Linked Life Data

9576616

Source:http://linkedlifedata.com/resource/pubmed/id/9576616

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-6-11
pubmed:abstractText
The NF-kappaB transcription factor complex plays a key role in the expression of genes involved in immune responses. Nuclear NF-kappaB is induced in B lymphocytes by engagement of either the antigen receptor (sIg) or the CD40 receptor for a T cell activation antigen, although different intracellular pathways appear to be involved. In the present study the protein composition of NF-kappaB complexes triggered by sIg and CD40 was probed by electrophoretic mobility shift, supershift, shift-Western, and Western blot analyses. At the time of peak NF-kappaB induction (2 h), the NF-kappaB components detected in the complexes induced through sIg and through CD40 were the same. However, with continued stimulation RelB completely disappeared from anti-Ig-stimulated kappaB binding material, but remained a component of CD40L-induced NF-kappaB. The loss of DNA-binding RelB from anti-Ig-induced NF-kappaB did not result from depletion of RelB from B cell nuclei, suggesting specific regulation of RelB function which is not directly attributed to IkappaB function. These results indicate that NF-kappaB complexes may undergo protein-specific alterations in a time- and receptor-dependent fashion that may be associated with differences in the outcomes of B cell stimulation through sIg and CD40.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
285-93
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Receptor-specific induction of NF-kappaB components in primary B cells.
pubmed:affiliation
Department of Pathology, Boston University Medical Center, MA 02118, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.