| First Author | Byrne JA | Year | 1996 |
| Journal | Genomics | Volume | 35 |
| Issue | 3 | Pages | 523-32 |
| PubMed ID | 8812487 | Mgi Jnum | J:34618 |
| Mgi Id | MGI:82073 | Doi | 10.1006/geno.1996.0393 |
| Citation | Byrne JA, et al. (1996) Definition of the tumor protein D52 (TPD52) gene family through cloning of D52 homologues in human (hD53) and mouse (mD52). Genomics 35(3):523-32 |
| abstractText | Cloning is reported of a cDNA homologue to the breast carcinoma-associated D52 cDNA, termed D53, and of a mouse 052 cDNA (HGMW-approved symbols TPD52L1 and TPD52). Human D53 and mouse D52 proteins are predicted to be 52 and 86% identical to human D52, respectively. Analysis of the three protein se quences identified a coiled-coil domain and N- and C terminally located PEST domains in each, The conservation of homology between the D52 and the D53 sequences, combined with a lack of homology between these and known proteins, defines a new mammalian gene/protein family, the D52 family. The human D52 locus has been previously mapped to chromosome 8q21, and using in situ mapping in the present study, a human D53 locus was mapped to chromosome 6q22-q23. We observed coexpression of the human 052 and D53 genes in some breast tumors and derivative cell lines and found that maintenance of D52 and D53 transcript levels in estrogen receptor-positive MCF7 breast carcinoma cells depends upon estradiol. However, D52 and D53 genes were specifically expressed in HL-60 and K-562 leukemia cells, respectively, with 12-O- tetradecanoylphorbol-13-acetate treatment decreasing D52 and D53 transcript levels in these cell lines. The presence of a coiled-coil domain, combined with observed co- or independent expression of the D52 and D53 genes, suggests that D52 and D53 proteins may be capable of hetero and/or homodimer formation. (C) 1996 Academic Press, Inc. |
