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An optimum dose of c-H-ras is a prerequisite for hormone-dependent conversion of a cell between cancerous and normal states in tissue culture.

作者信息

Xu Z Z, Miyahara K, Liszczynsky H, Seno S, Naora H

机构信息

Research School of Biological Sciences, Australian National University, Canberra, A.C.T.

出版信息

Cell Biol Int Rep. 1991 Jul;15(7):595-606. doi: 10.1016/0309-1651(91)90006-5.

DOI:10.1016/0309-1651(91)90006-5
PMID:1657409
Abstract

We have established a few cell lines which can be reversibly converted from cancerous to normal and vice versa by the addition to, or removal from the culture medium of glucocorticoid hormone. These cell lines were derived from mouse NIH 3T3 cells and possessed the integrated gene pairs on chromosomes, which are composed of human mutated c-H-ras fused with mouse mammary tumour virus long terminal repeat and E. coli xanthine-guanine phosphoribosyltransferase gene with the SV40 promoter. We have characterised these cell lines in order to elucidate an essential requirement for the conversion of the state of a cell. It was found that the presence of at least two to three copies of the gene pair per diploid genome are essential. An approximate threshold level of c-H-ras 1.6 kb RNA required for reversible conversion was estimated.

摘要

相似文献

1
An optimum dose of c-H-ras is a prerequisite for hormone-dependent conversion of a cell between cancerous and normal states in tissue culture.
Cell Biol Int Rep. 1991 Jul;15(7):595-606. doi: 10.1016/0309-1651(91)90006-5.
2
Gene ecology: a cis-acting gene-to-gene interaction due to the spatial arrangement of genes in chromosomes affects neighbouring transfected c-H-ras expression.基因生态学:由于染色体中基因的空间排列而导致的顺式作用基因与基因之间的相互作用影响相邻转染的c-H-ras表达。
Chromosome Res. 1994 May;2(3):171-83. doi: 10.1007/BF01553317.
3
Tumor-promoting phorbol ester and ras oncogene expression inhibit the glucocorticoid-dependent transcription from the mouse mammary tumor virus long terminal repeat.促肿瘤佛波酯和ras癌基因的表达抑制了来自小鼠乳腺肿瘤病毒长末端重复序列的糖皮质激素依赖性转录。
Mol Endocrinol. 1989 Oct;3(10):1659-65. doi: 10.1210/mend-3-10-1659.
4
The v-mos and H-ras oncogene expression represses glucocorticoid hormone-dependent transcription from the mouse mammary tumor virus LTR.
EMBO J. 1986 Oct;5(10):2609-16. doi: 10.1002/j.1460-2075.1986.tb04541.x.
5
Glucocorticoid dexamethasone reversibly complements EJ-RAS oncogene to transform mouse embryo BALB-3T3 cells.糖皮质激素地塞米松可逆转补充EJ-RAS癌基因,从而使小鼠胚胎BALB-3T3细胞发生转化。
J Cell Biochem. 1989 Dec;41(4):171-7. doi: 10.1002/jcb.240410402.
6
Expression and phenotypic alterations caused by an inducible transforming ras oncogene introduced into rat liver epithelial cells.导入大鼠肝上皮细胞的可诱导转化型ras癌基因所引起的表达及表型改变。
Oncogene. 1988 Sep;3(3):245-56.
7
Differential growth factor expression in transformed mouse NIH-3T3 cells.转化的小鼠NIH-3T3细胞中生长因子的差异表达。
J Cell Biochem. 1990 Jan;42(1):45-57. doi: 10.1002/jcb.240420105.
8
Cooperation between structural elements in hormono-regulated transcription from the mouse mammary tumor virus promoter.来自小鼠乳腺肿瘤病毒启动子的激素调节转录中结构元件之间的合作。
Nucleic Acids Res. 1991 Apr 11;19(7):1563-9. doi: 10.1093/nar/19.7.1563.
9
Glucocorticoid receptor-dependent disruption of a specific nucleosome on the mouse mammary tumor virus promoter is prevented by sodium butyrate.丁酸钠可防止糖皮质激素受体依赖性对小鼠乳腺肿瘤病毒启动子上特定核小体的破坏。
Proc Natl Acad Sci U S A. 1990 May;87(10):3977-81. doi: 10.1073/pnas.87.10.3977.
10
Plasmid rescue of an oncogenic sequence containing a mouse mammary tumor virus gene.包含小鼠乳腺肿瘤病毒基因的致癌序列的质粒拯救
Anticancer Res. 1994 Mar-Apr;14(2A):597-601.

引用本文的文献

1
Altered cellular responses by varying expression of a ribosomal protein gene: sequential coordination of enhancement and suppression of ribosomal protein S3a gene expression induces apoptosis.通过改变核糖体蛋白基因的表达来改变细胞反应:核糖体蛋白S3a基因表达增强与抑制的顺序协调诱导细胞凋亡。
J Cell Biol. 1998 May 4;141(3):741-53. doi: 10.1083/jcb.141.3.741.
2
Gene ecology: a cis-acting gene-to-gene interaction due to the spatial arrangement of genes in chromosomes affects neighbouring transfected c-H-ras expression.基因生态学:由于染色体中基因的空间排列而导致的顺式作用基因与基因之间的相互作用影响相邻转染的c-H-ras表达。
Chromosome Res. 1994 May;2(3):171-83. doi: 10.1007/BF01553317.