Premium
cDNA sequence for human bcr, the gene that translocates to the abl oncogene in chronic myeloid leukaemia.
Author(s) -
Hariharan I.K.,
Adams J.M.
Publication year - 1987
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1987.tb04727.x
Subject(s) - biology , complementary dna , breakpoint cluster region , gene , coding region , philadelphia chromosome , chromosomal translocation , genetics , abl , microbiology and biotechnology , breakpoint , tyrosine kinase , signal transduction
The hallmark of human chronic myeloid leukaemia is a 9;22 chromosome translocation that fuses most of the c‐abl oncogene to the 5′ portion of the breakpoint cluster region (bcr) gene, such that a hybrid bcr‐abl mRNA and polypeptide are generated. To clarify further the nature of this translocation, we have analysed the structure of normal human bcr mRNA by isolating large cDNA clones that collectively span the entire coding region and extend 2.6 kb upstream of those previously described. The 3150‐bp nucleotide sequence reported here includes 534 bp of a GC‐rich 5′ non‐coding segment and indicates, in conjunction with published sequences, that the bcr polypeptide comprises 1271 amino acid residues. The predicted polypeptide is unrelated to serine or tyrosine kinases, or indeed to any previously published sequence; its structure provides no evidence of a transmembrane region. Since probes from throughout the 4.8‐kb cloned region hybridized to both the 4.5 and 6.7 kb normal bcr transcripts, both RNAs contain most or all of that region.