FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1774296075> ?p ?o ?g. }

• W1774296075 abstract "The pathogenic bacterium Staphylococcus aureus has the ability to cause a wide variety of human diseases, ranging from superficial abscesses and wound infections to deep and systemic infections such as osteomyelitis, endocarditis and septicaemia. The ability to cause disease has been attributed to a large number of toxins and digesting enzymes as well as to proteins at the bacterial surface that bind various host molecules. These so-called virulence factors are accessory, and are supposed to be synthesised in response to the specific needs during the course of the infectious process. The work described in this thesis aims at a better understanding of the mechanisms that regulate the expression of virulence factors. Two interacting regulatory systems, agr (accessory gene regulator) and sar (staphylococcal accessory regulator), are involved in this regulation. The agr locus, which encodes a two-component signal transduction system responding to cell density, controls the expression of at least 25 different virulence factors. The effector molecule of the agr system is a regulatory RNA molecule, named RNAIII. The sar locus has been shown to regulate several staphylococcal virulence genes by modulating the activity of agr, but also via agr-independent mechanisms. The effector of the sar locus is a 14.7 kDa DNA binding protein, SarA. In animal models of infection both agr and sarA have been shown to affect virulence. How RNAIII and sarA function at the molecular level is, however, poorly understood. The structure and function of the RNAIII promoter have been studied in detail showing that SarA, which regulates the synthesis of RNAIII under certain growth conditions, binds to multiple sites within the RNAIII promoter region. It has also been shown that a region of 93 bp upstream of the transcription start point is sufficient for agr-dependent regulation of RNAIII synthesis. The RNAIII genes of several coagulase negative staphylococcal species –S. epidermidis, S. simulans and S. warneri– have been identified and analysed. The RNAIII molecules from the coagulase negative staphylococci were able to partially complement an RNAIII deficient S. aureus mutant. By the construction of hybrid RNAIII molecules it has also been demonstrated that highly conserved primary and secondary structures in both the 5 and the 3 -half of the RNAIII molecule are required for regulation of virulence genes, and that separate parts of the molecule were involved in regulation of different target genes. Several genes known to be regulated by RNAIII have been demonstrated to be regulated by the sarA locus, independent of its effect on expression of RNAIII. By electrophoresis mobility shift experiments and DNase footprinting, SarA has been found to bind in a very similar way to the promoter regions of genes that are either activated or repressed by sarA. SarA does not appear to recognise a conserved DNA sequence motif but rather binds to AT-rich sequences. New potential regulators of agr (RNAIII), hla (alpha-hemolysin), ssp (serine protease) and spa (protein A) have been searched for using specific promoter DNA linked to magnetic beads. Of several new candidate regulators, one protein with a high degree of similarity to SarA, named SarH1 (Sar Homologue 1) has been characterised and found to be part of the agr-sarA regulatory network controlling virulence gene expression. By computer searches in the unfinished S. aureus genome databases four additional Sar homologues have been found, some of which may also be involved in this regulatory network." @default.
• W1774296075 created "2016-06-24" @default.
• W1774296075 creator A5002416631 @default.
• W1774296075 date "2000-11-24" @default.
• W1774296075 modified "2023-09-27" @default.
• W1774296075 title "Regulation of virulence gene expression in Staphylococcus aureus" @default.
• W1774296075 cites W135808647 @default.
• W1774296075 cites W1492779378 @default.
• W1774296075 cites W1508139133 @default.
• W1774296075 cites W1511569985 @default.
• W1774296075 cites W1513370477 @default.
• W1774296075 cites W1518474490 @default.
• W1774296075 cites W1522327688 @default.
• W1774296075 cites W1533663942 @default.
• W1774296075 cites W1538375169 @default.
• W1774296075 cites W1543120839 @default.
• W1774296075 cites W1549526607 @default.
• W1774296075 cites W1562798956 @default.
• W1774296075 cites W1575455249 @default.
• W1774296075 cites W1587979806 @default.
• W1774296075 cites W159005137 @default.
• W1774296075 cites W1602775195 @default.
• W1774296075 cites W1603766972 @default.
• W1774296075 cites W1623295381 @default.
• W1774296075 cites W1628177336 @default.
• W1774296075 cites W1645243440 @default.
• W1774296075 cites W1727598810 @default.
• W1774296075 cites W1783815881 @default.
• W1774296075 cites W1785056813 @default.
• W1774296075 cites W1790927204 @default.
• W1774296075 cites W1819722519 @default.
• W1774296075 cites W1827553092 @default.
• W1774296075 cites W1828740938 @default.
• W1774296075 cites W1831646357 @default.
• W1774296075 cites W1835640114 @default.
• W1774296075 cites W1854017712 @default.
• W1774296075 cites W1884980943 @default.
• W1774296075 cites W1905790971 @default.
• W1774296075 cites W1911942190 @default.
• W1774296075 cites W191752848 @default.
• W1774296075 cites W1919005082 @default.
• W1774296075 cites W1924294726 @default.
• W1774296075 cites W1929816290 @default.
• W1774296075 cites W1937918507 @default.
• W1774296075 cites W1938591788 @default.
• W1774296075 cites W1941142806 @default.
• W1774296075 cites W1942690337 @default.
• W1774296075 cites W1947813675 @default.
• W1774296075 cites W1952814327 @default.
• W1774296075 cites W1956780777 @default.
• W1774296075 cites W1962827003 @default.
• W1774296075 cites W1965432401 @default.
• W1774296075 cites W1968366930 @default.
• W1774296075 cites W1970582294 @default.
• W1774296075 cites W1971289275 @default.
• W1774296075 cites W1972312133 @default.
• W1774296075 cites W1975161261 @default.
• W1774296075 cites W1977538040 @default.
• W1774296075 cites W1982285611 @default.
• W1774296075 cites W1982290773 @default.
• W1774296075 cites W1982310237 @default.
• W1774296075 cites W1982503880 @default.
• W1774296075 cites W1982777646 @default.
• W1774296075 cites W1987314736 @default.
• W1774296075 cites W1993488180 @default.
• W1774296075 cites W1995204810 @default.
• W1774296075 cites W1995364663 @default.
• W1774296075 cites W1996872292 @default.
• W1774296075 cites W1997884783 @default.
• W1774296075 cites W2001079530 @default.
• W1774296075 cites W2001550673 @default.
• W1774296075 cites W2005091466 @default.
• W1774296075 cites W2005853237 @default.
• W1774296075 cites W2009159314 @default.
• W1774296075 cites W2009937211 @default.
• W1774296075 cites W2012249586 @default.
• W1774296075 cites W2013013376 @default.
• W1774296075 cites W2014839221 @default.
• W1774296075 cites W2014962591 @default.
• W1774296075 cites W2015400027 @default.
• W1774296075 cites W2017808200 @default.
• W1774296075 cites W2019196439 @default.
• W1774296075 cites W2023135875 @default.
• W1774296075 cites W2025013124 @default.
• W1774296075 cites W2026565784 @default.
• W1774296075 cites W2028510005 @default.
• W1774296075 cites W2031281479 @default.
• W1774296075 cites W2032619610 @default.
• W1774296075 cites W2033278525 @default.
• W1774296075 cites W2034928517 @default.
• W1774296075 cites W2035499888 @default.
• W1774296075 cites W2037622389 @default.
• W1774296075 cites W2040199933 @default.
• W1774296075 cites W2042412127 @default.
• W1774296075 cites W2043266069 @default.
• W1774296075 cites W2044878310 @default.
• W1774296075 cites W2047160000 @default.
• W1774296075 cites W2047929024 @default.
• W1774296075 cites W2050634720 @default.
• W1774296075 cites W2052687085 @default.

• next