{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T19:07:15Z","timestamp":1791140835167,"version":"4.1.0"},"reference-count":52,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2003,2,15]],"date-time":"2003-02-15T00:00:00Z","timestamp":1045267200000},"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":["J Bacteriol"],"published-print":{"date-parts":[[2003,2,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The group A\n                    <jats:italic>Streptococcus<\/jats:italic>\n                    (GAS)\n                    <jats:italic>sof<\/jats:italic>\n                    gene encodes the serum opacity factor protein, which is capable of opacifying mammalian sera and binding at least two host proteins, fibronectin and fibrinogen. The\n                    <jats:italic>sof<\/jats:italic>\n                    gene exists in approximately 50% of clinical isolates, and there is a classical association of so-called nephritogenic strains with the opacity factor-positive phenotype. In both a type\n                    <jats:italic>emm49<\/jats:italic>\n                    strain and a type\n                    <jats:italic>emm12<\/jats:italic>\n                    strain, the sequences upstream of the 5\u2032 end of\n                    <jats:italic>sof<\/jats:italic>\n                    and downstream of the putative terminator were determined to be nearly identical to a region in the M type 1 genome approximately 10 kb upstream of the\n                    <jats:italic>emm1<\/jats:italic>\n                    gene. This close genetic linkage is likely reflected in the strict correlation of opacity factor phenotype with specific\n                    <jats:italic>emm<\/jats:italic>\n                    genotypes. A new fibronectin-binding protein gene,\n                    <jats:italic>sfbX<\/jats:italic>\n                    , was discovered immediately downstream of\n                    <jats:italic>sof<\/jats:italic>\n                    in\n                    <jats:italic>emm12<\/jats:italic>\n                    and\n                    <jats:italic>emm49<\/jats:italic>\n                    strains and in several other\n                    <jats:italic>sof<\/jats:italic>\n                    -positive strains. The\n                    <jats:italic>sof<\/jats:italic>\n                    and\n                    <jats:italic>sfbX<\/jats:italic>\n                    genes were found to be expressed on the same transcription unit, which was correlated with the putative promoter and rho-independant terminator sequences that flank these two genes. The\n                    <jats:italic>sfbX<\/jats:italic>\n                    genes from different\n                    <jats:italic>emm<\/jats:italic>\n                    types are predicted to encode \u223c650-residue surface-bound proteins sharing 89 to 92% sequence identity. SfbX residues approximately 1 to 480 are not highly similar to those of other known proteins, with the closest match being the\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    coagulase protein. The remaining portions of these proteins (residues 481 to 650) contain four putative fibronectin-binding repeats highly similar to those of other streptococcal fibronectin-binding proteins and a potential LP(X)SG cell wall anchor motif. Targeted in-frame allelic-exchange mutagenesis, complementation, and heterologous-expression studies found that serum opacification is encoded by\n                    <jats:italic>sof<\/jats:italic>\n                    alone and that\n                    <jats:italic>sfbX<\/jats:italic>\n                    encodes a fibronectin-binding function. A recombinant SfbX protein was found to bind immobilized fibronectin and to partially inhibit GAS adherence to fibronectin. The\n                    <jats:italic>sfbX<\/jats:italic>\n                    gene was found to be present only in\n                    <jats:italic>sof<\/jats:italic>\n                    -positive strains, and together these genes could influence the spectrum of tissues colonized by\n                    <jats:italic>sof<\/jats:italic>\n                    -positive GAS.\n                  <\/jats:p>","DOI":"10.1128\/jb.185.4.1208-1217.2003","type":"journal-article","created":{"date-parts":[[2003,1,31]],"date-time":"2003-01-31T15:03:10Z","timestamp":1044025390000},"page":"1208-1217","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":139,"title":["Molecular Genetic Analysis of a Group A\n                    <i>Streptococcus<\/i>\n                    Operon Encoding Serum Opacity Factor and a Novel Fibronectin-Binding Protein, SfbX"],"prefix":"10.1128","volume":"185","author":[{"given":"Arthur","family":"Jeng","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Infectious Diseases, University of California, San Diego, School of Medicine, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Varja","family":"Sakota","sequence":"additional","affiliation":[{"name":"Respiratory Diseases Branch, Division of Bacterial and Mycotic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhongya","family":"Li","sequence":"additional","affiliation":[{"name":"Respiratory Diseases Branch, Division of Bacterial and Mycotic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vivekananda","family":"Datta","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Infectious Diseases, University of California, San Diego, School of Medicine, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard","family":"Beall","sequence":"additional","affiliation":[{"name":"Respiratory Diseases Branch, Division of Bacterial and Mycotic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victor","family":"Nizet","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Division of Pediatric Infectious Diseases, University of California, San Diego, School of Medicine, La Jolla, California"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.184.8.2181-2191.2002"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1099\/00221287-146-5-1195"},{"key":"e_1_3_2_4_2","doi-asserted-by":"crossref","first-page":"10078","DOI":"10.1073\/pnas.152298499","volume":"99","year":"2002","unstructured":"Beres, S. 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