PU.1 regulates glutathione peroxidase expression in neutrophils

Stacy L. Throm, Michael Klemsz

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Based on knockout models, the transcription factor PU.1 has been shown to be important for the maturation of neutrophils. As the list of genes PU.1 directly regulates in neutrophils is still quite limited, defining PU.1 target genes for this lineage will provide valuable insight into how this factor regulates neutrophil development and terminal function. Using the combined techniques of representational difference analysis and a cDNA library screen, we identified four genes that were differentially expressed in the PU.1-expressing 503PU myeloid cell line but not the PU.1 null parent cell line 503. Two of these genes, glutathione peroxidase (GPx) and serine leukoprotease inhibitor, are involved in protecting neutrophils from the products they make to destroy pathogens and were analyzed further to determine if PU.1 directly regulates their expression. These studies showed that PU.1 directly regulated the expression of only the GPx gene through binding sites in the promoter and a 3′ regulatory region. Thus, PU.1 not only regulates the expression of molecules involved in the production of reactive oxygen species but also a gene that protects the neutrophils from these same destructive enzymes.

Original languageEnglish
Pages (from-to)111-117
Number of pages7
JournalJournal of Leukocyte Biology
Volume74
Issue number1
DOIs
StatePublished - Jul 2003

Fingerprint

Glutathione Peroxidase
Neutrophils
Genes
Cell Line
Null Lymphocytes
Nucleic Acid Regulatory Sequences
Myeloid Cells
Gene Library
Serine
Reactive Oxygen Species
Binding Sites
Enzymes

Keywords

  • Blood cell
  • Gene expression
  • Transcription

ASJC Scopus subject areas

  • Cell Biology

Cite this

PU.1 regulates glutathione peroxidase expression in neutrophils. / Throm, Stacy L.; Klemsz, Michael.

In: Journal of Leukocyte Biology, Vol. 74, No. 1, 07.2003, p. 111-117.

Research output: Contribution to journalArticle

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