2r7z

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Revision as of 10:10, 23 January 2008

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spinqualitylabelsall models 2r7z, resolution 3.80Å Show:Asymmetric Unit Biological Assembly Drag the structure with the mouse to rotate   Export Animated Image

Cisplatin lesion containing RNA polymerase II elongation complex

Overview

The anticancer drug cisplatin forms 1,2-d(GpG) DNA intrastrand cross-links, (cisplatin lesions) that stall RNA polymerase II (Pol II) and trigger, transcription-coupled DNA repair. Here we present a structure-function, analysis of Pol II stalling at a cisplatin lesion in the DNA template. Pol, II stalling results from a translocation barrier that prevents delivery of, the lesion to the active site. AMP misincorporation occurs at the barrier, and also at an abasic site, suggesting that it arises from nontemplated, synthesis according to an 'A-rule' known for DNA polymerases. Pol II can, bypass a cisplatin lesion that is artificially placed beyond the, translocation barrier, even in the presence of a G.A mismatch. Thus, the, barrier prevents transcriptional mutagenesis. The stalling mechanism, differs from that of Pol II stalling at a photolesion, which involves, delivery of the lesion to the active site and lesion-templated, misincorporation that blocks transcription.

About this Structure

2R7Z is a Protein complex structure of sequences from Saccharomyces cerevisiae with , and as ligands. Active as DNA-directed RNA polymerase, with EC number 2.7.7.6 Full crystallographic information is available from OCA.

Reference

Mechanism of transcriptional stalling at cisplatin-damaged DNA., Damsma GE, Alt A, Brueckner F, Carell T, Cramer P, Nat Struct Mol Biol. 2007 Nov 11;. PMID:17994106

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