A MECHANISM OF INTERFERON ACTION
干扰素的作用机制
基本信息
- 批准号:3177699
- 负责人:
- 金额:$ 8.08万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:1984
- 资助国家:美国
- 起止时间:1984-08-01 至 1991-05-31
- 项目状态:已结题
- 来源:
- 关键词:Golgi apparatus Vesiculovirus autoradiography clone cells complementary DNA defective virus electron microscopy gel electrophoresis glycosylation immunofluorescence technique interferons ionophores membrane activity membrane permeability membrane proteins protein biosynthesis protein metabolism protein structure protein transport sialate thrombospondins tissue /cell culture transfection virus infection mechanism virus morphology virus protein virus replication
项目摘要
Interferons (IFNs) have an unusual mechanism of action against
some membrane-associated viruses. IFN-treated cells produce
defective virus particles that have decreased infectivity because
they are deficient in a membrane-associated glycoprotein. This is
the principal antiviral activity of IFNs against retroviruses, but it
is also an important mechanism for inhibiting the replication of
vesicular stomatitis virus (VSV) in some cells such as IFN-treated
LB cells which produce VSV particles of low infectivity that are
deficient in VSV-G glycoprotein.
In the IFN-treated cells G does not efficiently localize in the
plasma membrane from which site it is ordinarily incorporated
into budding VSV particles. Recent findings indicate that in IFN-
treated cells the G protein of VSV is inefficiently transported to
the plasma membrane from a cytoplasmic structure. Preliminary
biochemical and morphological data suggest that this structure is
the trans compartment of the Golgi complex (GC).
The aims of this proposal are to analyze this localization in a
clone of LB cells in which a large majority of the cells clearly
manifest the cytoplasmic localization of G in IFN-treated cells.
Experiments in IFN-treated cells will be carried out to study the
morphological and biochemical localization of G. We also plan to
analyze the transport of G protein within the GC. Other
experiments will be focused on what biochemical effects of IFN
might be involved in the inhibition of G transport such as changes
in the pH of acid vesicles, in the fatty-acid composition of the
cell, or in association of G with membranes.
These studies may be useful in enlarging our understanding of how
proteins are targeted by processing.
干扰素(IFN)有一种不寻常的作用机制,
一些膜相关病毒。 IFN处理的细胞产生
有缺陷的病毒颗粒具有降低的传染性,
它们缺乏膜结合糖蛋白。 这是
IFN对逆转录病毒的主要抗病毒活性,但它
也是一个重要的机制,抑制复制
水泡性口炎病毒(VSV)在一些细胞,如IFN-处理
LB细胞产生低感染性的VSV颗粒,
缺乏VSV-G糖蛋白。
在IFN-处理的细胞中,G不能有效地定位于细胞内。
质膜,它通常从该位点结合
变成了萌芽的VSV粒子 最近的研究结果表明,在干扰素-
VSV的G蛋白被低效地转运到处理的细胞中,
从细胞质结构中分离出质膜。 初步
生物化学和形态学数据表明,这种结构是
高尔基复合体的反式隔室(GC)。
本建议的目的是分析这种本地化,
LB细胞的克隆,其中大部分细胞清楚地
表明G在IFN处理的细胞中的细胞质定位。
将在IFN处理的细胞中进行实验,以研究
形态和生化定位。 我们还计划
分析G蛋白在GC内的转运。 其他
实验将集中在什么样的生物化学效应干扰素
可能参与G转运的抑制,如改变
在酸性囊泡的pH值中,在
细胞,或与膜G的协会。
这些研究可能有助于扩大我们对
蛋白质是加工的目标。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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ROBERT M FRIEDMAN其他文献
ROBERT M FRIEDMAN的其他文献
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{{ truncateString('ROBERT M FRIEDMAN', 18)}}的其他基金
INHIBITION OF HUMAN ONCOGENE EXPRESSION BY INTERFERON
干扰素对人类癌基因表达的抑制
- 批准号:
3175183 - 财政年份:1984
- 资助金额:
$ 8.08万 - 项目类别:
INHIBITION OF HUMAN ONCOGENE EXPRESSION BY INTERFERON
干扰素对人类癌基因表达的抑制
- 批准号:
3175179 - 财政年份:1984
- 资助金额:
$ 8.08万 - 项目类别:
INHIBITION OF HUMAN ONCOGENE EXPRESSION BY INTERFERON
干扰素对人类癌基因表达的抑制
- 批准号:
6632930 - 财政年份:1984
- 资助金额:
$ 8.08万 - 项目类别:
INHIBITION OF HUMAN ONCOGENE EXPRESSION BY INTERFERON
干扰素对人类癌基因表达的抑制
- 批准号:
3175180 - 财政年份:1984
- 资助金额:
$ 8.08万 - 项目类别:
INHIBITION OF HUMAN ONCOGENE EXPRESSION BY INTERFERON
干扰素对人类癌基因表达的抑制
- 批准号:
6024372 - 财政年份:1984
- 资助金额:
$ 8.08万 - 项目类别:
INHIBITION OF HUMAN ONCOGENE EXPRESSION BY INTERFERON
干扰素对人类癌基因表达的抑制
- 批准号:
6045146 - 财政年份:1984
- 资助金额:
$ 8.08万 - 项目类别: