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12型腺病毒E1A基因转化的细胞对二酰基甘油介导的细胞杀伤具有高敏感性。

The high sensitivity of cells transformed by E1A gene of adenovirus type 12 to diacylglycerol-mediated cell killing.

作者信息

Shimura H, Matsuzaki A, Shiroki K, Ohtsu M, Fujinaga K, Onodera K, Kimura G

机构信息

Department of Virology, Kyushu University, Fukuoka, Japan.

出版信息

Cancer Lett. 1989 Feb;44(2):143-9. doi: 10.1016/0304-3835(89)90009-8.

DOI:10.1016/0304-3835(89)90009-8
PMID:2920374
Abstract

Viability of rat 3Y1 fibroblasts transformed by adenovirus type 12 (Ad12) was markedly impaired by the administration of dilinoleoylglycerol (DLG) to the culture medium. To identify the gene(s) of Ad12 responsible for the high sensitivity to DLG, we established several transformed sublines of 3Y1 induced by the viral E1A gene or by the mutants of Ad12 which have mutations in the E1A region. All of the transformed sublines of 3Y1 expressing either the 12S or the 13S message from the E1A region were highly sensitive to the cytotoxicity of DLG. We propose that the high sensitivity of Ad12-transformed cells to the DLG mediated cytotoxicity is attributable to the common function of E1A-12S and E1A-13S mRNA products.

摘要

向培养基中添加二亚油酰甘油(DLG)可显著损害由12型腺病毒(Ad12)转化的大鼠3Y1成纤维细胞的活力。为了鉴定Ad12中对DLG高度敏感负责的基因,我们建立了几个由病毒E1A基因或E1A区域有突变的Ad12突变体诱导的3Y1转化亚系。所有表达来自E1A区域的12S或13S信息的3Y1转化亚系对DLG的细胞毒性都高度敏感。我们提出,Ad12转化细胞对DLG介导的细胞毒性的高度敏感性归因于E1A - 12S和E1A - 13S mRNA产物的共同功能。

相似文献

1
The high sensitivity of cells transformed by E1A gene of adenovirus type 12 to diacylglycerol-mediated cell killing.12型腺病毒E1A基因转化的细胞对二酰基甘油介导的细胞杀伤具有高敏感性。
Cancer Lett. 1989 Feb;44(2):143-9. doi: 10.1016/0304-3835(89)90009-8.
2
Mechanism of selective killing by dilinoleoylglycerol of cells transformed by the E1A gene of adenovirus type 12.12型腺病毒E1A基因转化细胞被二亚油酰甘油选择性杀伤的机制
Cancer Res. 1989 Oct 15;49(20):5702-7.
3
Selective cytotoxicity of phospholipids and diacylglycerols to rat 3Y1 fibroblasts transformed by adenovirus type 12 or its E1A gene.磷脂和二酰基甘油对腺病毒12型或其E1A基因转化的大鼠3Y1成纤维细胞的选择性细胞毒性。
Cancer Res. 1988 Feb 1;48(3):578-83.
4
Suppression of block to entry into S phase in cell-cycle mutants of rat 3Y1 fibroblasts after transformation by adenovirus type 12.
Virology. 1988 Jul;165(1):57-65. doi: 10.1016/0042-6822(88)90658-7.
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Mutations in the E1a gene of type 5 adenovirus result in oncogenic transformation of Fischer rat embryo cells.5型腺病毒E1a基因的突变导致费希尔大鼠胚胎细胞发生致癌转化。
J Cell Biochem. 1987 Feb;33(2):117-26. doi: 10.1002/jcb.240330206.
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Tumorigenicity of adenovirus-transformed cells: region E1A of adenovirus 12 confers resistance to natural killer cells.腺病毒转化细胞的致瘤性:腺病毒12的E1A区域赋予对自然杀伤细胞的抗性。
Virology. 1985 Dec;147(2):413-21. doi: 10.1016/0042-6822(85)90143-6.
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Suppression of adenovirus type 5 E1A-mediated transformation and expression of the transformed phenotype by caffeic acid phenethyl ester (CAPE).咖啡酸苯乙酯(CAPE)对5型腺病毒E1A介导的转化作用及转化表型表达的抑制
Mol Carcinog. 1991;4(3):231-42. doi: 10.1002/mc.2940040310.
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Highly efficient focus formation by Rous sarcoma virus on adenovirus type 12 E1A-transformed rat 3Y1 cells.劳氏肉瘤病毒在12型腺病毒E1A转化的大鼠3Y1细胞上高效形成病灶。
J Virol. 1992 Mar;66(3):1449-57. doi: 10.1128/JVI.66.3.1449-1457.1992.
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Dissection of overlapping functions within the adenovirus type 5 E1A gene.5型腺病毒E1A基因重叠功能剖析
EMBO J. 1984 Aug;3(8):1907-12. doi: 10.1002/j.1460-2075.1984.tb02066.x.
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Region E1a of highly oncogenic adenovirus 12 in transformed cells protects against NK but not LAK cytolysis.在转化细胞中,高致癌性腺病毒12的E1a区域可抵御自然杀伤细胞(NK)的细胞溶解作用,但对淋巴因子激活的杀伤细胞(LAK)的细胞溶解作用无效。
Virology. 1986 Dec;155(2):644-54. doi: 10.1016/0042-6822(86)90224-2.

引用本文的文献

1
Selective syncytium formation by murine leukemia virus in rat 3Y1 fibroblasts transformed by adenovirus type 12 or its E1A gene.
Arch Virol. 1990;115(1-2):123-6. doi: 10.1007/BF01310628.
2
Adenovirus E1A proteins stimulate inositol phospholipid metabolism in PC12 cells.腺病毒E1A蛋白刺激PC12细胞中的肌醇磷脂代谢。
J Virol. 1992 Oct;66(10):6093-8. doi: 10.1128/JVI.66.10.6093-6098.1992.
3
Highly efficient focus formation by Rous sarcoma virus on adenovirus type 12 E1A-transformed rat 3Y1 cells.劳氏肉瘤病毒在12型腺病毒E1A转化的大鼠3Y1细胞上高效形成病灶。
J Virol. 1992 Mar;66(3):1449-57. doi: 10.1128/JVI.66.3.1449-1457.1992.