PubMed Journals: Nature

  Source:		PMID: 9069290

    		Nature. 1997 Mar 20;386(6622):296-9.
			Activation of the transcription factor MEF2C
			by the MAP kinase p38 in inflammation.

			Han J(1), Jiang Y, Li Z, Kravchenko VV,
			Ulevitch RJ.

			Author Information
			(1) Department of Immunology,
			The Scripps Research Institute, La Jolla,
			California 92037, USA. jhan@scripps.edu

			For cells of the innate immune system to
			mount a host defence response to infection,
			they must recognize products of microbial
			pathogens such as lipopolysaccharide (LPS),
			the endotoxin secreted by Gram-negative
			bacteria. These cellular responses require
			intracellular signalling pathways, such
			as the four MAP kinase (MAPK) pathways.
			In mammalian cells the MAPK p38 is thought
			to play an important role in the regulation
			of cellular responses during infection through
			its effects on the expression of proinflammatory
			molecules. One means of understanding the
			role of p38 in these responses is to identify
			proteins with functions regulated by p38-catalysed
			phosphorylation. Here we demonstrate a link
			between the p38 pathway and a member of
			the myocyte-enhancer factor 2 (MEF2) group
			of transcription factors. We found that
			in monocytic cells, LPS increases the
			transactivation activity of MEF2C through
			p38-catalysed phosphorylation. One consequence
			of MEF2C activation is increased c-jun gene
			transcription. Our results show that p38
			may influence host defence and inflammation
			by maintaining the balance of c-Jun protein
			consumed during infection.

			DOI: 10.1038/386296a0 PMID: 9069290 [Indexed
			for MEDLINE]

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