GENE FOR LYMPHOID ENHANCER-BINDING FACTOR-I (LEF1) MAPPED TO HUMAN CHROMOSOME-4 (Q23-Q25) AND MOUSE CHROMOSOME-3 NEAR EGF

GENE FOR LYMPHOID ENHANCER-BINDING FACTOR-I (LEF1) MAPPED TO HUMAN CHROMOSOME-4 (Q23-Q25) AND MOUSE CHROMOSOME-3 NEAR EGF
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DOI:
10.1016/0888-7543(91)90030-i
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发表时间:
1991-12-01
期刊:
影响因子:
4.4
通讯作者:
FRANCKE, U
FRANCKE, U
中科院分区:
生物学3区
文献类型:
--
作者:
MILATOVICH, A;TRAVIS, A;FRANCKE, U

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Lef-1是一种54 kDa的核蛋白,在前B细胞和T细胞中特异表达。它与T细胞受体α增强子中的一个重要功能部位结合,有助于发挥最大的增强子活性。Lef-1是与高迁移率族蛋白1(HMG1)同源的调节蛋白家族的成员。LEF1基因在人类和小鼠染色体上的位置是通过使用小鼠cDNA探针对种间体细胞杂交的DNA进行Southern印迹分析来确定的。在所有保留了人类染色体区域4cen-q31.2的体细胞杂交中都检测到了人类特有的DNA片段。与生物素标记的两个重叠的人类基因组宇宙进行荧光原位杂交,发现在4q23-q25处有特异的杂交信号。通过对啮齿动物×小鼠杂交细胞DNA的Southern分析,将小鼠的同源基因定位在3号染色体上。利用重组近交系小鼠品系的限制性片段长度多态性(RFLP)证实了这一染色体定位。RFLP分析的结果表明,小鼠Lef-1基因与Pmv-39和Egf紧密连锁,可能位于这两个基因座之间,这两个基因都被定位到小鼠3号染色体的远端。我们的定位结果没有表明该基因参与了先前定位的遗传疾病或已知的肿瘤相关易位断裂点。
LEF-1 is a 54-kDa nuclear protein that is expressed specifically in pre-B and T-cells. It binds to a functionally important site in the T-cell receptor α enhancer and contributes to maximal enhancer activity. LEF-1 is a member of a family of regulatory proteins that share homology with the high mobility group protein 1 (HMG1). The location of the LEF1 gene on human and mouse chromosomes was determined by Southern blot analysis of DNA from panels of interspecies somatic cell hybrids using a murine cDNA probe. Human-specific DNA fragments were detected in all somatic cell hybrids that retained the human chromosomal region 4cen-q31.2. Fluorescentin situhybridization with two biotin-labeled overlapping human genomic cosmids revealed a specific hybridization signal at 4q23-q25. The homologous locus in the mouse was mapped to chromosome 3 by Southern analysis of rodent × mouse hybrid cell DNA. This chromosomal location was confirmed by the use of a restriction fragment length polymorphism (RFLP) in recombinant inbred mouse strains. The results of this RFLP analysis indicated that the mouseLef-1gene was closely linked toPmv-39andEgfand was likely placed between these loci, both of which were previously mapped to distal mouse chromosome 3. Our mapping results did not suggest involvement of this gene in previously mapped genetic disorders or in known neoplasia-associated translocation breakpoints.