys. Biochem., Yale Univ., New Haven, CT 06511, USA). Biochemistry, 26(7), 1987-95 (English) 1987.There are some reagents with their cas registry numbers 39389-47-4 and 28718-90-3 are used in this study. CODEN: BICHAW. ISSN: 0006-2960. DOCUMENT TYPE: Journal CA Section: 6 (General Biochemistry) Section cross-reference(s): 1, 3 The effects of 6 DNA-binding drugs upon initiation at the lac UV5 promoter by Escherichia coli RNA polymerase were examd. Expts. were directed at detg. the influence of added drug on open complex formation, open complex stability, initiation from the open complex, and stability of the resulting initiated complex. The narrow groovebinding drugs distamycin and 4',6-diamidino-2-phenylindole were more effective in inhibiting initiation through their effect on the 1st 3 of these factors than were the intercalators ethidium bromide, daunomycin, and actinomycin. The bisintercalator bis(daunomycin) inhibited open complex formation better than its parent daunomycin. With the possible exception of actinomycin, the drugs tested were not able to disrupt preformed initiated complex, in contrast to their destabilizing effect upon the open complex. Combined with other results, the data suggest that the antitumor activity of daunomycin is unlikely to result from its effect on transcription. The relative effectiveness of the drugs were compared with the known phys. properties of the corresponding drug-DNA interactions. The rate of open complex formation seems to be influenced by both the on and off rates of the drug, probably due to the relative slowness of open complex formation. This is in contrast to elongation, a much quicker process, which seems to be limited by the drug off rate alone; these considerations may possibly rationalize the difference in relative effect of particular drugs upon initiation and elongation. All drugs were able to actively disrupt open complex, although to substantially different extents; some possible mechanisms for this disruption and the insensitivity of the initiated complex, are discussed. .