Haupt Y, Barri G, Adams J M
Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Victoria, Australia.
Mol Biol Rep. 1992 Nov;17(1):17-20. doi: 10.1007/BF01006395.
The ability of Moloney murine leukemia virus to accelerate lymphomagenesis in E mu-myc transgenic mice is frequently associated with proviral integration within a locus denoted bmi-1. This locus contains not only the bmi-1 gene implicated as a collaborator with myc in lymphomagenesis but also just upstream an unknown gene denoted bup. The nucleotide sequence reported here for bup cDNA and flanking genomic sequences reveals that this widely expressed gene comprises at least 7 exons and potentially encodes a polypeptide of 195 amino acid residues. Computer searches with this polypeptide sequence revealed no close homolog in the databases, nor any conserved motifs, and it is unrelated to the product of the mel-13 gene, which lies just upstream from the bmi-1 homolog mel-18.
莫洛尼鼠白血病病毒在Eμ-myc转基因小鼠中加速淋巴瘤发生的能力，常常与前病毒整合到一个名为bmi-1的基因座内有关。这个基因座不仅包含在淋巴瘤发生中被认为是与myc协同作用的bmi-1基因，而且在其上游还有一个未知基因bup。这里报道的bup cDNA及侧翼基因组序列的核苷酸序列显示，这个广泛表达的基因至少由7个外显子组成，可能编码一个由195个氨基酸残基组成的多肽。用这个多肽序列进行的计算机搜索在数据库中未发现紧密同源物，也未发现任何保守基序，并且它与位于bmi-1同源物mel-18上游的mel-13基因的产物无关。
