| First Author | Zhang P | Year | 1998 |
| Journal | J Exp Med | Volume | 188 |
| Issue | 6 | Pages | 1173-84 |
| PubMed ID | 9743535 | Mgi Jnum | J:50031 |
| Mgi Id | MGI:1289765 | Doi | 10.1084/jem.188.6.1173 |
| Citation | Zhang P, et al. (1998) Upregulation of interleukin 6 and granulocyte colony-stimulating factor receptors by transcription factor CCAAT enhancer binding protein alpha (C/EBP alpha) is critical for granulopoiesis. J Exp Med 188(6):1173-84 |
| abstractText | Cytokines stimulate granulopoiesis through signaling via receptors whose expression is controlled by lineage- specific transcription factors. Previously, we demonstrated that granulocyte colony-stimulating factor (G- CSF) receptor mRNA was undetectable and granulocyte maturation blocked in CCAAT enhancer binding protein or (C/ EBP alpha)-deficient mice. This phenotype is distinct from that of G-CSF receptor(-/-) mice, suggesting that other genes are likely to be adversely affected by loss of C/EBP alpha. Here we demonstrate loss of interleukin 6 (IL-6) receptor and IL-6-responsive colony-forming units (CFU- IL6) in C/EBP alpha(-/-) mice. The observed failure of granulopoiesis could be rescued by the addition of soluble IL-6 receptor and IL-6 or by retroviral transduction of G- CSF receptors, demonstrating that loss of both of these receptors contributes to the absolute block in granulocyte maturation observed in C/EBP alpha-deficient hematopoietic cells. The results of these and other studies suggest that additional C/EBP alpha target genes, possibly other cytokine receptors, are also important for the block in granulocyte differentiation observed in vivo in C/EBP alpha-deficient mice. |
