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Overview
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Background
Mechanism of Action
Blasticidin S HCl inhibits protein synthesis in prokaryotic and eukaryotic cells by binding to the ribosomal P-site which strengthens tRNA binding and slows down and prevents subsequent peptide synthesis.
Mechanisms of Resistance
Resistance to Blasticidin S is conferred by bsr, BSD, and bls resistance genes isolated from Bacillus cereus K55-S1, Aspergillus terreus, and Streptoverticillum spp, respectively.
The bsr resistance gene is a 420 bp fragment and encodes a 15 kDa Blasticidin S deaminase which catalyzes the reaction of blasticidin S to deaminohydroxyblasticidin S. Deaminohydroxyblasticidin S is a biologically inactive derivative of blasticidin S and does not interact with or inhibit prokaryotic or eukaryotic ribosomes.
The BSD resistance gene is a 393 bp fragment and also encodes a Blasticidin S deaminase enzyme which catalyzes a similar reaction to the BSR deaminase. A study by Kimura et al. found the transfection frequency with bsd to be 80X greater than with bsr when using FM3A cells.
The bls gene resistance gene encodes an acetyltransferase which interacts with acetyl-coenzyme A and prevents blasticidin S from inhibiting protein synthesis.
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Overview