WhiB7, a transcriptional activator that coordinates physiology with intrinsic drug resistance in Mycobacterium tuberculosis.
Identifieur interne : 001910 ( Main/Exploration ); précédent : 001909; suivant : 001911WhiB7, a transcriptional activator that coordinates physiology with intrinsic drug resistance in Mycobacterium tuberculosis.
Auteurs : Ján Burian [Canada] ; Santiago Ram N-García ; Charles G. Howes ; Charles J. ThompsonSource :
- Expert review of anti-infective therapy [ 1744-8336 ] ; 2012.
Descripteurs français
- KwdFr :
- Antituberculeux (pharmacologie), Facteurs de transcription (composition chimique), Facteurs de transcription (génétique), Facteurs de transcription (physiologie), Mycobacterium tuberculosis (effets des médicaments et des substances chimiques), Mycobacterium tuberculosis (génétique), Mycobacterium tuberculosis (métabolisme), Oxydoréduction (MeSH), Protéines bactériennes (composition chimique), Protéines bactériennes (génétique), Protéines bactériennes (physiologie), Régulation de l'expression des gènes bactériens (MeSH), Régulon (effets des médicaments et des substances chimiques), Régulon (physiologie), Résistance bactérienne aux médicaments (génétique).
- MESH :
- composition chimique : Facteurs de transcription, Protéines bactériennes.
- effets des médicaments et des substances chimiques : Mycobacterium tuberculosis, Régulon.
- génétique : Facteurs de transcription, Mycobacterium tuberculosis, Protéines bactériennes, Résistance bactérienne aux médicaments.
- métabolisme : Mycobacterium tuberculosis.
- pharmacologie : Antituberculeux.
- physiologie : Facteurs de transcription, Protéines bactériennes, Régulon.
- Oxydoréduction, Régulation de l'expression des gènes bactériens.
English descriptors
- KwdEn :
- Antitubercular Agents (pharmacology), Bacterial Proteins (chemistry), Bacterial Proteins (genetics), Bacterial Proteins (physiology), Drug Resistance, Bacterial (genetics), Gene Expression Regulation, Bacterial (MeSH), Mycobacterium tuberculosis (drug effects), Mycobacterium tuberculosis (genetics), Mycobacterium tuberculosis (metabolism), Oxidation-Reduction (MeSH), Regulon (drug effects), Regulon (physiology), Transcription Factors (chemistry), Transcription Factors (genetics), Transcription Factors (physiology).
- MESH :
- chemical , chemistry : Bacterial Proteins, Transcription Factors.
- chemical , genetics : Bacterial Proteins, Transcription Factors.
- chemical , pharmacology : Antitubercular Agents.
- chemical , physiology : Bacterial Proteins, Transcription Factors.
- drug effects : Mycobacterium tuberculosis, Regulon.
- genetics : Drug Resistance, Bacterial, Mycobacterium tuberculosis.
- metabolism : Mycobacterium tuberculosis.
- physiology : Regulon.
- Gene Expression Regulation, Bacterial, Oxidation-Reduction.
Abstract
Current tuberculosis treatment regimens are notoriously limited, lengthy and becoming increasingly ineffective due to the emergence of drug-resistant mutant strains of Mycobacterium tuberculosis. The intrinsic resistance of M. tuberculosis to the majority of available drugs relies both on the impermeability of its cell envelope, and its ability to activate specific genes and physiological states. WhiB7 is a transcriptional regulatory protein underlying this adaptive process. Transcription of the whiB7 gene is upregulated in response to a variety of antibiotics having different structures and targets, as well as in response to metabolic signals. The whiB7 regulon activates various systems of intrinsic drug resistance involving antibiotic export, antibiotic inactivation (by chemical modifications of the drug or its target) and significant changes to thiol redox balance. Drugs have been identified that inactivate resistance determinants in the whiB7 regulon, thereby potentiating the activities of diverse antibiotics against M. tuberculosis.
DOI: 10.1586/eri.12.90
PubMed: 23106278
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Howes</name></author><author><name sortKey="Thompson, Charles J" sort="Thompson, Charles J" uniqKey="Thompson C" first="Charles J" last="Thompson">Charles J. 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The intrinsic resistance of M. tuberculosis to the majority of available drugs relies both on the impermeability of its cell envelope, and its ability to activate specific genes and physiological states. WhiB7 is a transcriptional regulatory protein underlying this adaptive process. Transcription of the whiB7 gene is upregulated in response to a variety of antibiotics having different structures and targets, as well as in response to metabolic signals. The whiB7 regulon activates various systems of intrinsic drug resistance involving antibiotic export, antibiotic inactivation (by chemical modifications of the drug or its target) and significant changes to thiol redox balance. Drugs have been identified that inactivate resistance determinants in the whiB7 regulon, thereby potentiating the activities of diverse antibiotics against M. tuberculosis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23106278</PMID><DateCompleted><Year>2013</Year><Month>03</Month><Day>27</Day></DateCompleted><DateRevised><Year>2012</Year><Month>10</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1744-8336</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>9</Issue><PubDate><Year>2012</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Expert review of anti-infective therapy</Title><ISOAbbreviation>Expert Rev Anti Infect Ther</ISOAbbreviation></Journal><ArticleTitle>WhiB7, a transcriptional activator that coordinates physiology with intrinsic drug resistance in Mycobacterium tuberculosis.</ArticleTitle><Pagination><MedlinePgn>1037-47</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1586/eri.12.90</ELocationID><Abstract><AbstractText>Current tuberculosis treatment regimens are notoriously limited, lengthy and becoming increasingly ineffective due to the emergence of drug-resistant mutant strains of Mycobacterium tuberculosis. The intrinsic resistance of M. tuberculosis to the majority of available drugs relies both on the impermeability of its cell envelope, and its ability to activate specific genes and physiological states. WhiB7 is a transcriptional regulatory protein underlying this adaptive process. Transcription of the whiB7 gene is upregulated in response to a variety of antibiotics having different structures and targets, as well as in response to metabolic signals. The whiB7 regulon activates various systems of intrinsic drug resistance involving antibiotic export, antibiotic inactivation (by chemical modifications of the drug or its target) and significant changes to thiol redox balance. Drugs have been identified that inactivate resistance determinants in the whiB7 regulon, thereby potentiating the activities of diverse antibiotics against M. tuberculosis.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Burian</LastName><ForeName>Ján</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ramón-García</LastName><ForeName>Santiago</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Howes</LastName><ForeName>Charles G</ForeName><Initials>CG</Initials></Author><Author ValidYN="Y"><LastName>Thompson</LastName><ForeName>Charles J</ForeName><Initials>CJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MOP-82855</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Rev Anti Infect Ther</MedlineTA><NlmUniqueID>101181284</NlmUniqueID><ISSNLinking>1478-7210</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000995">Antitubercular Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000995" MajorTopicYN="N">Antitubercular Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D024881" MajorTopicYN="N">Drug Resistance, Bacterial</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015964" MajorTopicYN="Y">Gene Expression Regulation, Bacterial</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009169" MajorTopicYN="N">Mycobacterium tuberculosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018085" MajorTopicYN="N">Regulon</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>3</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23106278</ArticleId><ArticleId IdType="doi">10.1586/eri.12.90</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Colombie-Britannique </li></region><settlement><li>Vancouver</li></settlement><orgName><li>Université de la Colombie-Britannique</li></orgName></list><tree><noCountry><name sortKey="Howes, Charles G" sort="Howes, Charles G" uniqKey="Howes C" first="Charles G" last="Howes">Charles G. Howes</name><name sortKey="Ram N Garcia, Santiago" sort="Ram N Garcia, Santiago" uniqKey="Ram N Garcia S" first="Santiago" last="Ram N-García">Santiago Ram N-García</name><name sortKey="Thompson, Charles J" sort="Thompson, Charles J" uniqKey="Thompson C" first="Charles J" last="Thompson">Charles J. Thompson</name></noCountry><country name="Canada"><region name="Colombie-Britannique "><name sortKey="Burian, Jan" sort="Burian, Jan" uniqKey="Burian J" first="Ján" last="Burian">Ján Burian</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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