| First Author | Shapiro DN | Year | 1994 |
| Journal | Genomics | Volume | 23 |
| Issue | 1 | Pages | 282-5 |
| PubMed ID | 7829091 | Mgi Jnum | J:20739 |
| Mgi Id | MGI:68810 | Doi | 10.1006/geno.1994.1496 |
| Citation | Shapiro DN, et al. (1994) Assignment of the human MAD and MXI1 genes to chromosomes 2p12-p13 and 10q24-q25. Genomics 23(1):282-5 |
| abstractText | 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 non-lymphocytic 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. |
