2g9w | pdb_00002g9w

Crystal Structure of Rv1846c, a Putative Transcriptional Regulatory Protein of Mycobacterium Tuberculosis

spinqualitylabelsall models 2g9w, resolution 1.80Å Show:Asymmetric Unit Biological Assembly Drag the structure with the mouse to rotate   Export Animated Image   Print3D Structural highlights 2g9w is a 2 chain structure with sequence from Mycobacterium tuberculosis H37Rv. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance. Method: X-ray diffraction, Resolution 1.8Å Ligands: CL, MSE Resources: FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT Function BLAI_MYCTU Transcription regulator that binds to an inverted DNA repeat with the consensus sequence 5'-TAC[GT]AC-NNNNN-GT[AC]GTA-3' and regulates genes involved in antibiotic transport, detoxification and cell wall function. Also regulates its own transcription. Binds DNA as a dimer. Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. Publication Abstract from PubMed Comparative genomics with Staphylococcus aureus suggested the existence of a regulatory system governing beta-lactamase (BlaC) production in Mycobacterium tuberculosis. The crystal structure of Rv1846c, a winged helix regulator of previously unknown function, was solved thus revealing strong similarity to the BlaI and MecI repressors of S. aureus, which both respond to beta-lactam treatment. Using chromatin immunoprecipitation and hybridization to microarrays (ChIP-on-chip), the Rv1846c regulon was shown to comprise five separate genomic loci. Two of these mediate responses and resistance to beta-lactam antibiotics (rv1845c, rv1846c-rv1847; blaC-sigC); two encode membrane proteins of unknown function (rv1456c, rv3921c) while the last codes for ATP synthase (rv1303-atpBEFHAGDC-rv1312). The ChIP-on-chip findings were confirmed independently using electrophoretic mobility shift assays, DNAse footprinting and transcript analysis leading to Rv1846c being renamed BlaI. When cells were treated with beta-lactams, BlaI was released from its operator sites causing derepression of the regulon and upregulation of ATP synthase transcription. The existence of a potential regulatory loop between cell wall integrity and ATP production was previously unknown. Genome-wide regulon and crystal structure of BlaI (Rv1846c) from Mycobacterium tuberculosis.,Sala C, Haouz A, Saul FA, Miras I, Rosenkrands I, Alzari PM, Cole ST Mol Microbiol. 2009 Mar;71(5):1102-16. Epub 2009 Jan 16. PMID:19154333 From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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