ASSIGNMENT OF THE HUMAN MAD AND MXI1 GENES TO CHROMOSOMES 2P12-P13 AND 10Q24-Q25

被引:45
作者
SHAPIRO, DN
VALENTINE, V
EAGLE, L
YIN, XY
MORRIS, SW
PROCHOWNIK, EV
机构
[1] ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL ONCOL, MEMPHIS, TN 38101 USA
[2] ST JUDE CHILDRENS RES HOSP, DEPT EXPTL ONCOL, MEMPHIS, TN 38101 USA
[3] UNIV TENNESSEE, COLL MED, DEPT PEDIAT, MEMPHIS, TN USA
[4] CHILDRENS HOSP PITTSBURGH, HEMATOL ONCOL SECT, PITTSBURGH, PA 15213 USA
[5] UNIV PITTSBURGH, MED CTR, DEPT MOLEC GENET & BIOCHEM, PITTSBURGH, PA 15213 USA
关键词
D O I
10.1006/geno.1994.1496
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
MAD and MXI1, two recently described members of the basic helix-loop-helix (bHLH) gene family, encode proteins that dimerize with and modulate the DNA binding of max. In turn, mad-max or mxi1-max heterodimers or max homodimers can compete for DNA binding sites with dimers formed between max and myc oncoproteins and antagonize the transcriptional activities of this latter class of proteins. Using a combination of somatic cell mapping and fluorescence in situ hybridization techniques, we have determined the chromosomal locations of the MAD and MXI1 genes. The MAD gene maps to chromosome 2p12-p13, a region involved in translocations and deletions in acute and chronic lymphocytic leukemias as well as nonlymphocytic leukemias and Hodgkin disease. The MXI1 gene localizes to chromosome 10q24-q25, a region involved in translocations and deletions in acute and chronic lymphocytic leukemias and prostatic carcinomas. The availability of genomic clones of MAD and MXI1 will permit an assessment of their involvement in these diseases at the molecular level. (C) 1994 Academic Press, Inc.
引用
收藏
页码:282 / 285
页数:4
相关论文
共 23 条
[1]   TRANSCRIPTIONAL ACTIVATION BY THE HUMAN C-MYC ONCOPROTEIN IN YEAST REQUIRES INTERACTION WITH MAX [J].
AMATI, B ;
DALTON, S ;
BROOKS, MW ;
LITTLEWOOD, TD ;
EVAN, GI ;
LAND, H .
NATURE, 1992, 359 (6394) :423-426
[2]   CHROMOSOME STUDY OF 5 CANCERS OF THE PROSTATE [J].
ATKIN, NB ;
BAKER, MC .
HUMAN GENETICS, 1985, 70 (04) :359-364
[3]   MAD - A HETERODIMERIC PARTNER FOR MAX THAT ANTAGONIZES MYC TRANSCRIPTIONAL ACTIVITY [J].
AYER, DE ;
KRETZNER, L ;
EISENMAN, RN .
CELL, 1993, 72 (02) :211-222
[4]  
BIRD ML, 1989, LEUKEMIA, V3, P182
[5]   SEQUENCE-SPECIFIC DNA-BINDING BY THE C-MYC PROTEIN [J].
BLACKWELL, TK ;
KRETZNER, L ;
BLACKWOOD, EM ;
EISENMAN, RN ;
WEINTRAUB, H .
SCIENCE, 1990, 250 (4984) :1149-1151
[6]   MAX - A HELIX-LOOP-HELIX ZIPPER PROTEIN THAT FORMS A SEQUENCE-SPECIFIC DNA-BINDING COMPLEX WITH MYC [J].
BLACKWOOD, EM ;
EISENMAN, RN .
SCIENCE, 1991, 251 (4998) :1211-1217
[7]  
BRITOBABAPULLE V, 1986, BLOOD, V67, P516
[8]   MOUSE CHROMOSOME-19 [J].
GUENET, JL ;
POIRIER, C .
MAMMALIAN GENOME, 1993, 4 :S261-S268
[9]   MAX - FUNCTIONAL DOMAINS AND INTERACTION WITH C-MYC [J].
KATO, GJ ;
LEE, WMF ;
CHEN, LL ;
DANG, CV .
GENES & DEVELOPMENT, 1992, 6 (01) :81-92
[10]   AN AMINO-TERMINAL C-MYC DOMAIN REQUIRED FOR NEOPLASTIC TRANSFORMATION ACTIVATES TRANSCRIPTION [J].
KATO, GJ ;
BARRETT, J ;
VILLAGARCIA, M ;
DANG, CV .
MOLECULAR AND CELLULAR BIOLOGY, 1990, 10 (11) :5914-5920