嘌呤N-3在聚腺苷酸（poly(A)）和聚肌苷酸（poly(I)）生物活性中的作用。

Role of purine N-3 in the biologic activities of poly(A) and poly(I).

作者信息

de Clercq E, Torrence P F, Fukui T, Ikehara M

出版信息

Nucleic Acids Res. 1976 Jun;3(6):1591-601. doi: 10.1093/nar/3.6.1591.

DOI:10.1093/nar/3.6.1591

PMID:60741

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC343016/

Abstract

Poly(c3A) (poly 3-deazaadenylic acid) and poly(c3I) (poly 3-deazainosinic acid) differ in biological reactivity from their parent compounds poly(A) and poly(I) and from their 7-deaza counterparts poly(c7A) and poly(c7I). Three parameters of biological reactivity were evaluated : (1 degree) interferon induction, (2 degrees) anti-complement activity, (3 degrees) reverse transcriptase inhibition. Unlike poly(A)-poly(U), poly(I)-poly(C) and poly(I)-poly(br5C), the mixtures of poly(c3A) + POLY(U), poly(c3I) + poly(C), and poly(c3I) + poly(br5C) failed to elicit an interferon response in "super-induced" primary rabbit kidney cells; Poly(I) and its analogs poly(c3I) and poly(c7I) inhibited hemolytic complement activity, whereas poly(A) and its analogs poly(c3A) and poly(c7A) failed to do so. Both poly(I) and poly(c7I), but not poly(c3I), lost their anti-complement potency when annealed to either poly(C) or poly(A)-poly(U). Similarly, poly(I) and poly(c7I), but not poly(c3I), suppressed the interferon inducing ability of poly(A)-poly(U), suggesting that both poly(I) and poly(c7I), but not poly(c3I), added to poly(A)-poly(U) to form a triple-helical structure. Poly(I), poly(C7I) and poly(c7A)exerted a distinct inhibitory effect on turine leukemia virus, while under the same conditions poly(c3I) and poly(c3A) showed little, if any, inhibitory effect.

摘要

聚（c3A）（聚3 - 脱氮腺苷酸）和聚（c3I）（聚3 - 脱氮肌苷酸）在生物学活性上与其母体化合物聚（A）和聚（I）以及它们的7 - 脱氮类似物聚（c7A）和聚（c7I）不同。评估了生物学活性的三个参数：（1）干扰素诱导，（2）抗补体活性，（3）逆转录酶抑制。与聚（A）-聚（U）、聚（I）-聚（C）和聚（I）-聚（br5C）不同，聚（c3A）+聚（U）、聚（c3I）+聚（C）以及聚（c3I）+聚（br5C）的混合物在“超诱导”的原代兔肾细胞中未能引发干扰素反应；聚（I）及其类似物聚（c3I）和聚（c7I）抑制溶血补体活性，而聚（A）及其类似物聚（c3A）和聚（c7A）则无此作用。当与聚（C）或聚（A）-聚（U）退火时，聚（I）和聚（c7I）（而非聚（c3I））失去其抗补体效力。同样，聚（I）和聚（c7I）（而非聚（c3I））抑制聚（A）-聚（U）的干扰素诱导能力，这表明聚（I）和聚（c7I）（而非聚（c3I））添加到聚（A）-聚（U）中形成了三螺旋结构。聚（I）、聚（C7I）和聚（c7A）对鼠白血病病毒有明显的抑制作用，而在相同条件下聚（c3I）和聚（c3A）几乎没有抑制作用（如果有抑制作用的话也很小）。