Molecular biology of Friend viral erythroleukemia.
Molecular biology of Friend viral erythroleukemia.
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弗兰德病毒性红白血病的分子生物学。
DOI：
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发表时间：
1989
影响因子：
--
通讯作者：
D. Kabat
中科院分区：
文献类型：
--
作者：
D. Kabat
Friend病毒显然为理解癌症的分子生物学提供了一个重要的模型。此外，红白血病的最重要方面可以由单一SFFV感染在没有任何辅助病毒的情况下引起。SFFV env基因编码膜糖蛋白gp 55。这种糖蛋白在成红细胞表面表达时，引起组成性有丝分裂。然而，SFFV感染很少增加细胞的自我更新能力或废除其分化的承诺。因此，感染的后果最初是多克隆成红细胞增多症。这种多克隆增殖通常导致细胞分化和恢复，除非存在辅助病毒引起新成红细胞的持续感染。然而，极其罕见的SFFV前病毒整合导致细胞分化的承诺被废除，并伴随获得细胞永生。这些永生化的前病毒整合只发生在小鼠基因组中的少数位点。因此，现在已知红白血病的促有丝分裂和永生化阶段是由离散的遗传事件引起的-第一个涉及SFFV env基因，第二个涉及罕见的前病毒整合位点。在Friend病毒的早期研究中，第一阶段总是在第二阶段之前至少几周。现在我们知道，第二阶段的延迟完全是由统计数据引起的。每一个SFFV感染的成红细胞是有丝分裂激活，但只有很少的SFFV前病毒整合产生永生。白血病发生的两个步骤可以同时在成红细胞中由罕见的单一SFFV前病毒整合引起。逆转录病毒env基因介导的发病机制引起了人们极大的兴趣。这种发病机制最近已与大多数自然传播的逆转录病毒疾病，包括艾滋病。这些致病机制涉及不同的病毒免疫抑制、贫血、神经病和白血病（Mathes等，1978; Simon等，1984，1987;韦斯等，1985; Lifson等，1986; Riedel等，1986; Sitbon等，1986; Sodroski等，1986; Mitani等，1987;施密特等，1987; Klase等人，1988; Overbaugh等人，1988 a，B）。与鼠逆转录病毒白血病发生相关的改组和动态env基因重排现在也见于FeLV-FAIDS和HIV（Fisher et al. 1988; Overbaugh et al. 1 t88 b; Saag et al. 1988; Tersmette et al. 1988）。Friend病毒提供了这种env基因发病机制的重要实例。虽然我们仍然不清楚gp 55是如何引起成红细胞有丝分裂的，但这一领域的工作人员已经发现了可能导致答案的重要线索。（400字处截断摘要）
Friend virus clearly provides an important model for understanding the molecular biology of cancer. Moreover, the most important aspects of the erythroleukemia can be caused by a single SFFV infection in the absence of any helper virus. The SFFV env gene encodes a membrane glycoprotein, gp55. This glycoprotein, when expressed on erythroblast surfaces, causes a constitutive mitogenesis. However, SFFV infections only rarely increase the cell's self-renewal capability or abrogate its commitment to differentiate. Therefore, the consequence of infection is initially a polyclonal erythroblastosis. This polyclonal proliferation usually leads to cell differentiation and to recovery unless helper virus is present to cause continuing infection of new erythroblasts. Extremely rare SFFV proviral integrations, however, result in abrogation of the cell's commitment to differentiate and in the concomitant acquisition of cell immortality. These immortalizing proviral integrations occur at only a small number of sites in the mouse genome. Therefore, the mitogenic and immortalizing stages of erythroleukemia are now known to be caused by discrete genetic events--the first involving the SFFV env gene and the second involving the rare proviral integration sites. In early investigations of Friend virus, the first stage always preceded the second stage by at least several weeks. Now it is known that this delay in onset of the second stage is caused solely by statistics. Every SFFV-infected erythroblast is mitogenically activated, yet only rarely does the SFFV proviral integration produce immortality. Both steps in leukemogenesis can be caused simultaneously in an erythroblast by a rare single SFFV proviral integration. There has been an explosion of interest in retroviral env gene-mediated pathogenesis. Such pathogenesis has been recently associated with most of the naturally transmitted retroviral diseases including AIDS. Such pathogenesis involves in different viruses immunosuppression, anemia, neuropathy, and leukemia (Mathes et al. 1978; Simon et al. 1984, 1987; Weiss et al. 1985; Lifson et al. 1986; Riedel et al. 1986; Sitbon et al. 1986; Sodroski et al. 1986; Mitani et al. 1987; Schmidt et al. 1987; Klase et al. 1988; Overbaugh et al. 1988a, b). The shuffling and dynamic env gene rearrangements that have been associated with murine retroviral leukemogenesis have also now been seen in FeLV-FAIDS and HIV (Fisher et al. 1988; Overbaugh et al. 1 t88b; Saag et al. 1988; Tersmette et al. 1988). Friend virus provides an important established example of such env gene pathogenesis. Although we still do not understand precisely how gp55 causes erythroblast mitosis, workers in this field have discovered important clues that may lead to answers.(ABSTRACT TRUNCATED AT 400 WORDS)
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DOI：
10.1016/s0021-9258(19)45335-0
发表时间：
1982-12
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
T. Fitting;D. Kabat
通讯作者：
T. Fitting;D. Kabat
检测糖基化、不完全折叠形式的绒毛膜促性腺激素 β 亚基，该亚基是滋养层细胞中激素组装的前体。
DOI：
--
发表时间：
1987
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Ruddon,RW;Krzesicki,RF;Norton,SE;Beebe,JS;Peters,BP;Perini,F
通讯作者：
Perini,F
env 基因的特定序列决定了 Rauscher 病毒复合体的两种 XC 阴性病毒的宿主范围。
影响因子：
3.7
作者：
Vogt,M;Haggblom,C;Swift,S;Haas,M
通讯作者：
Haas,M
与致癌逆转录病毒跨膜成分同源的合成肽对多克隆 B 细胞活化的抑制作用。
DOI：
10.1073/pnas.84.1.237
发表时间：
1987
影响因子：
11.1
作者：
Mitani,M;Cianciolo,GJ;Snyderman,R;Yasuda,M;Good,RA;Day,NK
通讯作者：
Day,NK
鼠胎儿造血祖细胞的分离和各种红系前体细胞的选择性分级。
影响因子：
20.3
作者：
Nicola,NA;Metcalf,D;vonMelchner,H;Burgess,AW
通讯作者：
Burgess,AW