| First Author | Sasanuma H | Year | 2004 |
| Journal | Biochem Biophys Res Commun | Volume | 321 |
| Issue | 1 | Pages | 145-53 |
| PubMed ID | 15358227 | Mgi Jnum | J:91299 |
| Mgi Id | MGI:3046407 | Doi | 10.1016/j.bbrc.2004.06.126 |
| Citation | Sasanuma H, et al. (2004) Transcriptional regulation of SLP-76 family hematopoietic cell adaptor MIST/Clnk by STAT5. Biochem Biophys Res Commun 321(1):145-53 |
| abstractText | SLP-76-related adaptor protein MIST (also called Clnk) is expressed in a variety of cytokine-dependent hematopoietic cell lines of myeloid and lymphoid origin as well as some cytokine-independent mast cell lines. To understand the molecular mechanisms underlying the MIST gene expression, we have characterized the 5'-flanking region of the mouse MIST gene. We have identified an enhancer region (-773 to -709), which is active in P815 mast cells expressing the endogenous MIST gene, but not in EL-4 T cells lacking MIST expression. Outside of this enhancer region, one STAT element present in the MIST promoter (-44 to -36) was found to bind STAT5A when IC-2 mast cells were stimulated with IL-3. Mutation of this STAT element did not affect basal MIST promoter activity in P815 mast cells, but was required for STAT5-mediated activation of the MIST promoter. Furthermore, endogenous MIST gene expression was induced in mast cells by a constitutively activated form of STAT5A, but not by an active mutant of c-Kit receptor. These findings suggest that STAT5 is involved in cytokine-mediated up-regulation of MIST gene expression, probably in collaboration with other lineage-specific transcription factors that promote basal MIST expression in mast cells. |
