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Deoxyribonucleic acid binding

Meyer, T.E. and Habener, J.E (1993) Cyclic adenosine 3, 5 -monophosphate response element-binding protein (CREB) and related transcription-activating deoxyribonucleic acid-binding proteins. Endocr Rev 14 269-290. [Pg.43]

Ducouret, B., M. Tujague, J. Ashraf, N. Mouchel, N. Servel, Y. Valotaire and E.B. Thompson. Cloning of a teleost fish glucocorticoid receptor shows that it contains a deoxyribonucleic acid-binding domain different from that of mammals. Endocrinology 136 3774-3783, 1995. [Pg.388]

S- D. Kennedy and R. G. Bryant, Biophys.J., SO, 669 (1986). Manganese-Deoxyribonucleic Acid Binding Modes. [Pg.368]

Varanasi, U. and D.J. Gmur. 1980. Metabolic activation and covalent binding of benzo[a]pyrene to deoxyribonucleic acid catalyzed by liver enzymes of marine fish. Biochem. Pharmacol. 29 753-762. [Pg.1408]

Dichlorobenzidine was also shown to bind extensively to tissue deoxyribonucleic acid (DNA) in rats and mice. Single oral administration of 20 or 100 mg/kg radiolabeled 3,3 -dichlorobenzidine to male Sprague-Dawley rats and Swiss-Webster mice resulted in extensive binding of the compoimd to tissue (liver, bladder, and intestine) DNA at 12, 24, or 96 hours, and 9 or 14 days after treatment (Ghosal and Iba 1990). [Pg.48]

A snbstantial body of experimental evidence indicates that the formation of a covalent bond between chemical carcinogens and cellnlar macromolecnles represents the first critical step in the multistage process, eventually leading to tumor formation (see Geacintov et al. 1997, references therein). Most chemical carcinogens are not active on their own, but require metabolic activation to produce reactive intermediates capable of binding covalently with target macromolecnles, particularly with deoxyribonucleic acid (DNA), and thereby, initiate cancer. [Pg.186]

Because of the presence of the cyclic four-membered amide connected to the multicyclic ring systems, an effort to define their mechanism of action would be highly important. Despite a number of synthetic efforts, a relatively small amount of research had been focused on the use of compounds related to PAHs as anticancer agents. Bair et al. [152, 153] reported a close correlation between antitumor activity and the shape of the polyaromatic system. However, his group did not make a definitive correlation between the ability of these compounds to bind to deoxyribonucleic acid (DNA) and their cytotoxic activity. Bair s group developed... [Pg.363]

Brustad T, Jones WBG, Nakken KF (1971) On the binding of an organic nitroxide free radical to radiation-induced deoxyribonucleic acid (DNA) radicals under anoxic conditions. Int J Radiat Phys Chem 3 55-61... [Pg.208]

Povirk LF, Dattagupta N, Warf BC, Goldberg IH (1981) Neocarzinostatin chromophore binds to deoxyribonucleic acid by intercalation. Biochemistry 20 4007-4014 Powers EL, Gampel-Jobbagy Z (1972) Water-derived radicals and radiation sensitivity of bacteriophage T7. Int J Radiat Biol 21 353-359... [Pg.471]

Figure 7.5 Example of a chimeric oligonucleic acid and its modification. Chimeric RNA-DNA hybrids are used for correction of point mutations in target genes. One strand of this oligonucleic acid is composed of O-methyl-RNA (outline) with an interruption of 5 bases of deoxyribonucleic acid. X and Y are target residues for correction. In the complementary strand, there is a DNA nick, and T residues loop both ends. 3 -exonuclease and FEN-1 may act on the nick, PARP-1 possibly binds to and is activated by the nick, resulting in activation of damage response pathways. In the modified version, the 3 end is replaced by ribonucleic acids. The 5 end is extended, and the flipped back RNA tail is added. Thus, the nick is expected to be resistant to 3 -exonuclease and FEN-1. In addition, PARP-1 may not be activated by such a nick. Figure 7.5 Example of a chimeric oligonucleic acid and its modification. Chimeric RNA-DNA hybrids are used for correction of point mutations in target genes. One strand of this oligonucleic acid is composed of O-methyl-RNA (outline) with an interruption of 5 bases of deoxyribonucleic acid. X and Y are target residues for correction. In the complementary strand, there is a DNA nick, and T residues loop both ends. 3 -exonuclease and FEN-1 may act on the nick, PARP-1 possibly binds to and is activated by the nick, resulting in activation of damage response pathways. In the modified version, the 3 end is replaced by ribonucleic acids. The 5 end is extended, and the flipped back RNA tail is added. Thus, the nick is expected to be resistant to 3 -exonuclease and FEN-1. In addition, PARP-1 may not be activated by such a nick.
Blot overlays include the probing of membrane with various molecules to detect the presence of specific binding domains, for example, with guanine triphosphate (25,26) or proteoglycans (27). In the Southern or North Western blotting, the membrane is probed with deoxyribonucleic acid or ribonucleic acid molecules to detect nucleic-acid binding proteins (28). [Pg.121]

Immunocapture-polymerase chain reaction (IC-PCR) is a synthesis of two commonly used diagnostic tools. This method exploits the high-affinity binding of antibodies to provide a facile method of purification, usually from a complex matrix, supplying the substrate for PCR detection. PCR exponentially amplifies a deoxyribonucleic acid (DNA) template in a temperature-dependent fashion by the annealing of oligonucleotide primers, enzymatic extension of bound primers by a heat-stable polymerase, followed by denaturation of... [Pg.308]


See other pages where Deoxyribonucleic acid binding is mentioned: [Pg.235]    [Pg.352]    [Pg.235]    [Pg.352]    [Pg.171]    [Pg.220]    [Pg.156]    [Pg.47]    [Pg.532]    [Pg.11]    [Pg.170]    [Pg.6]    [Pg.253]    [Pg.423]    [Pg.197]    [Pg.216]    [Pg.128]    [Pg.4]    [Pg.7]    [Pg.1]    [Pg.64]    [Pg.244]    [Pg.403]    [Pg.413]    [Pg.686]    [Pg.193]    [Pg.6]    [Pg.28]    [Pg.134]    [Pg.507]    [Pg.147]    [Pg.147]   


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