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pubmed-article:18035491pubmed:abstractTextCerebral ischemia triggers inflammation and apoptosis, and the transcription factor NF-kappaB is a key regulator of both events. Here, we report on the induction of the peptidoglycan recognition protein-S (PGRP-S) in a mouse model of cerebral ischemia. Upregulation was reduced if the NF-kappaB subunit RelA was conditionally deleted in the brain. Regulation of PGRP-S transcription by RelA was confirmed in vitro. Cotransfection of a RelA expression plasmid stimulated the expression of a PGRP-S luciferase fusion gene. Mutation of two NF-kappaB response elements in the PGRP-S promoter disrupted stimulation by RelA. To investigate the function of PGRP-S in cerebral ischemia, we subjected PGRP-S(-/-) mice to cerebral ischemia. However, there was no difference in the infarct size in PGRP-S-deficient mice compared to controls. In summary, the data show that PGRP-S is induced in cerebral ischemia by RelA, but its role in ischemia is unclear.lld:pubmed
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pubmed-article:18035491pubmed:articleTitlePeptidoglycan recognition protein-S (PGRP-S) is upregulated by NF-kappaB.lld:pubmed
pubmed-article:18035491pubmed:affiliationInstitute of Pharmacology, University of Heidelberg, Im Neuenheimer Feld 366, 69120 Heidelberg, Germany. ming-fei.lang@pharma.uni-heidelberg.delld:pubmed
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