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. 2011 Aug 3;39(21):9306–9315. doi: 10.1093/nar/gkr619

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© The Author(s) 2011. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 7. — A dynamic system for Gln-tRNA^Gln synthesis, which limits free Glu-tRNA^Gln in H. pylori. The constants shown are the k_cat/K_M values calculated from the data in Table 2, for GluRS2 and GatCAB as free enzymes, and for the stoechiometric mix forming the Gln-transamidosome. Starting with tRNA^Gln, the Gln-transamidosome pathway is favoured, with a k_cat/K_M value greater than that of the GluRS2 pathway. Glu-tRNA^Gln which is formed outside the Gln-transamidosome is susceptible to deacylation by GluRS2, or to an efficient transamidation by free GatCAB. The entire system therefore regulates against the presence of free Glu-tRNA^Gln.