ArticleInfection and immunity1999
Molecular mechanism for the spontaneous generation of pigmentless Porphyromonas gingivalis mutants.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- The oral pathogen Porphyromonas gingivalis gains tolerance to the antimicrobial peptide DGL13K by synonymous mutations in hagA.PloS one · 2024Article
- Molecular basis for avirulence of spontaneous variants of Porphyromonas gingivalis: Genomic analysis of strains W50, BE1 and BR1.Molecular oral microbiology · 2022Article
- Porphyrin-mediated cell surface heme capture from hemoglobin by Porphyromonas gingivalis.Journal of bacteriology · 2003Article
- Role of polyphosphate kinase in biofilm formation by Porphyromonas gingivalis.Infection and immunity · 2002Article
- Specific antibodies to Porphyromonas gingivalis Lys-gingipain by DNA vaccination inhibit bacterial binding to hemoglobin and protect mice from infection.Infection and immunity · 2001Article
- vimA gene downstream of recA is involved in virulence modulation in Porphyromonas gingivalis W83.Infection and immunity · 2001Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Porphyromonas gingivalis is one of the pathogens associated with periodontal diseases, and its protease activity has been implicated as an important virulence factor. Kgp is the major Lys-gingipain protease of P. gingivalis and appears to be involved not only in enzyme activity but also in hemagglutination and the pigmented phenotype due to heme accumulation and/or hemoglobin binding. However, little information concerning the molecular mechanism for the spontaneous generation of pigmentless P. gingivalis mutants is currently available. In this study, several spontaneous pigmentless mutants of P. gingivalis were isolated and characterized. The results revealed that a portion of the kgp gene had been deleted from the chromosomes of the pigmentless mutants. This deletion appears to result from recombination between the highly homologous DNA sequences encoding the adhesin domains of the tandemly arranged hagA and kgp genes on the chromosomes of P. gingivalis strains.
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Registered trials
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