Ogino T, Rapp F
Proc Soc Exp Biol Med. 1976 Feb;151(2):280-4. doi: 10.3181/00379727-151-39192.
When rabbit kidney cells were infected with herpes simplex virus type 1 (strain Seibert) or herpes simplex virus type 2 (strain 316D), deoxycytidine kinase (CdR kinase) activity, assayed at 38 degrees, increased 5- to 15-fold relative to controls. The CdR kinase activity induced by type 2 virus was more thermolabile than the enzyme activity induced by type 1 virus. When CdR kinase activity was assayed at various temperatures between 0.5 and 38 degrees, maximum activity for type 1 enzyme was obtained at 16 degrees while maximum activities for host and type 2 enzymes were obtained at 38 degrees. Both type 1 and type 2 induced CdR kinase activities eluted at the same positions as deoxythymidine kinase activities on a Sephadex G-100 column. The estimated mol wt for HSV-1 (Seibert) and HSV-2 (316D) induced CdR kinases are 67,000 and 60,000, respectively.
当兔肾细胞被单纯疱疹病毒1型（赛伯特株）或单纯疱疹病毒2型（316D株）感染时，在38℃下测定的脱氧胞苷激酶（CdR激酶）活性相对于对照增加了5至15倍。2型病毒诱导的CdR激酶活性比1型病毒诱导的酶活性对热更不稳定。当在0.5至38℃之间的不同温度下测定CdR激酶活性时，1型酶的最大活性在16℃时获得，而宿主酶和2型酶的最大活性在38℃时获得。在Sephadex G - 100柱上，1型和2型诱导的CdR激酶活性与脱氧胸苷激酶活性在相同位置洗脱。单纯疱疹病毒1型（赛伯特株）和单纯疱疹病毒2型（316D株）诱导的CdR激酶的估计分子量分别为67,000和60,000。
