1zkj

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(New page: 200px<br /><applet load="1zkj" size="350" color="white" frame="true" align="right" spinBox="true" caption="1zkj, resolution 1.55&Aring;" /> '''Structural Basis for...)
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==Overview==
==Overview==
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The emergence and dissemination of extended-spectrum (ES) beta-lactamases, induce therapeutic failure and a lack of eradication of clinical isolates, even by third-generation beta-lactam antibiotics like ceftazidime. CMY-10, is a plasmid-encoded class C beta-lactamase with a wide spectrum of, substrates. Unlike the well-studied class C ES beta-lactamase from, Enterobacter cloacae GC1, the Omega-loop does not affect the active site, conformation and the catalytic activity of CMY-10. Instead, a, three-amino-acid deletion in the R2-loop appears to be responsible for the, ES activity of CMY-10. According to the crystal structure solved at 1.55 A, resolution, the deletion significantly widens the R2 active site, which, accommodates the R2 side-chains of beta-lactam antibiotics. This, observation led us to demonstrate the hydrolysing activity of CMY-10, towards imipenem with a long R2 substituent. The forced mutational, analyses of P99 beta-lactamase reveal that the introduction of deletion, mutations into the R2-loop is able to extend the substrate spectrum of, class C non-ES beta-lactamases, which is compatible with the isolation of, natural class C ES enzymes harbouring deletion mutations in the R2-loop., Consequently, the opening of the R2 active site by the deletion of some, residues in the R2-loop can be considered as an operative molecular, strategy of class C beta-lactamases to extend their substrate spectrum.
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The emergence and dissemination of extended-spectrum (ES) beta-lactamases induce therapeutic failure and a lack of eradication of clinical isolates even by third-generation beta-lactam antibiotics like ceftazidime. CMY-10 is a plasmid-encoded class C beta-lactamase with a wide spectrum of substrates. Unlike the well-studied class C ES beta-lactamase from Enterobacter cloacae GC1, the Omega-loop does not affect the active site conformation and the catalytic activity of CMY-10. Instead, a three-amino-acid deletion in the R2-loop appears to be responsible for the ES activity of CMY-10. According to the crystal structure solved at 1.55 A resolution, the deletion significantly widens the R2 active site, which accommodates the R2 side-chains of beta-lactam antibiotics. This observation led us to demonstrate the hydrolysing activity of CMY-10 towards imipenem with a long R2 substituent. The forced mutational analyses of P99 beta-lactamase reveal that the introduction of deletion mutations into the R2-loop is able to extend the substrate spectrum of class C non-ES beta-lactamases, which is compatible with the isolation of natural class C ES enzymes harbouring deletion mutations in the R2-loop. Consequently, the opening of the R2 active site by the deletion of some residues in the R2-loop can be considered as an operative molecular strategy of class C beta-lactamases to extend their substrate spectrum.
==About this Structure==
==About this Structure==
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[[Category: Enterobacter aerogenes]]
[[Category: Enterobacter aerogenes]]
[[Category: Single protein]]
[[Category: Single protein]]
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[[Category: An, Y.J.]]
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[[Category: An, Y J.]]
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[[Category: Cha, S.S.]]
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[[Category: Cha, S S.]]
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[[Category: Jung, H.I.]]
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[[Category: Jung, H I.]]
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[[Category: Lee, S.H.]]
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[[Category: Lee, S H.]]
[[Category: ACY]]
[[Category: ACY]]
[[Category: ZN]]
[[Category: ZN]]
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[[Category: plasmid]]
[[Category: plasmid]]
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Tue Jan 29 17:36:54 2008''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 16:16:29 2008''

Revision as of 14:16, 21 February 2008


1zkj, resolution 1.55Å

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Structural Basis for the Extended Substrate Spectrum of CMY-10, a Plasmid-Encoded Class C beta-lactamase

Overview

The emergence and dissemination of extended-spectrum (ES) beta-lactamases induce therapeutic failure and a lack of eradication of clinical isolates even by third-generation beta-lactam antibiotics like ceftazidime. CMY-10 is a plasmid-encoded class C beta-lactamase with a wide spectrum of substrates. Unlike the well-studied class C ES beta-lactamase from Enterobacter cloacae GC1, the Omega-loop does not affect the active site conformation and the catalytic activity of CMY-10. Instead, a three-amino-acid deletion in the R2-loop appears to be responsible for the ES activity of CMY-10. According to the crystal structure solved at 1.55 A resolution, the deletion significantly widens the R2 active site, which accommodates the R2 side-chains of beta-lactam antibiotics. This observation led us to demonstrate the hydrolysing activity of CMY-10 towards imipenem with a long R2 substituent. The forced mutational analyses of P99 beta-lactamase reveal that the introduction of deletion mutations into the R2-loop is able to extend the substrate spectrum of class C non-ES beta-lactamases, which is compatible with the isolation of natural class C ES enzymes harbouring deletion mutations in the R2-loop. Consequently, the opening of the R2 active site by the deletion of some residues in the R2-loop can be considered as an operative molecular strategy of class C beta-lactamases to extend their substrate spectrum.

About this Structure

1ZKJ is a Single protein structure of sequence from Enterobacter aerogenes with and as ligands. Active as Beta-lactamase, with EC number 3.5.2.6 Full crystallographic information is available from OCA.

Reference

Structural basis for the extended substrate spectrum of CMY-10, a plasmid-encoded class C beta-lactamase., Kim JY, Jung HI, An YJ, Lee JH, Kim SJ, Jeong SH, Lee KJ, Suh PG, Lee HS, Lee SH, Cha SS, Mol Microbiol. 2006 May;60(4):907-16. PMID:16677302

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