Intrinsic requirement for zinc finger transcription factor Gfi-1 in neutrophil differentiation.

[1]  M. Minden,et al.  Heterozygous PU.1 mutations are associated with acute myeloid leukemia. , 2002, Blood.

[2]  A. Friedman.  Transcriptional regulation of granulocyte and monocyte development , 2002, Oncogene.

[3]  S. Cameron,et al.  The zinc-finger proto-oncogene Gfi-1b is essential for development of the erythroid and megakaryocytic lineages. , 2002, Genes & development.

[4]  Hui Zeng,et al.  Inflammatory reactions and severe neutropenia in mice lacking the transcriptional repressor Gfi1 , 2002, Nature Genetics.

[5]  M. Minden,et al.  Heterozygous PU.1 mutations are associated with acute myeloid leukemia. , 2002, Blood.

[6]  H. Nakajima,et al.  Granulocyte colony-stimulating factor regulates myeloid differentiation through CCAAT/enhancer-binding protein epsilon. , 2001, Blood.

[7]  H P Koeffler,et al.  Neutrophil-specific granule deficiency: homozygous recessive inheritance of a frameshift mutation in the gene encoding transcription factor CCAAT/enhancer binding protein--epsilon. , 2001, Blood.

[8]  J. Lekstrom-Himes.  The Role of C/EBPε in the Terminal Stages of Granulocyte Differentiation , 2001 .

[9]  Pu Zhang,et al.  Dominant-negative mutations of CEBPA, encoding CCAAT/enhancer binding protein-α (C/EBPα), in acute myeloid leukemia , 2001, Nature Genetics.

[10]  J. Cowland,et al.  Regulation of human neutrophil granule protein expression. , 2001, Current opinion in hematology.

[11]  J. Lekstrom‐Himes,et al.  The role of C/EBP(epsilon) in the terminal stages of granulocyte differentiation. , 2001, Stem cells.

[12]  G. Behre,et al.  Dominant-negative mutations of CEBPA, encoding CCAAT/enhancer binding protein-alpha (C/EBPalpha), in acute myeloid leukemia. , 2001, Nature genetics.

[13]  J. Ihle,et al.  Granulocyte colony-stimulating factor regulates myeloid differentiation through CCAAT/enhancer-binding protein e , 2001 .

[14]  Stuart H. Orkin,et al.  Diversification of haematopoietic stem cells to specific lineages , 2000, Nature Reviews Genetics.

[15]  C. Klein,et al.  Comparative Analysis of Genetically Modified Dendritic Cells and Tumor Cells as Therapeutic Cancer Vaccines , 2000, The Journal of experimental medicine.

[16]  I. Weissman,et al.  A clonogenic common myeloid progenitor that gives rise to all myeloid lineages , 2000, Nature.

[17]  J. Lekstrom‐Himes,et al.  CCAAT/Enhancer Binding Protein ɛ Is Critical for Effective Neutrophil-Mediated Response to Inflammatory Challenge , 1999 .

[18]  Pu Zhang,et al.  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. , 1998 .

[19]  T. Möröy,et al.  Evidence implicating Gfi‐1 and Pim‐1 in pre‐T‐cell differentiation steps associated with β‐selection , 1998, The EMBO journal.

[20]  F. Pio,et al.  Neutrophils deficient in PU.1 do not terminally differentiate or become functionally competent. , 1998, Blood.

[21]  J. Walsh,et al.  PU.1 regulates both cytokine‐dependent proliferation and differentiation of granulocyte/macrophage progenitors , 1998, The EMBO journal.

[22]  D. Tenen,et al.  CCAAT/Enhancer Binding Protein α Is a Regulatory Switch Sufficient for Induction of Granulocytic Development from Bipotential Myeloid Progenitors , 1998, Molecular and Cellular Biology.

[23]  S. Mckercher,et al.  Use of RDA analysis of knockout mice to identify myeloid genes regulated in vivo by PU.1 and C/EBPalpha. , 1998, Nucleic acids research.

[24]  Tong-Yuan Yang,et al.  The Gfi-1B Proto-Oncoprotein Repressesp21WAF1 and Inhibits Myeloid Cell Differentiation , 1998, Molecular and Cellular Biology.

[25]  C. Barlow,et al.  Impaired granulopoiesis, myelodysplasia, and early lethality in CCAAT/enhancer binding protein epsilon-deficient mice. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[26]  J. Licht,et al.  Transcription factors, normal myeloid development, and leukemia. , 1997, Blood.

[27]  D. Tenen,et al.  CCAAT/enhancer binding protein epsilon is preferentially up-regulated during granulocytic differentiation and its functional versatility is determined by alternative use of promoters and differential splicing. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[28]  D. Tenen,et al.  Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein alpha-deficient mice. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[29]  P. Tsichlis,et al.  The Gfi-1 proto-oncoprotein contains a novel transcriptional repressor domain, SNAG, and inhibits G1 arrest induced by interleukin-2 withdrawal , 1996, Molecular and cellular biology.

[30]  A. Feeney,et al.  Targeted disruption of the PU.1 gene results in multiple hematopoietic abnormalities. , 1996, The EMBO journal.

[31]  P. Tsichlis,et al.  Gfi-1 encodes a nuclear zinc finger protein that binds DNA and functions as a transcriptional repressor , 1996, Molecular and cellular biology.

[32]  I. Weissman,et al.  Flow cytometric identification of murine neutrophils and monocytes. , 1996, Journal of immunological methods.

[33]  E. Scott,et al.  Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages. , 1994, Science.

[34]  H. Rosenberg,et al.  Neutrophil-specific granule deficiency includes eosinophils. , 1993, Blood.

[35]  A. Zlotnik,et al.  A developmental pathway involving four phenotypically and functionally distinct subsets of CD3-CD4-CD8- triple-negative adult mouse thymocytes defined by CD44 and CD25 expression. , 1993, Journal of immunology.

[36]  C. Gilks,et al.  Progression of interleukin-2 (IL-2)-dependent rat T cell lymphoma lines to IL-2-independent growth following activation of a gene (Gfi-1) encoding a novel zinc finger protein , 1993, Molecular and cellular biology.

[37]  D. Longo,et al.  Characterization and regulation of RB6-8C5 antigen expression on murine bone marrow cells. , 1991, Journal of immunology.

[38]  Anton Berns,et al.  Identification of cooperating oncogenes in Eμ-myc transgenic mice by provirus tagging , 1991, Cell.

[39]  J D Kemp,et al.  Resolution and characterization of pro-B and pre-pro-B cell stages in normal mouse bone marrow , 1991, The Journal of experimental medicine.

[40]  Rohrschneider Lr,et al.  Murine c-fms cDNA: cloning, sequence analysis and retroviral expression. , 1987 .

[41]  A. Coutinho,et al.  Lymphocyte Population Kinetics in the Mouse , 1986, Immunological reviews.

[42]  J. Gallin.  Neutrophil specific granule deficiency. , 1985, Annual review of medicine.

[43]  T. Springer,et al.  Tissue distribution, structural characterization, and biosynthesis of Mac-3, a macrophage surface glycoprotein exhibiting molecular weight heterogeneity. , 1983, The Journal of biological chemistry.

[44]  W. Crosby,et al.  Cytochemical identification of monocytes and granulocytes. , 1971, American journal of clinical pathology.