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Gene Review

tetK  -  tetracycline efflux protein

Staphylococcus lentus

 
 
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Disease relevance of tetK

 

High impact information on tetK

  • If an outwardly directed gradient of Na+ or K+ was present, Rb+ uptake occurred without energization in vesicles from cells transformed with a plasmid containing tetA(L) or tetK but not a control plasmid [1].
  • In summary, our data indicate that the observed dramatic enhancement by EGCg of tetracycline activity for resistant staphylococcal isolates is caused by impairment of tetracycline efflux pump activity and increased intracellular retention of the drug, suggesting a possible use of EGCg as an adjuvant in antibacterial therapy [4].
  • Mutations in the tetA(B) gene that cause a change in substrate specificity of the tetracycline efflux pump [5].
  • A double disc diffusion method has been developed to identify inducible resistance to minocycline and to distinguish between tetK, tetM and tetKM isolates [6].
  • Allele replacement of the femAB operon with the tetracycline resistance determinant tetK in a methicillin-resistant Staphylococcus aureus strain resulted in impaired growth, methicillin hypersusceptibility, and lysostaphin resistance [7].
 

Chemical compound and disease context of tetK

 

Biological context of tetK

 

Associations of tetK with chemical compounds

References

  1. Electrogenic antiport activities of the Gram-positive Tet proteins include a Na+(K+)/K+ mode that mediates net K+ uptake. Guffanti, A.A., Cheng, J., Krulwich, T.A. J. Biol. Chem. (1998) [Pubmed]
  2. Expression of the tetK gene from Staphylococcus aureus in Escherichia coli: comparison of substrate specificities of TetA(B), TetA(C), and TetK efflux proteins. Guay, G.G., Rothstein, D.M. Antimicrob. Agents Chemother. (1993) [Pubmed]
  3. Presence of the Tet M determinant in a clinical isolate of Acinetobacter baumannii. Ribera, A., Ruiz, J., Vila, J. Antimicrob. Agents Chemother. (2003) [Pubmed]
  4. Epigallocatechin-gallate enhances the activity of tetracycline in staphylococci by inhibiting its efflux from bacterial cells. Sudano Roccaro, A., Blanco, A.R., Giuliano, F., Rusciano, D., Enea, V. Antimicrob. Agents Chemother. (2004) [Pubmed]
  5. Mutations in the tetA(B) gene that cause a change in substrate specificity of the tetracycline efflux pump. Guay, G.G., Tuckman, M., Rothstein, D.M. Antimicrob. Agents Chemother. (1994) [Pubmed]
  6. Expression of resistance to tetracyclines in strains of methicillin-resistant Staphylococcus aureus. Trzcinski, K., Cooper, B.S., Hryniewicz, W., Dowson, C.G. J. Antimicrob. Chemother. (2000) [Pubmed]
  7. Cell wall monoglycine cross-bridges and methicillin hypersusceptibility in a femAB null mutant of methicillin-resistant Staphylococcus aureus. Strandén, A.M., Ehlert, K., Labischinski, H., Berger-Bächi, B. J. Bacteriol. (1997) [Pubmed]
  8. Analysis of mutations in the Staphylococcus aureus clfB promoter leading to increased expression. McAleese, F.M., Foster, T.J. Microbiology (Reading, Engl.) (2003) [Pubmed]
  9. DNA microarray for the detection of therapeutically relevant antibiotic resistance determinants in clinical isolates of Staphylococcus aureus. Strommenger, B., Schmidt, C., Werner, G., Roessle-Lorch, B., Bachmann, T.T., Witte, W. Mol. Cell. Probes (2007) [Pubmed]
  10. The tet(K) gene of plasmid pT181 of Staphylococcus aureus encodes an efflux protein that contains 14 transmembrane helices. Guay, G.G., Khan, S.A., Rothstein, D.M. Plasmid (1993) [Pubmed]
 
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