Journal of medicinal chemistry, 52(9), 3108-3111 (2009-04-10)
Poly(ADP-ribose) polymerases (PARPs) activate DNA repair mechanisms upon stress- and cytotoxin-induced DNA damage, and inhibition of PARP activity is a lead in cancer drug therapy. We present a structural and functional analysis of the PARP domain of human PARP-3 in
Journal of medicinal chemistry, 36(11), 1539-1547 (1993-05-28)
In order to obtain selective suicide substrates of trypsin-like proteases including plasminogen activators, plasmin, and thrombin, a series of cyclopeptides cyclo[Arg or Lys-aB(CH2X)-Gly4], in which a substituted o- or m-aminobenzoyl group constitutes a latent electrophile, have been prepared. Treatment of
Nanofibrous blends of HCl-doped poly(aniline-co-3-aminobenzoic acid) (3ABAPANI) copolymer and poly(lactic acid) (PLA) were fabricated by electrospinning solutions of the polymers, in varying relative proportions, in dimethyl sulfoxide/tetrahydrofuran mixture. The morphology, mechanical and electrical properties of the nanofibers were characterized and
H2O2 causes DNA damage, which activates poly(adenosine diphosphate ribose) polymerase (PARP), a nuclear enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate. When DNA strand breaks are extensive, consumption of NAD by PARP can cause adenosine triphosphate depletion. The
There is compelling evidence for the central role of oxidative damage in the aging process and for the participation of reactive oxygen species in tumor initiation and promotion. Caloric restriction (CR) or energy restriction retards age-associated increases in mitochondrial free-radical
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