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本帖最后由 细胞海洋 于 2012-3-26 13:34 编辑
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6 B D, n! ?% f; M3 D* K( _1 ACellular DNA is subjected to continual attack, both by reactive species inside
' m5 B% v( D: u( ccells and by environmental agents. Toxic and mutagenic consequences are1 L9 Y& a( \1 o) {; Q' }
minimized by distinct pathways of repair, and 130 known human DNA repair
' K% b: ]( ]4 E( l0 X; K$ agenes are described here. Notable features presently include four enzymes that
5 h2 A4 K- ]3 m' ucan remove uracil from DNA, seven recombination genes related to RAD51, and0 J4 J3 G; T$ q) ?& h
many recently discovered DNA polymerases that bypass damage, but only one! ]. R7 k3 J+ H, O" [0 g) A
system to remove the main DNA lesions induced by ultraviolet light. More
9 f$ S" G4 J1 d' E$ Chuman DNA repair genes will be found by comparison with model organisms' U& K5 t9 u. H; F, |: _2 C
and as common folds in three-dimensional protein structures are determined.- C! P) C" ^9 X) Q" {, E$ F3 L- {
Modulation of DNA repair should lead to clinical applications including im-
( d: y% x/ t) s6 ~provement of radiotherapy and treatment with anticancer drugs and an ad-5 k" v+ n+ q, P
vanced understanding of the cellular aging process.7 A/ |1 }0 P! [" o6 I$ T- W/ |' I
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