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病毒mos癌基因产物对胶原蛋白基因启动子的调控

Regulation of a collagen gene promoter by the product of viral mos oncogene.

作者信息

Schmidt A, Setoyama C, de Crombrugghe B

出版信息

Nature. 1985;314(6008):286-9. doi: 10.1038/314286a0.

DOI:10.1038/314286a0
PMID:2984572
Abstract

Oncogenic transformation of cells produces important changes in the biosynthetic pattern of certain cellular proteins. For example, the synthesis of type I collagen in transformed fibroblasts is severely reduced as a result of changes in transcription. Here we report the results of DNA-mediated transfection experiments using recombinant plasmids in which the promoter region of the alpha 2(I) collagen gene is fused to an easily recognizable marker gene, and cell lines expressing the marker gene are isolated. Our data show that the expression of the marker gene fused to the cloned alpha 2(I) collagen promoter is strongly inhibited by v-mos transformation, suggesting that a common mechanism inhibits both the transfected and endogeneous alpha 2(I) collagen promoters.

摘要

细胞的致癌转化会使某些细胞蛋白质的生物合成模式发生重要变化。例如,由于转录变化,转化的成纤维细胞中I型胶原蛋白的合成会严重减少。在此,我们报告了使用重组质粒进行DNA介导的转染实验的结果,其中α2(I)胶原蛋白基因的启动子区域与一个易于识别的标记基因融合,并分离出表达该标记基因的细胞系。我们的数据表明,与克隆的α2(I)胶原蛋白启动子融合的标记基因的表达受到v-mos转化的强烈抑制,这表明存在一种共同机制抑制转染的和内源性的α2(I)胶原蛋白启动子。

相似文献

1
Regulation of a collagen gene promoter by the product of viral mos oncogene.病毒mos癌基因产物对胶原蛋白基因启动子的调控
Nature. 1985;314(6008):286-9. doi: 10.1038/314286a0.
2
A common cellular pathway for v-mos and v-Ki-ras is not required for v-Ki-ras-induced tumorigenicity in a nonmalignant, v-mos-expressing revertant cell.在一个非恶性的、表达v-mos的回复细胞中,v-Ki-ras诱导的致瘤性并不需要v-mos和v-Ki-ras的共同细胞途径。
Mol Carcinog. 1990;3(2):103-13. doi: 10.1002/mc.2940030208.
3
Persistent expression of v-mos oncogene in transformed cells that revert to nonmalignancy after prolonged treatment with interferon.在用干扰素长时间处理后恢复为非恶性的转化细胞中v-mos癌基因的持续表达。
Proc Natl Acad Sci U S A. 1986 Aug;83(16):5764-8. doi: 10.1073/pnas.83.16.5764.
4
Functions of the mos oncogene family and associated gene products.mos癌基因家族及相关基因产物的功能。
Cancer Surv. 1986;5(2):243-55.
5
Coordinate regulation of the levels of type III and type I collagen mRNA in most but not all mouse fibroblasts.大多数(但并非所有)小鼠成纤维细胞中III型和I型胶原蛋白mRNA水平的协调调节。
J Biol Chem. 1985 Jan 10;260(1):531-6.
6
Long terminal repeat sequences impart hematopoietic transformation properties to the myeloproliferative sarcoma virus.长末端重复序列赋予骨髓增殖性肉瘤病毒造血转化特性。
Proc Natl Acad Sci U S A. 1985 Sep;82(17):5746-50. doi: 10.1073/pnas.82.17.5746.
7
Viral transfer, transcription, and rescue of a selectable myeloproliferative sarcoma virus in embryonal cell lines: expression of the mos oncogene.在胚胎细胞系中可选择的骨髓增殖性肉瘤病毒的病毒转移、转录及拯救:mos癌基因的表达
Mol Cell Biol. 1986 Jan;6(1):286-93. doi: 10.1128/mcb.6.1.286-293.1986.
8
Transformation of diploid human fibroblasts by DNA transfection with the v-sis oncogene.用v-sis癌基因通过DNA转染使二倍体人类成纤维细胞发生转化。
J Cell Physiol. 1986 Aug;128(2):313-21. doi: 10.1002/jcp.1041280225.
9
A threshold effect in the induction of tumorigenicity of an established human cell line by v-mos.v-mos对一种已建立的人类细胞系致瘤性诱导中的阈值效应。
Oncogene. 1988 Sep;3(3):295-9.
10
Differential transformation of C3H10T1/2 cells by v-mos: sequential expression of transformation parameters.v-mos对C3H10T1/2细胞的差异转化:转化参数的顺序表达
Mol Cell Biol. 1985 Sep;5(9):2204-11. doi: 10.1128/mcb.5.9.2204-2211.1985.

引用本文的文献

1
Assembly of cartilage collagen fibrils is disrupted by overexpression of normal type II collagen in transgenic mice.在转基因小鼠中,正常II型胶原蛋白的过表达会破坏软骨胶原纤维的组装。
Proc Natl Acad Sci U S A. 1993 May 1;90(9):3825-9. doi: 10.1073/pnas.90.9.3825.
2
Transcriptional control of the mouse alpha 2(I) collagen gene: functional deletion analysis of the promoter and evidence for cell-specific expression.小鼠α2(I)型胶原基因的转录调控:启动子的功能缺失分析及细胞特异性表达的证据
Mol Cell Biol. 1986 Feb;6(2):347-54. doi: 10.1128/mcb.6.2.347-354.1986.
3
Formation of a type I collagen RNA dimer by intermolecular base-pairing of a conserved sequence around the translation initiation site.
通过翻译起始位点周围保守序列的分子间碱基配对形成I型胶原RNA二聚体。
Nucleic Acids Res. 1987 Nov 11;15(21):8935-56. doi: 10.1093/nar/15.21.8935.
4
Regulatory elements in the first intron contribute to transcriptional control of the human alpha 1(I) collagen gene.第一个内含子中的调控元件有助于人类α1(I)型胶原蛋白基因的转录控制。
Proc Natl Acad Sci U S A. 1987 Dec;84(24):8869-73. doi: 10.1073/pnas.84.24.8869.
5
Interferons increase transcription of a major histocompatibility class I gene via a 5' interferon consensus sequence.干扰素通过一个5'干扰素共有序列增加主要组织相容性复合体I类基因的转录。
Mol Cell Biol. 1987 Jul;7(7):2625-30. doi: 10.1128/mcb.7.7.2625-2630.1987.
6
Introduction of the human pro alpha 1(I) collagen gene into pro alpha 1(I)-deficient Mov-13 mouse cells leads to formation of functional mouse-human hybrid type I collagen.将人类原α1(I)胶原蛋白基因导入缺乏原α1(I)的Mov-13小鼠细胞中,可导致功能性小鼠-人类杂合I型胶原蛋白的形成。
Proc Natl Acad Sci U S A. 1987 Feb;84(3):764-8. doi: 10.1073/pnas.84.3.764.
7
Developmental and tissue-specific expression directed by the alpha 2 type I collagen promoter in transgenic mice.α2 I型胶原启动子在转基因小鼠中指导的发育和组织特异性表达。
Proc Natl Acad Sci U S A. 1986 Feb;83(3):725-9. doi: 10.1073/pnas.83.3.725.
8
Deletion analysis of the mouse alpha 1(III) collagen promoter.小鼠α1(III)胶原启动子的缺失分析
Nucleic Acids Res. 1988 Aug 11;16(15):7513-26. doi: 10.1093/nar/16.15.7513.
9
Regulation of type VI collagen synthesis in transformed mesenchymal cells.转化间充质细胞中VI型胶原蛋白合成的调控
Biochem J. 1988 Jul 15;253(2):381-6. doi: 10.1042/bj2530381.
10
Neoplastic transformation inactivates specific trans-acting factor(s) required for the expression of the thyroglobulin gene.肿瘤转化使甲状腺球蛋白基因表达所需的特定反式作用因子失活。
Proc Natl Acad Sci U S A. 1988 Mar;85(6):1744-8. doi: 10.1073/pnas.85.6.1744.