Linked Life Data

18081698

Source:http://linkedlifedata.com/resource/pubmed/id/18081698

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-3-27
pubmed:abstractText
Although the nuclear factor-kappaB (NF-kappaB)-dependent gene expression is critical to the induction of an efficient immune response to infection or tissue injury, excessive or prolonged NF-kappaB signalling can contribute to the development of several inflammatory diseases. Therefore, the NF-kappaB signal transduction pathway is tightly regulated by several intracellular proteins. We have previously identified A20-binding inhibitor of NF-kappaB activation (ABIN)-3 as an lipopolysaccharide (LPS)-inducible protein in monocytes that negatively regulates NF-B activation in response to tumour necrosis factor (TNF) and LPS. Here we report that ABIN-3 expression is also up-regulated upon TNF treatment of monocytes and other non-myeloid cell types. We also found a significantly enhanced expression of ABIN-3 in monocytes of sepsis patients, which is restored to control levels by corticotherapy. To further understand the transcriptional regulation of ABIN-3 expression, we isolated the human ABIN-3 promoter and investigated its activation in response to TNF and LPS. This revealed that the LPS- and TNF-inducible expression of ABIN-3 is dependent on the binding of NF-kappaB to a specific B site in the ABIN-3 promoter. Altogether, these data indicate an important role for NF-kappaB-dependent gene expression of ABIN-3 in the negative feedback regulation of TNF receptor and toll-like receptor 4 induced NF-kappaB activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1582-1838
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
316-29
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:18081698-Adolescent, pubmed-meshheading:18081698-Adrenal Cortex Hormones, pubmed-meshheading:18081698-Base Sequence, pubmed-meshheading:18081698-Cell Nucleus, pubmed-meshheading:18081698-Cells, Cultured, pubmed-meshheading:18081698-Electrophoretic Mobility Shift Assay, pubmed-meshheading:18081698-Feedback, Physiological, pubmed-meshheading:18081698-Gene Expression Regulation, pubmed-meshheading:18081698-Humans, pubmed-meshheading:18081698-Lipopolysaccharides, pubmed-meshheading:18081698-Molecular Sequence Data, pubmed-meshheading:18081698-Monocytes, pubmed-meshheading:18081698-NF-kappa B, pubmed-meshheading:18081698-Proteins, pubmed-meshheading:18081698-RNA, Messenger, pubmed-meshheading:18081698-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18081698-Sepsis, pubmed-meshheading:18081698-Signal Transduction, pubmed-meshheading:18081698-Toll-Like Receptor 4, pubmed-meshheading:18081698-Tumor Necrosis Factor-alpha, pubmed-meshheading:18081698-Up-Regulation
pubmed:articleTitle
Expression of the NF-kappaB inhibitor ABIN-3 in response to TNF and toll-like receptor 4 stimulation is itself regulated by NF-kappaB.
pubmed:affiliation
Unit of Molecular Signal Transduction in Inflammation, Department for Molecular Biomedical Research, Ghent, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't