Genomic structure and chromosomal localization of GML (GPI-anchored molecule-like protein), a gene induced by p53

被引:28
作者
Kimura, Y
Furuhata, T
Urano, T
Hirata, K
Nakamura, Y
Tokino, T
机构
[1] UNIV TOKYO,INST MED SCI,MOL MED LAB,MINTO KU,TOKYO 108,JAPAN
[2] SAPPORO MED UNIV,DEPT SURG 1,SAPPORO,HOKKAIDO 060,JAPAN
关键词
D O I
10.1006/geno.1997.4680
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Among its known functions, tumor suppressor gene p53 serves as a transcriptional regulator and mediates various signals through activation of downstream genes, We recently identified a novel gene, GML (glycosylphosphatidylinositol (GPI)-anchored molecule-like protein), whose expression is specifically induced by wildtype p53, To characterize the GML gene further, we determined 35.8 kb of DNA sequence that included a consensus binding sequence for p53 and the entire GML gene. The GML gene consists of four exons, and the p53-binding sequence is present in the 5'-flanking region. in genomic organization this gene resembles genes encoding murine Ly-6 glycoproteins, a human homologue of the Ly-6 family called RIG-E, and CD59; products of these genes, known as GPI-anchored proteins, are variously involved in signal transduction, cell-cell adhesion, and cell-matrix attachment. FISH analysis revealed that the GML gene is located on human chromosome 8q24.3. Genes encoding at least two other GPI-anchored molecules, E48 and RIG-E, are also located in this region. (C) 1997 Academic Press.
引用
收藏
页码:477 / 480
页数:4
相关论文
共 20 条
[1]   HERPESVIRUS SAIMIRI HAS A GENE SPECIFYING A HOMOLOG OF THE CELLULAR MEMBRANE GLYCOPROTEIN CD59 [J].
ALBRECHT, JC ;
NICHOLAS, J ;
CAMERON, KR ;
NEWMAN, C ;
FLECKENSTEIN, B ;
HONESS, RW .
VIROLOGY, 1992, 190 (01) :527-530
[2]  
BOTHWELL A, 1988, J IMMUNOL, V140, P2815
[3]   THE HUMAN E48 ANTIGEN, HIGHLY HOMOLOGOUS TO THE MURINE LY-6 ANTIGEN THB, IS A GPI-ANCHORED MOLECULE APPARENTLY INVOLVED IN KERATINOCYTE CELL-CELL ADHESION [J].
BRAKENHOFF, RH ;
GERRETSEN, M ;
KNIPPELS, EMC ;
VANDIJK, M ;
VANESSEN, H ;
WEGHUIS, DO ;
SINKE, RJ ;
SNOW, GB ;
VANDONGEN, GAMS .
JOURNAL OF CELL BIOLOGY, 1995, 129 (06) :1677-1689
[4]   PREVENTION OF METASTASIS BY INHIBITION OF THE UROKINASE RECEPTOR [J].
CROWLEY, CW ;
COHEN, RL ;
LUCAS, BK ;
LIU, GH ;
SHUMAN, MA ;
LEVINSON, AD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (11) :5021-5025
[5]   DEFINITION OF A CONSENSUS BINDING-SITE FOR P53 [J].
ELDEIRY, WS ;
KERN, SE ;
PIETENPOL, JA ;
KINZLER, KW ;
VOGELSTEIN, B .
NATURE GENETICS, 1992, 1 (01) :45-49
[6]  
ELDEIRY WS, 1995, CANCER RES, V55, P2910
[7]  
FLEMING TJ, 1993, J IMMUNOL, V150, P5379
[8]  
GUMLEY TP, 1992, J IMMUNOL, V149, P2615
[9]  
GURUHATA T, 1996, ONCOGENE, V13, P1965
[10]   P53 MUTATIONS IN HUMAN CANCERS [J].
HOLLSTEIN, M ;
SIDRANSKY, D ;
VOGELSTEIN, B ;
HARRIS, CC .
SCIENCE, 1991, 253 (5015) :49-53