p100, a precursor of NF-κB2, inhibits c-Rel and reduces the expression of IL-23 in dendritic cells

Nuclear factor κB regulates various genes involved in the immune response, inflammation, cell survival, and development. NF-κB activation is controlled by proteins possessing ankyrin repeats, such as IκBs. A precursor of the NF-κB2 (p52) subunit, p100, contains ankyrin repeats in its C-terminal port...

Full description

Saved in:

Bibliographic Details
Published in:	Biochemical and biophysical research communications Vol. 453; no. 3; pp. 332 - 337
Main Authors:	Mise-Omata, Setsuko, Obata, Yuichi, Doi, Takahiro S
Format:	Journal Article
Language:	English
Published:	United States 24-10-2014
Subjects:	60 APPLIED LIFE SCIENCES Animals Base Sequence BONE MARROW DENDRITES Dendritic Cells - metabolism DNA Primers GENE REGULATION GENES GUANINE HEK293 Cells Humans HYPOXANTHINE INFLAMMATION INTERFERON Interleukin-23 - metabolism Mice NF-kappa B p52 Subunit - genetics NF-kappa B p52 Subunit - physiology Polymerase Chain Reaction PRECURSOR Proto-Oncogene Proteins c-rel - antagonists & inhibitors RECEPTORS STEADY-STATE CONDITIONS STIMULATION TRANSLOCATION Gene Regulation NF-κB p100 Cytokines Dendritic cells c-Rel
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Nuclear factor κB regulates various genes involved in the immune response, inflammation, cell survival, and development. NF-κB activation is controlled by proteins possessing ankyrin repeats, such as IκBs. A precursor of the NF-κB2 (p52) subunit, p100, contains ankyrin repeats in its C-terminal portion and has been found to act as a cytoplasmic inhibitor of RelA in the canonical pathway of NF-κB activation. Here, we demonstrate that p100 also suppresses c-Rel function in dendritic cells. Expression of the p19 and p40 subunits of IL-23, a c-Rel-dependent cytokine, was enhanced in p100-deficient cells, although expression of a RelA-dependent cytokine, TNF-α, was reduced. Nuclear translocation of c-Rel was enhanced in p100-deficient cells. p100, and not the processed p52 form, associated with c-Rel in the steady state and dissociated immediately after lipopolysaccharide stimulation in wild-type dendritic cells. Four hours after the stimulation, p100 was newly synthesized and associated with c-Rel again. In cells expressing both c-Rel and RelA, c-Rel is preferentially suppressed by p100.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0006-291X 1090-2104
DOI:	10.1016/j.bbrc.2014.09.143