Characterization of G1 transit induced by the mitogenic-oncogenic viral Ki-ras gene product
Characterization of G1 transit induced by the mitogenic-oncogenic viral Ki-ras gene product
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有丝分裂致癌病毒 Ki-ras 基因产物诱导的 G1 转运的表征
DOI：
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发表时间：
1986
影响因子：
5.3
通讯作者：
J. Whitfield
中科院分区：
文献类型：
--
作者：
J. Durkin;J. Whitfield
用Kirsten肉瘤病毒（ts 371）的温度敏感突变体感染的NRK大鼠肾细胞在36 ℃下转化，但由于病毒Ki-ras基因的致癌21千道尔顿产物的异常热不稳定性，在41 ℃下表型不转化。因此，tsK-NRK细胞通过在41 ℃的非允许的p21失活温度下在无血清培养基中孵育48小时而处于G 0-G1状态的静止状态。然后，通过在41 ℃加入血清刺激血清饥饿的细胞以非转化细胞的形式或通过将温度降低至p21活化的36 ℃作为转化细胞的形式，来刺激血清饥饿的细胞通过G1。病毒p21蛋白在刺激tsK-NRK细胞通过G1期并开始复制DNA方面与血清一样有效。虽然p21有效地刺激细胞过境G1，即使在非条件，无血清培养基，他们仍然需要细胞衍生的条件因素，随后分裂。p21蛋白也使细胞过境G1，尽管细胞外Ca 2+缺乏，抑制G1过境的血清刺激的细胞。需要p21活性来刺激早期和晚期G1事件。与血清相反，p21不刺激总RNA或蛋白质合成，但p21驱动的G1转运必须需要一些RNA和蛋白质合成，因为它可以被放线菌素D或放线菌酮阻止。
NRK rat kidney cells infected with a temperature-sensitive mutant of the Kirsten sarcoma virus (ts371) were transformed at 36 degrees C but were phenotypically nontransformed at 41 degrees C because of the abnormal thermolability of the oncogenic 21-kilodalton product of the viral Ki-ras gene. Thus tsK-NRK cells were rendered quiescent in a G0-G1 state by a 48-h incubation in serum-free medium at the nonpermissive, p21-inactivating temperature of 41 degrees C. The serum-starved cells could then be stimulated to transit G1 either as nontransformed cells by adding serum at 41 degrees C or as transformed cells by lowering the temperature to a p21-activating 36 degrees C. The viral p21 protein was as effective as serum in stimulating tsK-NRK cells to transit G1 and to start replicating DNA. While p21 effectively stimulated cells to transit G1 even in unconditioned, serum-free medium, they still needed cell-derived conditioning factors to subsequently divide. The p21 protein also enabled the cells to transit G1 in spite of an extracellular Ca2+ deficiency that inhibited the G1 transit of serum-stimulated cells. p21 activity was needed to stimulate both early and late G1 events. In contrast to serum, p21 did not stimulate total RNA or protein synthesis, but some RNA and protein synthesis must have been needed for the p21-driven G1 transit because it could be stopped by actinomycin D or cycloheximide.
影响因子：
56.9
作者：
DOOLITTLE, RF;HUNKAPILLER, MW;ANTONIADES, HN
通讯作者：
ANTONIADES, HN