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关于类固醇激素对培养的鼠细胞中C型病毒产生影响的一项调查。

A survey on the effect of steroid hormone on type C virus production from cultured murine cells.

作者信息

Wu A M, Richardson L S, Paran M, Gallo R C

出版信息

Cancer Res. 1976 Jun;36(6):2025-30.

PMID:178441
Abstract

Dexamethasone stimulates type C virus production induced by iododeoxyuridine (IdUrd) from several murine cell lines: uninfected BALB cells, virally transformed nonproducer K-BALB cells, mouse neuroblastoma N-4 cells, and rat tumor XC cells. Dexamethasone also stimulates virus production from BALB cells newly infected by some murine leukemia or leukemia sarcoma viruses, from a murine myelogenous leukemic cell line (M-1) producing type C virus, from K-BALB(l) cells (K-BALB producing cells previously induced by IdUrd), and from K-BALB cells rescued by Rauscher leukemia virus. However, this stimulatory effect is not universal, since we observed that dexamethasone did not stimulate virus production from BALB cells newly infected by B-tropic virus, from S2CL3 cells producing N-tropic virus (a clone of spontaneously transformed BALB cells), from virus producing normal rat kidney cells, and from a mouse adrenal gland tumor Y-1 cell line chronically producing type C virus. Some estrogenic hormones that do not have any stimulatory effect on virus production from BALB or K-BALB cells induced by IdUrd stimulate virus production from normal rat kidney cells induced by IdUrd. When there is no stimulation of virus production in a cell system by steroid hormones, very often there is some inhibitory activity. Furthermore, we observed that in JLSV10 cells chronically producing Rauscher leukemia virus and in K-BALB cells newly infected by Rauscher leukemia virus, virus production is enhanced by dexamethasone when the cells are still producing a low titer of virus but is not enhanced when the cells are producing a high titer of virus.

摘要

地塞米松可刺激几种鼠细胞系由碘脱氧尿苷(IdUrd)诱导产生C型病毒,这些细胞系包括:未感染的BALB细胞、病毒转化的非生产性K-BALB细胞、小鼠神经母细胞瘤N-4细胞和大鼠肿瘤XC细胞。地塞米松还可刺激一些新感染鼠白血病或白血病肉瘤病毒的BALB细胞产生病毒,刺激产生C型病毒的鼠骨髓白血病细胞系(M-1)产生病毒,刺激K-BALB(l)细胞(先前由IdUrd诱导产生病毒的K-BALB细胞)产生病毒,以及刺激经劳氏肉瘤病毒拯救的K-BALB细胞产生病毒。然而,这种刺激作用并非普遍存在,因为我们观察到地塞米松不能刺激新感染嗜B性病毒的BALB细胞产生病毒,不能刺激产生嗜N性病毒的S2CL3细胞(自发转化的BALB细胞克隆)产生病毒,不能刺激产生病毒的正常大鼠肾细胞产生病毒,也不能刺激长期产生C型病毒的小鼠肾上腺肿瘤Y-1细胞系产生病毒。一些对IdUrd诱导BALB或K-BALB细胞产生病毒没有刺激作用的雌激素,却能刺激IdUrd诱导正常大鼠肾细胞产生病毒。当类固醇激素在细胞系统中不刺激病毒产生时,往往会有一些抑制活性。此外,我们观察到,在长期产生劳氏肉瘤病毒的JLSV10细胞和新感染劳氏肉瘤病毒的K-BALB细胞中,当细胞仍产生低滴度病毒时,地塞米松可增强病毒产生,但当细胞产生高滴度病毒时则无增强作用。

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