pubmed-article:17483226 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C0445750 | lld:lifeskim |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C0929176 | lld:lifeskim |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C0450429 | lld:lifeskim |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C0206522 | lld:lifeskim |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C0449943 | lld:lifeskim |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
pubmed-article:17483226 | lifeskim:mentions | umls-concept:C1519595 | lld:lifeskim |
pubmed-article:17483226 | pubmed:issue | 13 | lld:pubmed |
pubmed-article:17483226 | pubmed:dateCreated | 2007-6-20 | lld:pubmed |
pubmed-article:17483226 | pubmed:abstractText | The Salmonella enterica serovar Typhimurium HilA protein is the key regulator for the invasion of epithelial cells. By a combination of genome-wide location and transcript analysis, the HilA-dependent regulon has been delineated. Under invasion-inducing conditions, HilA binds to most of the known target genes and a number of new target genes. The sopB, sopE, and sopA genes, encoding effector proteins secreted by the type III secretion system on Salmonella pathogenicity island 1 (SPI-1), were identified as being both bound by HilA and differentially regulated in an HilA mutant. This suggests a cooperative role for HilA and InvF in the regulation of SPI-1-secreted effectors. Also, siiA, the first gene of SPI-4, is both bound by HilA and differentially regulated in an HilA mutant, thus linking this pathogenicity island to the invasion key regulator. Finally, the interactions of HilA with the SPI-2 secretion system gene ssaH and the flagellar gene flhD imply a repressor function for HilA under invasion-inducing conditions. | lld:pubmed |
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