Linked Life Data

1715367

Source:http://linkedlifedata.com/resource/pubmed/id/1715367

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-9-27
pubmed:abstractText
In macrophages, the TNF-alpha promoter is specifically induced by bacterial endotoxin, and provides a good model for gene regulation during bacterial infections. We have analyzed the protein-binding characteristics and enhancer activity of four kappa B-like enhancers and of a MHC class II-like Y box found in the mouse TNF-alpha promoter. In addition to members of the NF-kappa B/rel transcription factor family, at least two of the kappa B sites also bound a nuclear protein identified as NF-GMa, a factor that binds to promoter sequences from many cytokines. When inserted upstream of an enhancer-less promoter, two of the kappa B sites were active as LPS-inducible enhancers in primary macrophages, whereas the other two were not. Mutations in nucleotides known to contact nuclear factors severely reduced affinity of the kappa B sites for NF-kappa B. Introduction of the same mutations into a construct containing 1059 bp of the TNF-alpha promoter coupled to a CAT reporter gene resulted in a stepwise reduction in inducibility by LPS; mutation of all four sites (11 bp of 1059) reduced inducibility by 90%, providing compelling evidence for the role of transcription factors belonging to the NF-kappa B/rel family in the activation of the TNF-alpha promoter. The TNF-alpha Y box bound an abundant nuclear factor, but had no detectable activity in our assays, either as an enhancer or as a mutation-sensitive controlling element.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1694-700
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Enhancers and transcription factors controlling the inducibility of the tumor necrosis factor-alpha promoter in primary macrophages.
pubmed:affiliation
Ludwig Institute for Cancer Research, Epalinges, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't