PU.1, Interferon Regulatory Factor 1, and Interferon Consensus Sequence-binding Protein Cooperate to Increase gp91 Expression

Abstract

gp91phox is a subunit of the phagocyte respiratory burst oxidase catalytic unit. Transcription of CYBB, the gene encoding gp91 phox , is restricted to terminally differentiated phagocytic cells. An element in the proximal CYBB promoter binds a protein complex, referred to as hematopoiesis-associated factor (HAF1), that is necessary for interferon-␥ (IFN␥)-induced gp91 phox expression. In these investigations, we determined that HAF1 was a multiprotein complex, cross-immunoreactive with the transcription factors PU.1, interferon regulatory factor 1 (IRF-1), and interferon consensus sequencebinding protein (ICSBP). In electrophoretic mobility shift assay, the

An IFN-γ-Inducible Transcription Factor, IFN Consensus Sequence Binding Protein (ICSBP), Stimulates IL-12 p40 Expression in Macrophages

“…What directs ICSBP and IRF-4 to act as an activator or a repressor is unclear at present, but presumably depends on the context of promoter sequences and proteins with which they interact. ICSBP is recently shown to activate the gp91 phox promoter in cooperation with PU.1 (52). In addition, it has been reported that not only ICSBP but Pip/IRF-4 can form complexes with PU.1 in macrophages and regulate transcription from PU.1/IRF-dependent promoters (53).…”

Oncogenic Ras upregulates NADPH oxidase 1 gene expression through MEK-ERK-dependent phosphorylation of GATA-6

“…Ras/ERK signaling upregulates Nox1 gene expression Y Adachi et al 1996) and PU.1 (Eklund et al, 1998), either positively or negatively, control the transcription of Nox2 in myeloid cells and neutrophils, respectively. Cyclic AMP response element-binding proteins have been found to be responsible for acid-induced expression of Nox5-S in barrett esophagel adenocarcinoma cells (Fu et al, 2006).…”

“…The activities of several Nox enzymes have been reported to be transcriptionally regulated. For example, the expression of Nox2 in mature phagocytes is induced by the inflammatory mediators including interferon-g (IFNg), where transcription of Nox2 involves the coordinate action of an Ets transcription factor PU.1 and IFNg regulatory factor 1 (Eklund et al, 1998), and Nox2 is transcriptionally repressed in chronic granulomatous diseases (Newburger et al, 1988). Similarly, expression of Nox1 mRNA is induced by the growth stimuli such as PDGF (Lasse`gue et al, 2001) and angiotensin II (Lasse`gue et al, 2001).…”

IFN-γ Up-Regulates IL-18 Gene Expression Via IFN Consensus Sequence-Binding Protein and Activator Protein-1 Elements in Macrophages

“…In contrast, in IFN-␥-treated nuclear extracts, the retardation of protein-DNA complex was seen by the addition of anti-IRF-1 Ab as well as anti-ICSBP Ab. Interaction between IRF-1 and ICSBP has been reported to increase gp91 phox expression (29). In this case, equal amounts of two factors bound to form hemopoiesis-associated factor 1 complex, which is necessary for IFN-␥-induced gp91 phox expression.…”