3pm1: Difference between revisions

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[[Image:3pm1.jpg|left|200px]]
<!--
The line below this paragraph, containing "STRUCTURE_3pm1", creates the "Structure Box" on the page.
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{{STRUCTURE_3pm1|  PDB=3pm1  |  SCENE=  }}  
{{STRUCTURE_3pm1|  PDB=3pm1  |  SCENE=  }}  
===Structure of QacR E90Q bound to Ethidium===
===Structure of QacR E90Q bound to Ethidium===
{{ABSTRACT_PUBMED_21264225}}


 
==Function==
<!--
[[http://www.uniprot.org/uniprot/QACR_STAAM QACR_STAAM]] Transcriptional repressor of qacA. Binds to IR1, an unusually long 28 bp operator, which is located downstream from the qacA promoter and overlaps its transcription start site. QacR is induced from its IR1 site by binding to one of many structurally dissimilar cationic lipophilic compounds, which are also substrates of QacA (By similarity).  
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{{ABSTRACT_PUBMED_21264225}}


==About this Structure==
==About this Structure==
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==Reference==
==Reference==
<ref group="xtra">PMID:021264225</ref><references group="xtra"/>
<ref group="xtra">PMID:021264225</ref><references group="xtra"/><references/>
[[Category: Staphylococcus aureus]]
[[Category: Staphylococcus aureus]]
[[Category: Schumacher, M A.]]
[[Category: Schumacher, M A.]]

Revision as of 07:42, 16 May 2013

Template:STRUCTURE 3pm1

Structure of QacR E90Q bound to Ethidium

Template:ABSTRACT PUBMED 21264225

Function

[QACR_STAAM] Transcriptional repressor of qacA. Binds to IR1, an unusually long 28 bp operator, which is located downstream from the qacA promoter and overlaps its transcription start site. QacR is induced from its IR1 site by binding to one of many structurally dissimilar cationic lipophilic compounds, which are also substrates of QacA (By similarity).

About this Structure

3pm1 is a 2 chain structure with sequence from Staphylococcus aureus. Full crystallographic information is available from OCA.

Reference

  1. Peters KM, Brooks BE, Schumacher MA, Skurray RA, Brennan RG, Brown MH. A single acidic residue can guide binding site selection but does not govern QacR cationic-drug affinity. PLoS One. 2011 Jan 17;6(1):e15974. PMID:21264225 doi:10.1371/journal.pone.0015974

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