本帖最后由 细胞海洋 于 2012-4-13 22:22 编辑 $ S( _) s; R6 s6 S" v ) ?1 n, k1 u& T# k$ u7 F4 o ! ]5 C2 w5 w0 j4 c1 xVolume 149, Issue 2: s) u3 K& m$ k9 r. l+ q+ a! i
On the cover: Congenital scoliosis is a human birth defect that results in , e+ w* i3 Q. W( o/ G3 }spinal curvature caused by vertebral defects. In this issue, Sparrow et al. (pp. j5 z1 T1 M! Y- O9 i, q
295–306) demonstrate that such defects in humans and mice can be caused by 3 C: c& ]' R3 ]$ a) C4 Whaploinsufficiency of Notch signaling pathway genes. In mice, this genetic risk 4 ^* @# N {0 O5 x; nfactor combined with an environmental condition (short-term hypoxia) 7 C1 `" Y- r# }/ h7 o7 o. U6 osignificantly increases the penetrance and severity of vertebral defects. The % T1 g" |$ ]% f+ U/ wcover photograph shows severe vertebral and rib defects of an embryonic mouse S: n. f. Z2 g7 {7 p- b" icontaining a null allele of a Notch signaling pathway target gene and exposed to ; f* |3 ]" U& _2 m2 T
a brief period of hypoxia during gestation.7 J' n4 a& e3 h- H. {0 X
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( E) q6 I- s8 v$ @2 K( m 作者: yxp 时间: 2012-4-14 15:06
