Abstract
C/EBPα and PU.1 are key regulators of early myeloid development. Mice lacking C/EBPα or PU.1 have reduced granulocytes and monocytes. Consistent with a model in which induction of PU.1 by C/EBPα contributes to monocyte lineage specification, mice with reduced PU.1 have diminished monocytes but retain granulocytes, C/EBPα directly activates PU.1 gene transcription, and exogenous C/EBPα increases monocytic lineage commitment from bipotential myeloid progenitors. In addition to C/EBPα, AP-1 proteins also have the capacity to induce monocytic maturation. C/EBPα:c-Jun or C/EBPα:c-Fos leucine zipper heterodimers induce monopoiesis more potently than C/EBPα or c-Jun homodimers or c-Fos:c-Jun heterodimers. C/EBPs and NF-κB cooperatively regulate numerous genes during the inflammatory response. The C/EBPα basic region interacts with NF-κB p50, but not p65, to induce bcl-2, and this interaction may be relevant to myeloid cell survival and development.
Original language | English (US) |
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Pages (from-to) | 340-343 |
Number of pages | 4 |
Journal | Blood Cells, Molecules, and Diseases |
Volume | 39 |
Issue number | 3 |
DOIs | |
State | Published - Nov 2007 |
Keywords
- C/EBPα
- Myeloid
- NF-κB
- PU.1
- c-Jun
ASJC Scopus subject areas
- Molecular Medicine
- Molecular Biology
- Hematology
- Cell Biology