Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.
Activation of erythropoietin receptors by Friend viral gp55 and by erythropoietin and down-modulation by the murine Fv-2r resistance gene.
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Friend 病毒 gp55 和促红细胞生成素激活促红细胞生成素受体，并通过鼠 Fv-2r 抗性基因下调。
DOI：
10.1073/pnas.87.24.9985
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发表时间：
1990
影响因子：
11.1
通讯作者：
Kabat,D
中科院分区：
文献类型：
--
作者：
Hoatlin,ME;Kozak,SL;Lilly,F;Chakraborti,A;Kozak,CA;Kabat,D
由Friend脾病灶形成病毒编码的致白血病膜糖蛋白（gp55）似乎与促红细胞生成素受体（EpoR）结合以刺激成红细胞增多症[Li，J. P.，D'Andrea，A.D.，Lodish，H.F. &巴尔的摩，D.（1990）Nature（伦敦）343，762 - 764]。为了直接比较gp55与促红细胞生成素（Epo）的作用，我们产生了编码gp55、Epo或EpoR的逆转录病毒体。EpoR病毒感染后，白细胞介素3依赖性DA-3细胞结合125 I标记的Epo，并在Epo存在下生长而不需要白细胞介素3。这些后者的细胞，但不是亲本DA-3细胞，成为因子独立的超感染后，无论是Epo病毒或朋友脾病灶形成病毒。此外，Epo病毒在小鼠中引起了一种类似Friend红白血病的疾病。尽管Fv-2r纯合子对所有其他逆转录病毒疾病易感，但它们对Epo病毒和Friend病毒性红白血病均具有抗性。这些结果表明，gp55和Epo刺激EpoR和Fv-2基因编码的蛋白质，控制这些配体的反应。然而，Fv-2蛋白不是EpoR，因为相应的基因映射到小鼠9号染色体的两端。这些结果对于理解EpoR的信号转导和宿主遗传变异在控制致癌蛋白易感性中的作用具有重要意义。
The leukemogenic membrane glycoprotein (gp55) encoded by Friend spleen focus-forming virus appears to bind to erythropoietin receptors (EpoR) sto stimulate erythroblastosis [Li, J.-P., D'Andrea, A.D., Lodish, H.F. & Baltimore, D. (1990) Nature (London) 343, 762-764]. To directly compare the effects of gp55 with erythropoietin (Epo), we produced retrovirions that encode either gp55, Epo, or EpoR. After infection with EpoR virus, interleukin 3-dependent DA-3 cells bound 125I-labeled Epo and grew without interleukin 3 in the presence of Epo. These latter cells, but not parental DA-3 cells, became factor-independent after superinfection either with Epo virus or with Friend spleen focus-forming virus. In addition, Epo virus caused a disease in mice that mimicked Friend erythroleukemia. Although Fv-2r homozygotes are susceptible to all other retroviral diseases, they are resistant to both Epo viral and Friend viral erythroleukemias. These results indicate that both gp55 and Epo stimulate EpoR and that the Fv-2 gene encodes a protein that controls response to these ligands. However, the Fv-2 protein is not EpoR because the corresponding genes map to opposite ends of mouse chromosome 9. These results have important implications for understanding signal transduction by EpoR and the role of host genetic variation in controlling susceptibility to an oncogenic protein.