Abnormal Stat Activation, Hematopoietic Homeostasis, and Innate Immunity in c-fes−/− Mice
- 1 September 2000
- Vol. 13 (3) , 397-407
- https://doi.org/10.1016/s1074-7613(00)00039-x
Abstract
No abstract availableKeywords
Funding Information
- National Institutes of Health
This publication has 61 references indexed in Scilit:
- PU.1 and Spi-B Are Required for Normal B Cell Receptor–Mediated Signal TransductionImmunity, 1999
- Overexpression of HOXB3 in Hematopoietic Cells Causes Defective Lymphoid Development and Progressive MyeloproliferationImmunity, 1997
- Co-expression with BCR Induces Activation of the FES Tyrosine Kinase and Phosphorylation of Specific N-terminal BCR Tyrosine ResiduesPublished by Elsevier ,1996
- PU.1 is not essential for early myeloid gene expression but is required for terminal myeloid differentiationImmunity, 1995
- Phosphorylation of a Fes-related Protein in Response to Granulocyte-Macrophage Colony Stimulating FactorPublished by Elsevier ,1995
- Antisense Strategies to Characterize the Role of Genes and Oncogenes Involved in Myeloid DifferentiationaAnnals of the New York Academy of Sciences, 1992
- Leukocyte-endothelial cell recognition: Three (or more) steps to specificity and diversityPublished by Elsevier ,1991
- Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogeneCell, 1991
- CYTOKINES: COORDINATORS OF IMMUNE AND INFLAMMATORY RESPONSESAnnual Review of Biochemistry, 1990
- Appearance of membrane-bound tyrosine kinase during differentiation of HL-60 leukemia cells by immune interferon and tumor necrosis factorBiochemical and Biophysical Research Communications, 1986