| First Author | Harada Y | Year | 2001 |
| Journal | Biochem Biophys Res Commun | Volume | 284 |
| Issue | 3 | Pages | 714-22 |
| PubMed ID | 11396961 | Mgi Jnum | J:72568 |
| Mgi Id | MGI:2153255 | Doi | 10.1006/bbrc.2001.5005 |
| Citation | Harada Y, et al. (2001) A hematopoietic-specific transmembrane protein, Art-1, is possibly regulated by AML1. Biochem Biophys Res Commun 284(3):714-22 |
| abstractText | The functions of AML1 in hematopoietic differentiation are repressed by AML1-mutants including the AML1/ETO chimeric protein, which is seen in t(8;21) acute myeloid leukemia. Erythroid progenitors of the patients with t(8;21) AML expressed AML1/ETO. To investigate the effect of AML1/ETO in erythroid cells, we made a tetracycline-regulated AML1/ETO overexpression system in mouse erythroleukemic (MEL) cells. Enforced AML1/ETO repressed the terminal erythroid differentiation. Furthermore, we performed representational difference analysis using this MEL cell system to clone the downstream targets of AML1 in erythroid cell differentiation. We cloned a novel transmembrane protein, Art-1 (AML1-regulated transmembrane protein 1), which is a member of tetramembrane spanning superfamily. Art-1 expression was restricted in hematopoietic cells. It was upregulated by AML1 and downregulated by AML1/ETO in both erythroid and myeloid cells, and increased during erythroid cell differentiation. Art-1 may play an important role in the differentiation of erythroid cells, possibly as a direct downstream target of AML1. Copyright 2001 Academic Press. |
