|  Help  |  About  |  Contact Us

Publication : Cloning and characterization of the human interleukin-3 (IL-3)/IL-5/ granulocyte-macrophage colony-stimulating factor receptor betac gene: regulation by Ets family members.

First Author  van Dijk TB Year  1998
Journal  Blood Volume  92
Issue  10 Pages  3636-46
PubMed ID  9808557 Mgi Jnum  J:50954
Mgi Id  MGI:1313079 Doi  10.1182/blood.v92.10.3636.422k45_3636_3646
Citation  van Dijk TB, et al. (1998) Cloning and characterization of the human interleukin-3 (IL-3)/IL-5/granulocyte-macrophage colony-stimulating factor receptor betac gene: regulation by Ets family members. Blood 92(10):3636-46
abstractText  High-affinity receptors for interleukin-3 (IL-3), IL-5, and granulocyte-macrophage colony-stimulating factor (GM-CSF) are composed of two distinct subunits, a ligand-specific chain and a common beta chain (betac). Whereas the mouse has two homologous beta subunits (betac and betaIL-3), in humans, only a single beta chain is identified. We describe here the isolation and characterization of the gene encoding the human IL-3/IL-5/GM-CSF receptor beta subunit. The gene spans about 25 kb and is divided into 14 exons, a structure very similar to that of the murine betac/ betaIL-3 genes. Surprisingly, we also found the remnants of a second betac chain gene directly downstream of betac. We identified a functional promoter that is active in the myeloid cell lines U937 and HL-60, but not in HeLa cells. The proximal promoter region, located from -103 to +33 bp, contains two GGAA consensus binding sites for members of the Ets family. Single mutation of those sites reduces promoter activity by 70% to 90%. The 5' element specifically binds PU.1, whereas the 3' element binds a yet-unidentified protein. These findings, together with the observation that cotransfection of PU.1 and other Ets family members enhances betac promoter activity in fibroblasts, reinforce the notion that GGAA elements play an important role in myeloid-specific gene regulation.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression