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1996-02-27
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Document 0075
DOCN M9630075
TI Inhibition of NF-AT-dependent transcription by NF-kappa B: implications
for differential gene expression in T helper cell subsets.
DT 9603
AU Casolaro V; Georas SN; Song Z; Zubkoff ID; Abdulkadir SA; Thanos D; Ono
SJ; Department of Medicine, Johns Hopkins University, Baltimore, MD;
21224, USA.
SO Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11623-7. Unique Identifier :
AIDSLINE MED/96102166
AB Activation of individual CD4+ T cells results in differential lymphokine
expression: interleukin 2 (IL-2) is preferentially produced by T helper
type 1 (TH1) cells, which are involved in cell-mediated immune
responses, whereas IL-4 is synthesized by TH2 cells, which are essential
for humoral immunity. The Ca(2+)-dependent factor NF-ATp plays a key
role in the inducible transcription of both these lymphokine genes.
However, while IL2 expression requires the contribution of Ca(2+)- and
protein kinase C-dependent signals, we report that activation of human
IL4 transcription through the Ca(2+)-dependent pathway is diminished by
protein kinase C stimulation in Jurkat T cells. This phenomenon is due
to mutually exclusive binding of NF-ATp and NF-kappa B to the P
sequence, an element located 69 bp upstream of the IL4 transcription
initiation site. Human IL4 promoter-mediated transcription is
downregulated in Jurkat cells stimulated with the NF-kappa B-activating
cytokine tumor necrosis factor alpha and suppressed in
RelA-overexpressing cells. In contrast, protein kinase C stimulation or
RelA overexpression does not affect the activity of a human IL4 promoter
containing a mouse P sequence, which is a higher-affinity site for
NF-ATp and a lower-affinity site for RelA. Thus, competition between two
general transcriptional activators, RelA and NF-ATp, mediates the
inhibitory effect of protein kinase C stimulation on IL4 expression and
may contribute to differential gene expression in TH cells.
DE Animal Base Sequence Cell Differentiation DNA-Binding
Proteins/*METABOLISM *Gene Expression Regulation Genes, Reporter
Human Interleukin-2/BIOSYNTHESIS/GENETICS
Interleukin-4/BIOSYNTHESIS/GENETICS Interleukins/*BIOSYNTHESIS/GENETICS
Mice Molecular Sequence Data NF-kappa B/*METABOLISM Promoter Regions
(Genetics) Protein Kinase C Species Specificity Support, Non-U.S.
Gov't Support, U.S. Gov't, P.H.S. T-Lymphocyte Subsets
T-Lymphocytes/*METABOLISM Th1 Cells Th2 Cells Transcription
Factors/*METABOLISM *Transcription, Genetic JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).