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E1A和ras癌基因在巨细胞病毒启动子的控制下,协同增强BHK - 21细胞中重组蛋白的产生。

E1A and ras oncogenes synergistically enhance recombinant protein production under control of the cytomegalovirus promoter in BHK-21 cells.

作者信息

Shirahata S, Watanabe J, Teruya K, Yano T, Osada K, Ohashi H, Tachibana H, Kim E H, Murakami H

机构信息

Graduate School of Genetic Resources Technology, Kyushu University, Fukuoka, Japan.

出版信息

Biosci Biotechnol Biochem. 1995 Feb;59(2):345-7. doi: 10.1271/bbb.59.345.

DOI:10.1271/bbb.59.345
PMID:7766037
Abstract

The amplified ras oncogene greatly enhanced the production of recombinant human interleukin-6 (hIL-6) under control of the cytomegalovirus immediate early promoter (CMV promoter) in BHK-21 cells. When the adenovirus E1A oncogene was further transfected into the above mentioned ras-amplified hIL-6 hyperproducing BHK cells, the transfectants had about 10 times higher productivity than non-transfectants. However, the E1A gene alone did not enhance productivity. These results implicate a ras and E1A synergistic ability that acts to enhance hIL-6 production.

摘要

在巨细胞病毒立即早期启动子(CMV启动子)的控制下,扩增的ras癌基因极大地增强了重组人白细胞介素-6(hIL-6)在BHK-21细胞中的产生。当将腺病毒E1A癌基因进一步转染到上述ras扩增的hIL-6高产BHK细胞中时,转染子的生产力比未转染子高约10倍。然而,单独的E1A基因并不能提高生产力。这些结果表明ras和E1A具有协同作用,可增强hIL-6的产生。

相似文献

1
E1A and ras oncogenes synergistically enhance recombinant protein production under control of the cytomegalovirus promoter in BHK-21 cells.E1A和ras癌基因在巨细胞病毒启动子的控制下,协同增强BHK - 21细胞中重组蛋白的产生。
Biosci Biotechnol Biochem. 1995 Feb;59(2):345-7. doi: 10.1271/bbb.59.345.
2
Ras oncogene enhances the production of a recombinant protein regulated by the cytomegalovirus promoter in BHK-21 cells.Ras癌基因增强了由巨细胞病毒启动子调控的重组蛋白在BHK - 21细胞中的产生。
Cytotechnology. 1994;16(3):167-78. doi: 10.1007/BF00749904.
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Ras amplification in BHK-21 cells produces a host cell line for further rapid establishment of recombinant protein hyper-producing cell lines.BHK-21细胞中的Ras扩增产生了一个宿主细胞系,用于进一步快速建立重组蛋白高产细胞系。
Biosci Biotechnol Biochem. 1995 Feb;59(2):341-4. doi: 10.1271/bbb.59.341.
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Adenovirus E1A 13S gene product up-regulates the cytomegalovirus major immediate early promoter.腺病毒E1A 13S基因产物上调巨细胞病毒主要立即早期启动子。
Am J Respir Cell Mol Biol. 1994 Apr;10(4):448-52. doi: 10.1165/ajrcmb.10.4.8136160.
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Cytomegalovirus immediate early genes upregulate interleukin-6 gene expression.巨细胞病毒立即早期基因上调白细胞介素-6基因的表达。
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Reduction of adenovirus E1A mRNA by RNAi results in enhanced recombinant protein expression in transiently transfected HEK293 cells.通过RNA干扰降低腺病毒E1A mRNA水平可增强瞬时转染的HEK293细胞中的重组蛋白表达。
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[The characteristics of the transformed phenotype and the expression of indicator plasmids in the cells of rat embryonic fibroblasts immortalized by oncogene E1Aad5 and transformed by oncogenes E1Aad5+c-Ha-ras].[由癌基因E1Aad5永生化并由癌基因E1Aad5 + c-Ha-ras转化的大鼠胚胎成纤维细胞中转化表型的特征及指示质粒的表达]
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Downregulation of c-fos gene transcription in cells transformed by E1A and cHa-ras oncogenes: a role of sustained activation of MAP/ERK kinase cascade and of inactive chromatin structure at c-fos promoter.E1A和c-Ha-ras癌基因转化的细胞中c-fos基因转录的下调:MAP/ERK激酶级联的持续激活及c-fos启动子处无活性染色质结构的作用
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Transient expression of E1A and Ras oncogenes causes downregulation of c-fos gene transcription in nontransformed REF52 cells.E1A和Ras癌基因的瞬时表达导致未转化的REF52细胞中c-fos基因转录下调。
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Trans-activation of human MYC: the second promoter is target for the stimulation by adenovirus E1a proteins.人类MYC的反式激活:第二个启动子是腺病毒E1a蛋白刺激的靶点。
Oncogene. 1989 May;4(5):535-41.

引用本文的文献

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Cytotechnology. 2003 Nov;43(1-3):11-7. doi: 10.1023/b:cyto.0000039901.92984.7a.
2
Productivity enhancement of recombinant protein in CHO cells via specific promoter activation by oncogenes.通过癌基因特异性启动子激活提高 CHO 细胞中重组蛋白的产量。
Cytotechnology. 1999 Sep;31(1-2):103-9. doi: 10.1023/A:1008048928053.
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A regulatable selective system facilitates isolation of heterologous protein hyper-producing mammalian cells without gene amplification.
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Cytotechnology. 2002 Nov;40(1-3):13-22. doi: 10.1023/A:1023945517446.
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An Approach to Further Enhance the Cellular Productivity of Exogenous Protein Hyper-producing Chinese Hamster Ovary (CHO) Cells.提高外源蛋白高产中国仓鼠卵巢(CHO)细胞的细胞产率的方法。
Cytotechnology. 2005 Jan;47(1-3):29-36. doi: 10.1007/s10616-005-3765-4.
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