{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ando T"],"funding":["NIGMS NIH HHS"],"pagination":["295-301"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC141823"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["185(1)"],"pubmed_abstract":["A recently identified Helicobacter pylori gene, hrgA, was previously reported to be present in 70 (33%) of 208 strains examined (T. Ando, T. M. Wassenaar, R. M. Peek, R. A. Aras, A. I. Tschumi, L.-J. Van Doorn, K. Kusugami, and M. J. Blaser, Cancer Res. 62:2385-2389, 2002). Sequence analysis of nine such strains indicated that in each strain hrgA replaced hpyIIIR, which encodes a restriction endonuclease and which, together with the gene for its cognate methyltransferase, constitutes the hpyIII locus. As a consequence of either the hrgA insertion or independent mutations, hpyIIIM function was lost in 11 (5%) of the 208 strains examined, rendering chromosomal DNA sensitive to MboI digestion. The evolutionary history of the locus containing either hpyIII or hrgA was reconstructed. By homolog"],"journal":["Journal of bacteriology"],"pubmed_title":["Evolutionary history of hrgA, which replaces the restriction gene hpyIIIR in the hpyIII locus of Helicobacter pylori."],"pmcid":["PMC141823"],"funding_grant_id":["R01 GM063270","R01 GM 63270"],"pubmed_authors":["Wassenaar TM","Ando T","Blaser MJ","Aras RA","Kusugami K"],"additional_accession":[]},"is_claimable":false,"name":"Evolutionary history of hrgA, which replaces the restriction gene hpyIIIR in the hpyIII locus of Helicobacter pylori.","description":"A recently identified Helicobacter pylori gene, hrgA, was previously reported to be present in 70 (33%) of 208 strains examined (T. Ando, T. M. Wassenaar, R. M. Peek, R. A. Aras, A. I. Tschumi, L.-J. Van Doorn, K. Kusugami, and M. J. Blaser, Cancer Res. 62:2385-2389, 2002). Sequence analysis of nine such strains indicated that in each strain hrgA replaced hpyIIIR, which encodes a restriction endonuclease and which, together with the gene for its cognate methyltransferase, constitutes the hpyIII locus. As a consequence of either the hrgA insertion or independent mutations, hpyIIIM function was lost in 11 (5%) of the 208 strains examined, rendering chromosomal DNA sensitive to MboI digestion. The evolutionary history of the locus containing either hpyIII or hrgA was reconstructed. By homolog","dates":{"release":"2003-01-01T00:00:00Z","publication":"2003 Jan","modification":"2025-04-21T14:55:46.026Z","creation":"2019-03-26T23:29:36Z"},"accession":"S-EPMC141823","cross_references":{"pubmed":["12486066"],"doi":["10.1128/jb.185.1.295-301.2003","10.1128/JB.185.1.295-301.2003"]}}