First Author | Yamanaka R | Year | 1997 |
Journal | Proc Natl Acad Sci U S A | Volume | 94 |
Issue | 24 | Pages | 13187-92 |
PubMed ID | 9371821 | Mgi Jnum | J:76024 |
Mgi Id | MGI:2178285 | Doi | 10.1073/pnas.94.24.13187 |
Citation | Yamanaka R, et al. (1997) Impaired granulopoiesis, myelodysplasia, and early lethality in CCAAT/enhancer binding protein epsilon-deficient mice. Proc Natl Acad Sci U S A 94(24):13187-92 |
abstractText | Polymorphonuclear leukocytes are essential for host defense to infectious diseases. CCAAT/enhancer binding protein epsilon (C/EBP epsilon) is preferentially expressed in granulocytes and lymphoid cells. Mice with a null mutation in C/EBP epsilon develop normally and are fertile but fail to generate functional neutrophils and eosinophils. Opportunistic infections and tissue destruction lead to death by 3-5 months of age. Furthermore, end-stage mice develop myelodysplasia, characterized by proliferation of atypical granulocytes that efface the bone marrow and result in severe tissue destruction. Thus, C/EBP epsilon is essential for terminal differentiation and functional maturation of committed granulocyte progenitor cells. |