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Macrolide resistance based on the Erm-mediated rRNA methylation (CROSBI ID 111234)

Prilog u časopisu | pregledni rad (znanstveni) | međunarodna recenzija

Maravić, Gordana Macrolide resistance based on the Erm-mediated rRNA methylation // Current drug targets. Infectious disorders, 4 (2004), 3; 193-202-x

Podaci o odgovornosti

Maravić, Gordana

engleski

Macrolide resistance based on the Erm-mediated rRNA methylation

Macrolide, lincosamide and streptogramin B (MLSB) antibiotics are extensively used for the treatment of wide variety of clinically important Gram-positive bacteria. MLSB antibiotics inhibit protein biosynthesis by targeting the peptidyl transferase centre within the 50S ribosomal subunit. The most widespread mechanism of bacterial resistance to MLSB antibiotics, reported early after their introduction into clinical practice is the modification of the target site exhibited by a family of rRNA methyltransferases designated Erm. Using S-adenosyl-L-methionine, Erm enzymes catalyze mono- or dimethylation of a specific adenine residue in the 23S rRNA. The methyl group sterically hinders the MLSB binding site and disrupts the hydrogen bonding between the macrolides and the rRNA, thus rendering bacteria resistant. This review summarizes the current understanding of Erm-mediated resistance, in light of high-resolution structural data of bacterial ribosome and with specific focus on the results of recent genetic, biochemical and structural studies of Erm methyltransferases and their cognate rRNA substrate. Although many features of MLSB resistance remain indistinct, the present knowledge can now serve as the guidance for development of both new antimicrobial drugs and potential inhibitors of Erm enzymes, hence providing a new lead to solve the urgent problem of the macrolide resistance based on the ribosome methylation.

antibiotics; MLSB resistance; Erm methyltransferases; inhibitors

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Podaci o izdanju

4 (3)

2004.

193-202-x

objavljeno

1568-0053

Povezanost rada

Biologija

Indeksiranost