Mitsudomi T, Kimura G
J Virol. 1985 Dec;56(3):951-7. doi: 10.1128/JVI.56.3.951-957.1985.
In quiescent rat 3Y1 fibroblasts infected with simian virus 40 (SV40), sodium butyrate elongated the time lag before entry into S phase in a concentration-dependent fashion. In spite of the elongated time lags, SV40-infected cells entered S phase in a very synchronous mode, irrespective of the butyrate concentrations. The elongated time lag seemed to be at least partially due to a delayed synthesis and a delayed accumulation of large T antigen caused by butyrate. The entry into S phase was also delayed even when butyrate was added to the cultures after expression of T antigen to an extent sufficient for untreated cells to enter S phase. This suggests that butyrate may also inhibit a cellular event(s) that is required for entry into S phase after expression of the T antigen. In contrast, serum-stimulated cells were more sensitive to butyrate with respect to entry into S phase than SV40-infected cells, and the distribution of the time lag among cell populations increased (i.e., asynchrony in entry into S phase increased) with an increase in the butyrate concentration.
在感染了猿猴病毒40(SV40)的静止大鼠3Y1成纤维细胞中,丁酸钠以浓度依赖的方式延长了进入S期前的时间间隔。尽管时间间隔延长,但SV40感染的细胞以非常同步的模式进入S期,与丁酸钠浓度无关。延长的时间间隔似乎至少部分是由于丁酸钠导致大T抗原的合成延迟和积累延迟。即使在T抗原表达后向培养物中添加丁酸钠,进入S期也会延迟,延迟程度足以使未处理的细胞进入S期。这表明丁酸钠也可能抑制T抗原表达后进入S期所需的细胞事件。相比之下,血清刺激的细胞在进入S期方面比SV40感染的细胞对丁酸钠更敏感,并且随着丁酸钠浓度的增加,细胞群体中时间间隔的分布增加(即进入S期的异步性增加)。