Difference between revisions of "User:Scmohr/Antibiotic-res cat page"
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==Introduction to Antibiotic Resistance== | ==Introduction to Antibiotic Resistance== | ||
| − | The established mechanisms of antibiotic resistance include the following: | + | The established mechanisms of antibiotic resistance include the following: (1.) Enzymes that inactivate the antibiotic [famously (a). beta-lactamases that destroy penicillins and related compounds and (b) enzymes that acetylate chloramphenicol]. (2.) Proteins that keep antibiotics from entering the cell (by blocking the outer-membrane pores). (3) Membrane-embedded channel proteins that actively pump antibiotics out of the cell. (4.) Proteins (and RNAs?) with altered drug binding sites. (Vancomycin resistance comes from a switch in the chemistry of the cell-wall cross-linking peptide). This category also includes mutations in ribosomal RNA -- ribosomes are one of the main targets of both prokaryote- and eukaryote-directed antibiotics. (5.) Proteins that enable substitution of an alternative metabolic pathway (as in the case of sulfonamide resistance). |
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==Parts by Category== | ==Parts by Category== | ||
Revision as of 15:08, 23 July 2008
Contents
Antibiotic Resistance Parts
Introduction to Antibiotic Resistance
The established mechanisms of antibiotic resistance include the following: (1.) Enzymes that inactivate the antibiotic [famously (a). beta-lactamases that destroy penicillins and related compounds and (b) enzymes that acetylate chloramphenicol]. (2.) Proteins that keep antibiotics from entering the cell (by blocking the outer-membrane pores). (3) Membrane-embedded channel proteins that actively pump antibiotics out of the cell. (4.) Proteins (and RNAs?) with altered drug binding sites. (Vancomycin resistance comes from a switch in the chemistry of the cell-wall cross-linking peptide). This category also includes mutations in ribosomal RNA -- ribosomes are one of the main targets of both prokaryote- and eukaryote-directed antibiotics. (5.) Proteins that enable substitution of an alternative metabolic pathway (as in the case of sulfonamide resistance).