蛋氨酸氨基肽酶2的缺失不会改变细胞对烟曲霉素或苯甲酰胺类药物的反应。
Depletion of methionine aminopeptidase 2 does not alter cell response to fumagillin or bengamides.
作者信息
Kim Sunkyu, LaMontagne Kenneth, Sabio Michael, Sharma Sushil, Versace Richard W, Yusuff Naeem, Phillips Penny E
机构信息
Novartis Pharmaceuticals, East Hanover, New Jersey 07936, USA.
出版信息
Cancer Res. 2004 May 1;64(9):2984-7. doi: 10.1158/0008-5472.can-04-0019.
Inhibition of endothelial cell growth by fumagillin has been assumed to be mediated by inhibition of the molecular target methionine aminopeptidase 2 (MetAp2). New data show that depletion of MetAp2 by siRNA does not inhibit endothelial cell growth. Moreover, MetAp2-depleted endothelial cells remain responsive to inhibition by either fumagillin or a newly identified MetAp2 enzyme inhibitor. These data suggest that MetAp2 function is not required for endothelial cell proliferation.
烟曲霉素对内皮细胞生长的抑制作用被认为是通过抑制分子靶点甲硫氨酸氨基肽酶2（MetAp2）介导的。新数据表明，小干扰RNA（siRNA）使MetAp2缺失并不会抑制内皮细胞生长。此外，MetAp2缺失的内皮细胞对烟曲霉素或新发现的MetAp2酶抑制剂的抑制作用仍有反应。这些数据表明，MetAp2功能并非内皮细胞增殖所必需。
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