MOLECULAR ASPECTS OF COLON EPITHELIUM DIFFERENTIATION AND TUMOR FORMATION
MOLECULAR ASPECTS OF COLON EPITHELIUM DIFFERENTIATION AND TUMOR FORMATION
批准号:
3752747
负责人:
J LAUTENBERGER
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至
关键词:
DNA binding protein cell differentiation cell growth regulation colon neoplasms complementary DNA conformation epithelium gene expression human tissue messenger RNA molecular oncology mutant neoplasm /cancer genetics neoplastic transformation oncogenes open reading frames protein structure protein structure function ribosomal proteins tissue /cell culture transfection tumor suppressor genes
中文摘要
我们报道了用差异杂交技术分离到的一条cdna。
分化和未分化的结肠癌细胞。这部小说
转录本,CORI-1,是对基因5‘非翻译区的补充
Krev-1抑癌基因mRNA.CORI-1mRNA有一个开放阅读框架,
编码一种与大鼠S29核糖体蛋白相同的蛋白质。这
蛋白质有一个潜在的锌指基序,由四个半胱氨酸组成
残留物。为了检测蛋白质的生物学功能,
在大肠杆菌中合成的突变的Cori-1蛋白被固定在膜上
变性后与55Zn孵育。只有野生型的
用55Zn标记,表明这种形式的蛋白质,而不是
突变形式,可能采取锌指构象。野生型和
将突变的Cori-1基因插入到表达载体中,
转染HT1080人纤维肉瘤细胞。在HT1080细胞中
转导突变型Cori-1后,细胞的体内外生长均明显增强
与仅转载体的细胞相比,其表达增强。论
另一方面,细胞在体外和体内的生长在以下情况下并没有得到促进
介绍了野生型CORI-1。KREV-1 AS的表达
由mRNA或蛋白质决定的基因不会因导入而改变。
野生型或突变型Cori-1导入HT1080细胞。这些结果
提示内源性CORI-1的反显性抑制
基因突变型促进细胞生长和致癌
表型。突变体Cori-1的这一功能是由
干扰依赖于锌指结构域的功能而不需要
影响krev-1的表达。
英文摘要
We have reported a cDNA isolated by differential hybridization between
differentiated and undifferentiated colon carcinoma cells. The novel
transcript, cori-1, is complementary to the 5' untranslated region of the
krev-1 anti-oncogene mRNA. Cori-1 mRNA has an open reading frame which
encodes a protein identical with the rat S29 ribosomal protein. This
protein has a potential zinc finger motif consisting of four cysteine
residues. In order to examine the biological function of the protein,
mutant cori-1 proteins synthesized in E. coli were fixed on a membrane
and incubated with 55Zn after denaturation. Only the wild type was
labeled with 55Zn, indicating that this form of the protein, but not the
mutant form, may take a zinc finger conformation. The wild type and
mutant cori-1 genes were inserted into an expression vector and
transfected into HT1080 human fibrosarcoma cells. In HT1080 cells
transfected with mutant cori-1, both in vitro and in vivo cell growth was
enhanced compared with the cells transfected with vector only. On the
other hand, cell growth both in vitro and in vivo was not enhanced when
the wild type cori-1 was introduced. The expression of krev-1 as
determined by either mRNA or protein was not changed by introducing
either wild type or mutant cori-1 into HT1080 cells. These results
suggest that the trans-dominant suppression of endogenous cori-1 by the
mutant form of the gene enhanced cell growth and the tumorigenic
phenotype. This function of the mutant cori-1 is conferred by
interfering with a function dependent on the zinc finger domain without
affecting krev-1 expression.
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会议论文
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批准号:3916926
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项目类别:
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资助金额:$0.0万
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财政年份:--
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负责人:J LAUTENBERGER
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依托单位:
BIOCHEMICAL AND FUNCTIONAL PROPERTIES OF THE ETS PROTO-ONCOGENES
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批准号:5201515
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项目类别:
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资助金额:$0.0万
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负责人:J LAUTENBERGER
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TUMOR SUPPRESSOR ACTIVITIES OF ETS1 GENE PRODUCTS
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项目类别:
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负责人:J LAUTENBERGER
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依托单位:
TRANSGENIC MOUSE MODEL SYSTEM FOR THE ETS-1 AND ETS-2 PROTO-ONCOGENE FUNCTION
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批准号:5201517
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项目类别:
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资助金额:$0.0万
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财政年份:--
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负责人:J LAUTENBERGER
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依托单位:
海外基金