Linked Life Data

12522000

Source:http://linkedlifedata.com/resource/pubmed/id/12522000

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2003-4-22
pubmed:abstractText
In vitro models of granulopoiesis involving the inducible expression of either CCAAT enhancer binding protein alpha (C/EBP alpha) or C/EBP epsilon in myeloid cells have been shown to lead to the induction of a granulocytic maturation program accompanied by the expression of myeloid-specific genes. Since members of the C/EBP family of transcription factors recognize and bind to similar DNA-binding motifs, it has been difficult to elucidate the specific role of each of the C/EBP family members in eliciting myeloid gene expression. In order to address this issue, we focused on the expression of the lactoferrin (LF) gene. LF expression is transcriptionally regulated in a C/EBP-dependent manner in myeloid cells. Using chromatin immunoprecipitation (ChIP) analysis we demonstrate that C/EBP alpha binds to the LF promoter in nonexpressing cells. Upon induction of maturation, C/EBP epsilon binds to the LF promoter, which correlates with LF expression. Lack of LF expression in the acute promyelocytic leukemia cell line NB4, which harbors the t(15;17) translocation, cannot be correlated with aberrant binding at the C/EBP site in the LF promoter. It is, however, associated with the persistent binding of the silencer CCAAT displacement protein (CDP/cut) to the LF promoter in these cells. We conclude that C/EBP alpha, C/EBP epsilon, and CDP/cut all play definitive roles in regulating late gene expression during normal myeloid development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3460-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:12522000-CCAAT-Enhancer-Binding Protein-alpha, pubmed-meshheading:12522000-CCAAT-Enhancer-Binding Proteins, pubmed-meshheading:12522000-Cell Differentiation, pubmed-meshheading:12522000-Chromatin, pubmed-meshheading:12522000-Gene Expression Regulation, Leukemic, pubmed-meshheading:12522000-Homeodomain Proteins, pubmed-meshheading:12522000-Humans, pubmed-meshheading:12522000-Lactoferrin, pubmed-meshheading:12522000-Leukemia, Promyelocytic, Acute, pubmed-meshheading:12522000-Myeloid Cells, pubmed-meshheading:12522000-Neoplasm Proteins, pubmed-meshheading:12522000-Nuclear Proteins, pubmed-meshheading:12522000-Precipitin Tests, pubmed-meshheading:12522000-Promoter Regions, Genetic, pubmed-meshheading:12522000-Protein Binding, pubmed-meshheading:12522000-Repressor Proteins, pubmed-meshheading:12522000-Transcriptional Activation, pubmed-meshheading:12522000-Tretinoin, pubmed-meshheading:12522000-Tumor Cells, Cultured
pubmed:year
2003
pubmed:articleTitle
Chromatin immunoprecipitation (ChIP) studies indicate a role for CCAAT enhancer binding proteins alpha and epsilon (C/EBP alpha and C/EBP epsilon ) and CDP/cut in myeloid maturation-induced lactoferrin gene expression.
pubmed:affiliation
Section of Hematology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't