Linked Life Data

14568969

Source:http://linkedlifedata.com/resource/pubmed/id/14568969

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2003-10-21
pubmed:abstractText
Development of type I diabetes requires coordinated expression of myriad genes responsible for the initiation and progression of the disease. Expression of these genes are regulated by a small number of transcription factors including the Rel/NF-kappaB family. To determine the roles of the Rel/NF-kappaB family in type I diabetes, we studied multiple low-dose streptozotocin-induced diabetes in mice deficient in either c-Rel or NF-kappaB1. We found that mice deficient in each of these NF-kappaB subunits were resistant to streptozotocin-induced diabetes. However, the mechanisms of the disease resistance may differ in different cases. Deficiency in c-Rel selectively reduced Th1, but not Th2 responses, whereas NF-kappaB1 deficiency had little effect on T cell responses to anti-CD3 stimulation. Death of dendritic cells was accelerated in the absence of NF-kappaB1, whereas death of macrophages and granulocytes was affected primarily by c-Rel deficiency. Furthermore, Stat-1 expression was significantly reduced in macrophages deficient in NF-kappaB1, but not c-Rel. These results indicate that both c-Rel and NF-kappaB1are essential for the development of type I diabetes and that strategies targeting each of these subunits would be effective in preventing the disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
171
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4886-92
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:14568969-Animals, pubmed-meshheading:14568969-Apoptosis, pubmed-meshheading:14568969-DNA-Binding Proteins, pubmed-meshheading:14568969-Dendritic Cells, pubmed-meshheading:14568969-Diabetes Mellitus, Experimental, pubmed-meshheading:14568969-Diabetes Mellitus, Type 1, pubmed-meshheading:14568969-Dose-Response Relationship, Immunologic, pubmed-meshheading:14568969-Immunity, Innate, pubmed-meshheading:14568969-Interferon-gamma, pubmed-meshheading:14568969-Lipopolysaccharides, pubmed-meshheading:14568969-Lymphocyte Activation, pubmed-meshheading:14568969-Macrophages, pubmed-meshheading:14568969-Mice, pubmed-meshheading:14568969-Mice, Inbred C57BL, pubmed-meshheading:14568969-Mice, Knockout, pubmed-meshheading:14568969-Myeloid Cells, pubmed-meshheading:14568969-NF-kappa B, pubmed-meshheading:14568969-NF-kappa B p50 Subunit, pubmed-meshheading:14568969-Proto-Oncogene Proteins c-rel, pubmed-meshheading:14568969-STAT1 Transcription Factor, pubmed-meshheading:14568969-Signal Transduction, pubmed-meshheading:14568969-Streptozocin, pubmed-meshheading:14568969-T-Lymphocyte Subsets, pubmed-meshheading:14568969-Th1 Cells, pubmed-meshheading:14568969-Th2 Cells, pubmed-meshheading:14568969-Trans-Activators, pubmed-meshheading:14568969-Transcription, Genetic
pubmed:year
2003
pubmed:articleTitle
Transcriptional regulation of type I diabetes by NF-kappa B.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.