A general genetic approach in Escherichia coli for determining the mechanism(s) of action of tumoricidal agents: application to DMP 840, a tumoricidal agent.
Identifieur interne : 001233 ( Main/Exploration ); précédent : 001232; suivant : 001234A general genetic approach in Escherichia coli for determining the mechanism(s) of action of tumoricidal agents: application to DMP 840, a tumoricidal agent.
Auteurs : P K Chatterjee [États-Unis] ; N L SternbergSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1995.
Descripteurs français
- KwdFr :
- Analyse de séquence d'ADN (MeSH), Antinéoplasiques (pharmacologie), Arabinose (pharmacologie), Banque de gènes (MeSH), Cadres ouverts de lecture (génétique), Cartographie de restriction (MeSH), DNA topoisomerase IV (MeSH), Données de séquences moléculaires (MeSH), Escherichia coli (génétique), Gènes bactériens (MeSH), Inactivation métabolique (MeSH), Inhibiteurs de la topoisomérase-II (MeSH), Isoquinoléines (pharmacologie), Méthanesulfonates (pharmacologie), Nitroréductases (MeSH), Protéines Escherichia coli (MeSH), Protéines bactériennes (génétique), Régulation de l'expression des gènes bactériens (effets des médicaments et des substances chimiques), Résistance aux médicaments antinéoplasiques (MeSH), Résistance microbienne aux médicaments (génétique), Séquence d'acides aminés (MeSH), Séquence nucléotidique (MeSH), Tests de toxicité (méthodes).
- MESH :
- effets des médicaments et des substances chimiques : Régulation de l'expression des gènes bactériens.
- génétique : Cadres ouverts de lecture, Escherichia coli, Protéines bactériennes, Résistance microbienne aux médicaments.
- méthodes : Tests de toxicité.
- pharmacologie : Antinéoplasiques, Arabinose, Isoquinoléines, Méthanesulfonates.
- Analyse de séquence d'ADN, Banque de gènes, Cartographie de restriction, DNA topoisomerase IV, Données de séquences moléculaires, Gènes bactériens, Inactivation métabolique, Inhibiteurs de la topoisomérase-II, Nitroréductases, Protéines Escherichia coli, Résistance aux médicaments antinéoplasiques, Séquence d'acides aminés, Séquence nucléotidique.
English descriptors
- KwdEn :
- Amino Acid Sequence (MeSH), Antineoplastic Agents (pharmacology), Arabinose (pharmacology), Bacterial Proteins (genetics), Base Sequence (MeSH), DNA Topoisomerase IV (MeSH), Drug Resistance, Microbial (genetics), Drug Resistance, Neoplasm (MeSH), Escherichia coli (genetics), Escherichia coli Proteins (MeSH), Gene Expression Regulation, Bacterial (drug effects), Gene Library (MeSH), Genes, Bacterial (MeSH), Inactivation, Metabolic (MeSH), Isoquinolines (pharmacology), Mesylates (pharmacology), Molecular Sequence Data (MeSH), Nitroreductases (MeSH), Open Reading Frames (genetics), Restriction Mapping (MeSH), Sequence Analysis, DNA (MeSH), Topoisomerase II Inhibitors (MeSH), Toxicity Tests (methods).
- MESH :
- chemical , genetics : Bacterial Proteins.
- chemical , pharmacology : Antineoplastic Agents, Arabinose, Isoquinolines, Mesylates.
- drug effects : Gene Expression Regulation, Bacterial.
- genetics : Drug Resistance, Microbial, Escherichia coli, Open Reading Frames.
- methods : Toxicity Tests.
- Amino Acid Sequence, Base Sequence, DNA Topoisomerase IV, Drug Resistance, Neoplasm, Escherichia coli Proteins, Gene Library, Genes, Bacterial, Inactivation, Metabolic, Molecular Sequence Data, Nitroreductases, Restriction Mapping, Sequence Analysis, DNA, Topoisomerase II Inhibitors.
Abstract
We describe here a simple and easily manipulatable Escherichia coli-based genetic system that permits us to identify bacterial gene products that modulate the sensitivity of bacteria to tumoricidal agents, such as DMP 840, a bisnaphthalimide drug. To the extent that the action of these agents is conserved, these studies may expand our understanding agents is conserved, these studies may expand our understanding of how the agents work in mammalian cells. The approach briefly is to use a library of E. coli genes that are overexpressed in a high copy number vector to select bacterial clones that are resistant to the cytotoxic effects of drugs. AtolC bacterial mutant is used to maximize permeability of cells to hydrophobic organic molecules. By using DMP 840 to model the system, we have identified two genes, designated mdaA and mdaB, that impart resistance to DMP 840 when they are expressed at elevated levels. mdaB maps to E. coli map coordinate 66, is located between the parE and parC genes, and encodes a protein of 22 kDa. mdaA maps to E. coli map coordinate 18, is located adjacent to the glutaredoxin (grx) gene, and encodes a protein of 24 kDa. Specific and regulatable overproduction of both of these proteins correlates with DMP 840 resistance. Overproduction of the MdaB protein also imparts resistance to two mammalian topoisomerase inhibitors, Adriamycin and etoposide. In contrast, overproduction of the MdaA protein produces resistance only to Adriamycin. Based on its drug-resistance properties and its location between genes that encode the two subunits of the bacterial topoisomerase IV, we suggest that mdaB acts by modulating topoisomerase IV activity. The location of the mdaA gene adjacent to grx suggests it acts by a drug detoxification mechanism.
DOI: 10.1073/pnas.92.19.8950
PubMed: 7568050
PubMed Central: PMC41085
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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To the extent that the action of these agents is conserved, these studies may expand our understanding agents is conserved, these studies may expand our understanding of how the agents work in mammalian cells. The approach briefly is to use a library of E. coli genes that are overexpressed in a high copy number vector to select bacterial clones that are resistant to the cytotoxic effects of drugs. AtolC bacterial mutant is used to maximize permeability of cells to hydrophobic organic molecules. By using DMP 840 to model the system, we have identified two genes, designated mdaA and mdaB, that impart resistance to DMP 840 when they are expressed at elevated levels. mdaB maps to E. coli map coordinate 66, is located between the parE and parC genes, and encodes a protein of 22 kDa. mdaA maps to E. coli map coordinate 18, is located adjacent to the glutaredoxin (grx) gene, and encodes a protein of 24 kDa. Specific and regulatable overproduction of both of these proteins correlates with DMP 840 resistance. Overproduction of the MdaB protein also imparts resistance to two mammalian topoisomerase inhibitors, Adriamycin and etoposide. In contrast, overproduction of the MdaA protein produces resistance only to Adriamycin. Based on its drug-resistance properties and its location between genes that encode the two subunits of the bacterial topoisomerase IV, we suggest that mdaB acts by modulating topoisomerase IV activity. The location of the mdaA gene adjacent to grx suggests it acts by a drug detoxification mechanism.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">7568050</PMID><DateCompleted><Year>1995</Year><Month>10</Month><Day>23</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>01</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0027-8424</ISSN><JournalIssue CitedMedium="Print"><Volume>92</Volume><Issue>19</Issue><PubDate><Year>1995</Year><Month>Sep</Month><Day>12</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc Natl Acad Sci U S A</ISOAbbreviation></Journal><ArticleTitle>A general genetic approach in Escherichia coli for determining the mechanism(s) of action of tumoricidal agents: application to DMP 840, a tumoricidal agent.</ArticleTitle><Pagination><MedlinePgn>8950-4</MedlinePgn></Pagination><Abstract><AbstractText>We describe here a simple and easily manipulatable Escherichia coli-based genetic system that permits us to identify bacterial gene products that modulate the sensitivity of bacteria to tumoricidal agents, such as DMP 840, a bisnaphthalimide drug. To the extent that the action of these agents is conserved, these studies may expand our understanding agents is conserved, these studies may expand our understanding of how the agents work in mammalian cells. The approach briefly is to use a library of E. coli genes that are overexpressed in a high copy number vector to select bacterial clones that are resistant to the cytotoxic effects of drugs. AtolC bacterial mutant is used to maximize permeability of cells to hydrophobic organic molecules. By using DMP 840 to model the system, we have identified two genes, designated mdaA and mdaB, that impart resistance to DMP 840 when they are expressed at elevated levels. mdaB maps to E. coli map coordinate 66, is located between the parE and parC genes, and encodes a protein of 22 kDa. mdaA maps to E. coli map coordinate 18, is located adjacent to the glutaredoxin (grx) gene, and encodes a protein of 24 kDa. Specific and regulatable overproduction of both of these proteins correlates with DMP 840 resistance. Overproduction of the MdaB protein also imparts resistance to two mammalian topoisomerase inhibitors, Adriamycin and etoposide. In contrast, overproduction of the MdaA protein produces resistance only to Adriamycin. Based on its drug-resistance properties and its location between genes that encode the two subunits of the bacterial topoisomerase IV, we suggest that mdaB acts by modulating topoisomerase IV activity. The location of the mdaA gene adjacent to grx suggests it acts by a drug detoxification mechanism.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chatterjee</LastName><ForeName>P K</ForeName><Initials>PK</Initials><AffiliationInfo><Affiliation>DuPont Merck Pharmaceutical Company, Glenolden, PA 19036, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sternberg</LastName><ForeName>N L</ForeName><Initials>NL</Initials></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>GENBANK</DataBankName><AccessionNumberList><AccessionNumber>U18655</AccessionNumber><AccessionNumber>U18656</AccessionNumber></AccessionNumberList></DataBank></DataBankList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029968">Escherichia coli Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007546">Isoquinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C095690">MdaB protein, E coli</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008698">Mesylates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D059005">Topoisomerase II 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MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001089" MajorTopicYN="N">Arabinose</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D027101" MajorTopicYN="N">DNA Topoisomerase IV</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004352" MajorTopicYN="N">Drug Resistance, Microbial</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019008" MajorTopicYN="Y">Drug Resistance, 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uniqKey="Sternberg N" first="N L" last="Sternberg">N L Sternberg</name></noCountry><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Chatterjee, P K" sort="Chatterjee, P K" uniqKey="Chatterjee P" first="P K" last="Chatterjee">P K Chatterjee</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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