Literature DB >> 21447698

Molecular signaling mechanisms of the periopathogen, Treponema denticola.

J R Frederick1, J Sarkar, J V McDowell, R T Marconi.   

Abstract

In the healthy subgingiva, oral treponemes account for a small percentage of the total bacteria. However, in diseased periodontal pockets, treponemes thrive and become a dominant component of the bacterial population. Oral treponemes are uniquely adept at capitalizing on the environmental conditions that develop with periodontal disease. The molecular basis of adaptive responses of oral treponemes is just beginning to be investigated and defined. The completion of several treponeme genome sequences and the characterization of global regulatory systems provide an important starting point in the analysis of signaling and adaptive responses. In this review, we discuss existing literature focused on the genetic regulatory mechanisms of Treponema denticola and present an overview of the possible roles of regulatory proteins identified through genome analyses. This information provides insight into the possible molecular mechanisms utilized by oral spirochetes to survive in the periodontal pocket and transition from a minor to a dominant organism.

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Year:  2011        PMID: 21447698      PMCID: PMC3173007          DOI: 10.1177/0022034511402994

Source DB:  PubMed          Journal:  J Dent Res        ISSN: 0022-0345            Impact factor:   6.116


  58 in total

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Review 6.  C4-dicarboxylate carriers and sensors in bacteria.

Authors:  I G Janausch; E Zientz; Q H Tran; A Kröger; G Unden
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7.  The diversity of periodontal spirochetes by 16S rRNA analysis.

Authors:  F E Dewhirst; M A Tamer; R E Ericson; C N Lau; V A Levanos; S K Boches; J L Galvin; B J Paster
Journal:  Oral Microbiol Immunol       Date:  2000-06

8.  Detection of putative periodontal pathogens in non-insulin-dependent diabetes mellitus and non-diabetes mellitus by polymerase chain reaction.

Authors:  K Yuan; C J Chang; P C Hsu; H S Sun; C C Tseng; J R Wang
Journal:  J Periodontal Res       Date:  2001-02       Impact factor: 4.419

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Journal:  Proc Natl Acad Sci U S A       Date:  2001-10-23       Impact factor: 11.205

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Authors:  Andrew T Revel; Adel M Talaat; Michael V Norgard
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  13 in total

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2.  On the role, ecology, phylogeny, and structure of dual-family immunophilins.

Authors:  Sailen Barik
Journal:  Cell Stress Chaperones       Date:  2017-05-31       Impact factor: 3.667

3.  Development of a modified gentamicin resistance cassette for genetic manipulation of the oral spirochete Treponema denticola.

Authors:  Jiang Bian; J Christopher Fenno; Chunhao Li
Journal:  Appl Environ Microbiol       Date:  2012-01-13       Impact factor: 4.792

4.  Filifactor alocis interactions with gingival epithelial cells.

Authors:  C E Moffatt; S E Whitmore; A L Griffen; E J Leys; R J Lamont
Journal:  Mol Oral Microbiol       Date:  2011-09-13       Impact factor: 3.563

5.  Inactivation of cyclic Di-GMP binding protein TDE0214 affects the motility, biofilm formation, and virulence of Treponema denticola.

Authors:  Jiang Bian; Xiangyang Liu; Yi-Qiang Cheng; Chunhao Li
Journal:  J Bacteriol       Date:  2013-06-21       Impact factor: 3.490

6.  The Treponema denticola PAS Domain-Containing Histidine Kinase Hpk2 Is a Heme Binding Sensor of Oxygen Levels.

Authors:  Juni Sarkar; Daniel P Miller; Lee D Oliver; Richard T Marconi
Journal:  J Bacteriol       Date:  2018-08-24       Impact factor: 3.490

7.  Kanamycin Resistance Cassette for Genetic Manipulation of Treponema denticola.

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Journal:  Appl Environ Microbiol       Date:  2015-04-17       Impact factor: 4.792

8.  The Treponema denticola AtcR LytTR domain-containing response regulator interacts with three architecturally distinct promoter elements: implications for understanding the molecular signaling mechanisms that drive the progression of periodontal disease.

Authors:  D P Miller; J R Frederick; J Sarkar; R T Marconi
Journal:  Mol Oral Microbiol       Date:  2014-07-24       Impact factor: 3.563

Review 9.  Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response.

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