{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T20:15:22Z","timestamp":1790972122105,"version":"4.1.0"},"reference-count":30,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2006,9,1]],"date-time":"2006-09-01T00:00:00Z","timestamp":1157068800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2006,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Enterococcus faecalis<\/jats:italic>\n            , the third most frequent cause of bacterial endocarditis, appears to be equipped with diverse surface-associated proteins showing structural-fold similarity to the immunoglobulin-fold family of staphylococcal adhesins. Among the putative\n            <jats:italic>E. faecalis<\/jats:italic>\n            surface proteins, the previously characterized adhesin Ace, which shows specific binding to collagen and laminin, was detectable in surface protein preparations only after growth at 46\u00b0C, mirroring the finding that adherence was observed in 46\u00b0C, but not 37\u00b0C, grown\n            <jats:italic>E. faecalis<\/jats:italic>\n            cultures. To elucidate the influence of different growth and host parameters on\n            <jats:italic>ace<\/jats:italic>\n            expression, we investigated\n            <jats:italic>ace<\/jats:italic>\n            expression using\n            <jats:italic>E. faecalis<\/jats:italic>\n            OG1RF grown in routine laboratory media (brain heart infusion) and found that\n            <jats:italic>ace<\/jats:italic>\n            mRNA levels were low in all growth phases. However, quantitative reverse transcription-PCR showed 18-fold-higher\n            <jats:italic>ace<\/jats:italic>\n            mRNA amounts in cells grown in the presence of collagen type IV compared to the controls. Similarly, a marked increase was observed when cells were either grown in the presence of collagen type I or serum but not in the presence of fibrinogen or bovine serum albumin. The production of Ace after growth in the presence of collagen type IV was demonstrated by immunofluorescence microscopy, mirroring the increased\n            <jats:italic>ace<\/jats:italic>\n            mRNA levels. Furthermore, increased Ace expression correlated with increased collagen and laminin adhesion. Collagen-induced Ace expression was also seen in three of three other\n            <jats:italic>E. faecalis<\/jats:italic>\n            strains of diverse origins tested, and thus it appears to be a common phenomenon. The observation of host matrix signal-induced adherence of\n            <jats:italic>E. faecalis<\/jats:italic>\n            may have important implications on our understanding of this opportunistic pathogen.\n          <\/jats:p>","DOI":"10.1128\/iai.00476-06","type":"journal-article","created":{"date-parts":[[2006,8,22]],"date-time":"2006-08-22T22:13:07Z","timestamp":1156284787000},"page":"4982-4989","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["Ligand-Signaled Upregulation of\n            <i>Enterococcus faecalis ace<\/i>\n            Transcription, a Mechanism for Modulating Host-\n            <i>E. faecalis<\/i>\n            Interaction"],"prefix":"10.1128","volume":"74","author":[{"given":"Sreedhar R.","family":"Nallapareddy","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine"},{"name":"Center for the Study of Emerging and Re-emerging Pathogens"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara E.","family":"Murray","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine"},{"name":"Center for the Study of Emerging and Re-emerging Pathogens"},{"name":"Department of Microbiology and Molecular Genetics, University of Texas Medical School, Houston, Texas 77030"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.1999.tb13762.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1089\/107662901750152765"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(98)01400-0"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0378-1097(97)00421-7"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.66.7.3170-3178.1998"},{"key":"e_1_3_2_7_2","first-page":"301","year":"2002","unstructured":"Gilmore, M. 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