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雅巴肿瘤痘病毒感染CV-1细胞期间与质膜和细胞器相关的酶的变化。

Alterations of enzymes associated with plasma membranes and cellular organelles during infection of CV-1 cells with Yaba tumor poxvirus.

作者信息

Milo G E, Yohn D S

出版信息

Cancer Res. 1975 Jan;35(1):199-206.

PMID:162862
Abstract

The formation of cellular aggregates (foci) in CV-1 cells following infection with Yaba tumor poxvirus is dependent upon cell passage level, temperatue of incubation, and calcium concentration in the medium. Resistance of older cells can be reversed by maintaining calcium at 0.1 mM or by adding cortisone acetate (1 mug/ml), hydrocortisone, or estradiol-17beta to the cultures. In susceptible cells, foci formation was inhibited slightly by methyltestosterone and inhibited completely by dexamethasone, aldosterone and progesterone. Activities and patterns of enzymes associated with cytoplasmic membranes (alkaline phosphatase, mononucleotidase, and Na+-K+-adenosine triphosphatase) and lysosomes (beta-glucuronidase and acid phosphatase) of the younger susceptible and the older resistant CV-1 cells differed. These differences apparently occurred in concert with phenotypic changes in the membranes that reduced the mobility of older resistant cells. In susceptible culture, unifected cells migrated to the infected cell and participated in foci formation. Reduction of the calcium content to 0.1 mM apparently removed some of the constraints on mobility of the resistant cells. Although the hormones may have had a similar effect, the changes in enzyme patterns indicated basic alterations in protein synthesis. The development of resistance to foci formation occurred between the 45th and 50th passage level. Hormonal reversal of this resistance resulted in enzyme profiles that reflected the pattern of young susceptible cells.

摘要

雅巴肿瘤痘病毒感染CV - 1细胞后细胞聚集体(病灶)的形成取决于细胞传代水平、培养温度和培养基中的钙浓度。通过将钙浓度维持在0.1 mM或向培养物中添加醋酸可的松(1微克/毫升)、氢化可的松或雌二醇 - 17β,可以逆转老龄细胞的抗性。在易感细胞中,甲基睾酮对病灶形成有轻微抑制作用,而地塞米松、醛固酮和孕酮则完全抑制病灶形成。年轻易感和老龄抗性CV - 1细胞的与细胞质膜相关的酶(碱性磷酸酶、单核苷酸酶和钠钾 - 腺苷三磷酸酶)以及溶酶体相关的酶(β - 葡萄糖醛酸酶和酸性磷酸酶)的活性和模式存在差异。这些差异显然与膜的表型变化同时发生,这些变化降低了老龄抗性细胞的流动性。在易感培养物中,未感染的细胞迁移到感染细胞并参与病灶形成。将钙含量降低到0.1 mM显然消除了对抗性细胞流动性的一些限制。尽管激素可能有类似的作用,但酶模式的变化表明蛋白质合成发生了基本改变。对病灶形成抗性的发展发生在第45代到第50代传代水平之间。这种抗性的激素逆转导致酶谱反映年轻易感细胞的模式。

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