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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
24
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pubmed:dateCreated |
1998-1-8
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pubmed: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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-1372394,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-1391942,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-1436033,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-1870982,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-2112087,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7481803,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7521686,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7530603,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7566171,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7652557,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7744000,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7829869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-7849512,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8467792,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8541551,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8601314,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8639758,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8661101,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8755574,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8861914,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8899290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-8934575,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-9012825,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-9032264,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-9177240,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9371821-9226149
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
94
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
13187-92
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:9371821-Animals,
pubmed-meshheading:9371821-CCAAT-Enhancer-Binding Proteins,
pubmed-meshheading:9371821-Cytokines,
pubmed-meshheading:9371821-DNA-Binding Proteins,
pubmed-meshheading:9371821-Genes, Lethal,
pubmed-meshheading:9371821-Granulocytes,
pubmed-meshheading:9371821-Hematopoiesis,
pubmed-meshheading:9371821-Hematopoietic Cell Growth Factors,
pubmed-meshheading:9371821-Mice,
pubmed-meshheading:9371821-Mice, Mutant Strains,
pubmed-meshheading:9371821-Myelodysplastic Syndromes,
pubmed-meshheading:9371821-Nuclear Proteins,
pubmed-meshheading:9371821-Recombination, Genetic
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pubmed:year |
1997
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pubmed:articleTitle |
Impaired granulopoiesis, myelodysplasia, and early lethality in CCAAT/enhancer binding protein epsilon-deficient mice.
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pubmed:affiliation |
Clinical Gene Therapy Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article
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