21 research outputs found
Determinants of a transcriptionally competent environment at the GM-CSF promoter
Granulocyte macrophage-colony stimulating factor
(GM-CSF) is produced by T cells, but not B cells,
in response to immune signals. GM-CSF gene
activation in response to T-cell stimulation requires
remodelling of chromatin associated with the
gene promoter, and these changes do not occur in
B cells. While the CpG methylation status of the
murine GM-CSF promoter shows no correlation with
the ability of the gene to respond to activation, we
find that the basal chromatin environment of the
gene promoter influences its ability to respond to
immune signals. In unstimulated T cells but not B
cells, the GM-CSF promoter is selectively marked
by enrichment of histone acetylation, and association
of the chromatin-remodelling protein BRG1.
BRG1 is removed from the promoter upon activation
concomitant with histone depletion and BRG1
is required for efficient chromatin remodelling and
transcription. Increasing histone acetylation at
the promoter in T cells is paralleled by increased
BRG1 recruitment, resulting in more rapid chromatin
remodelling, and an associated increase in GM-CSF
mRNA levels. Furthermore, increasing histone
acetylation in B cells removes the block in chromatin
remodelling and transcriptional activation
of the GM-CSF gene. These data are consistent
with a model in which histone hyperacetylation
and BRG1 enrichment at the GM-CSF promoter,
generate a chromatin environment competent
to respond to immune signals resulting in gene
activation
Determinants of a transcriptionally competent environment at the GM-CSF promoter
Granulocyte macrophage-colony stimulating factor (GM-CSF) is produced by T cells, but not B cells, in response to immune signals. GM-CSF gene activation in response to T-cell stimulation requires remodelling of chromatin associated with the gene promoter, and these changes do not occur in B cells. While the CpG methylation status of the murine GM-CSF promoter shows no correlation with the ability of the gene to respond to activation, we find that the basal chromatin environment of the gene promoter influences its ability to respond to immune signals. In unstimulated T cells but not B cells, the GM-CSF promoter is selectively marked by enrichment of histone acetylation, and association of the chromatin-remodelling protein BRG1. BRG1 is removed from the promoter upon activation concomitant with histone depletion and BRG1 is required for efficient chromatin remodelling and transcription. Increasing histone acetylation at the promoter in T cells is paralleled by increased BRG1 recruitment, resulting in more rapid chromatin remodelling, and an associated increase in GM-CSF mRNA levels. Furthermore, increasing histone acetylation in B cells removes the block in chromatin remodelling and transcriptional activation of the GM-CSF gene. These data are consistent with a model in which histone hyperacetylation and BRG1 enrichment at the GM-CSF promoter, generate a chromatin environment competent to respond to immune signals resulting in gene activation
Does Private Islamic Schooling Promote Terrorism? An Analysis of the Educational Background of Successful American Homegrown Terrorists
Some commentators argue that private religious schools are less likely to inculcate the attributes of good citizenship than traditional public schools, specifically proposing that private Islamic schools are relatively more likely to produce individuals sympathetic to terrorism. This study offers a preliminary examination of the question by studying the educational backgrounds of Western educated terrorists. While data are limited, in accord with prior work findings indicate the vast majority of both Islamic and reactionary terrorists attended traditional public schools and had no religious education; hence findings suggest that early religious training and identification may actually encourage prosocial behavior