Transcriptional response pathways in a yeast strain sensitive to saframycin a and a more potent analog: evidence for a common basis of activity.
Identifieur interne : 001959 ( Main/Exploration ); précédent : 001958; suivant : 001960Transcriptional response pathways in a yeast strain sensitive to saframycin a and a more potent analog: evidence for a common basis of activity.
Auteurs : Alleyn T. Plowright [États-Unis] ; Scott E. Schaus ; Andrew G. MyersSource :
- Chemistry & biology [ 1074-5521 ] ; 2002.
Descripteurs français
- KwdFr :
- ADN fongique (analyse), ADN fongique (génétique), ADN fongique (isolement et purification), Acides gras (biosynthèse), Acétyl coenzyme A (métabolisme), Altération de l'ADN (génétique), Analyse de profil d'expression de gènes (MeSH), Cellules cancéreuses en culture (MeSH), Dioxoles (pharmacologie), Génome fongique (MeSH), Humains (MeSH), Isoquinoléines (pharmacologie), Protéines fongiques (génétique), Protéines fongiques (métabolisme), Quinoléines (pharmacologie), Relation structure-activité (MeSH), Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Stress oxydatif (MeSH), Séquençage par oligonucléotides en batterie (MeSH), Trabectédine (MeSH), Transcription génétique (effets des médicaments et des substances chimiques), Tétrahydroisoquinoléines (MeSH).
- MESH :
- analyse : ADN fongique.
- biosynthèse : Acides gras.
- croissance et développement : Saccharomyces cerevisiae.
- effets des médicaments et des substances chimiques : Régulation de l'expression des gènes fongiques, Saccharomyces cerevisiae, Transcription génétique.
- génétique : ADN fongique, Altération de l'ADN, Protéines fongiques, Saccharomyces cerevisiae.
- isolement et purification : ADN fongique.
- métabolisme : Acétyl coenzyme A, Protéines fongiques, Saccharomyces cerevisiae.
- pharmacologie : Dioxoles, Isoquinoléines, Quinoléines, Sirolimus.
- Analyse de profil d'expression de gènes, Cellules cancéreuses en culture, Génome fongique, Humains, Relation structure-activité, Stress oxydatif, Séquençage par oligonucléotides en batterie, Trabectédine, Tétrahydroisoquinoléines.
English descriptors
- KwdEn :
- Acetyl Coenzyme A (metabolism), DNA Damage (genetics), DNA, Fungal (analysis), DNA, Fungal (genetics), DNA, Fungal (isolation & purification), Dioxoles (pharmacology), Fatty Acids (biosynthesis), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (drug effects), Genome, Fungal (MeSH), Humans (MeSH), Isoquinolines (pharmacology), Oligonucleotide Array Sequence Analysis (MeSH), Oxidative Stress (MeSH), Quinolines (pharmacology), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Sirolimus (pharmacology), Structure-Activity Relationship (MeSH), Tetrahydroisoquinolines (MeSH), Trabectedin (MeSH), Transcription, Genetic (drug effects), Tumor Cells, Cultured (MeSH).
- MESH :
- chemical , analysis : DNA, Fungal.
- chemical , biosynthesis : Fatty Acids.
- chemical , genetics : DNA, Fungal, Fungal Proteins.
- chemical , isolation & purification : DNA, Fungal.
- chemical , metabolism : Acetyl Coenzyme A, Fungal Proteins.
- drug effects : Gene Expression Regulation, Fungal, Saccharomyces cerevisiae, Transcription, Genetic.
- genetics : DNA Damage, Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- chemical , pharmacology : Dioxoles, Isoquinolines, Quinolines, Sirolimus.
- Gene Expression Profiling, Genome, Fungal, Humans, Oligonucleotide Array Sequence Analysis, Oxidative Stress, Structure-Activity Relationship, Tetrahydroisoquinolines, Trabectedin, Tumor Cells, Cultured.
Abstract
Saframycin A (SafA) is a natural product that inhibits human cancer cell proliferation. Its synthetic analog, QAD, is a more potent inhibitor of these cells. SafA does not affect wild-type yeast, but it does inhibit growth of the strain CCY333 (DeltaPDR1/PDR3/ERG6) (IC50 = 0.9 microM). QAD is also a more effective inhibitor of CCY333 growth (IC50 = 0.4 microM). Transcription profiling of SafA- and QAD-treated CCY333 cultures showed that both drugs generated nearly identical profiles, with altered expression levels (> or =2-fold) of more than 240 genes. Both agents induced the overexpression of genes involved in glycolysis, oxidative stress, and protein degradation and repressed genes encoding histones, biosynthetic enzymes, and the cellular import machinery. Significantly, neither drug affected the expression of known DNA-damage repair genes, as might have been expected if their primary mechanism of action involved the covalent modification of DNA.
DOI: 10.1016/s1074-5521(02)00137-0
PubMed: 12031667
Affiliations:
Links toward previous steps (curation, corpus...)
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(MeSH)</term><term>Isoquinoléines (pharmacologie)</term><term>Protéines fongiques (génétique)</term><term>Protéines fongiques (métabolisme)</term><term>Quinoléines (pharmacologie)</term><term>Relation structure-activité (MeSH)</term><term>Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (croissance et développement)</term><term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term><term>Saccharomyces cerevisiae (génétique)</term><term>Saccharomyces cerevisiae (métabolisme)</term><term>Sirolimus (pharmacologie)</term><term>Stress oxydatif (MeSH)</term><term>Séquençage par oligonucléotides en batterie (MeSH)</term><term>Trabectédine (MeSH)</term><term>Transcription génétique (effets des médicaments et des substances chimiques)</term><term>Tétrahydroisoquinoléines (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>DNA, 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qualifier="métabolisme" xml:lang="fr"><term>Acétyl coenzyme A</term><term>Protéines fongiques</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Dioxoles</term><term>Isoquinoléines</term><term>Quinoléines</term><term>Sirolimus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Dioxoles</term><term>Isoquinolines</term><term>Quinolines</term><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Expression Profiling</term><term>Genome, Fungal</term><term>Humans</term><term>Oligonucleotide Array Sequence Analysis</term><term>Oxidative Stress</term><term>Structure-Activity Relationship</term><term>Tetrahydroisoquinolines</term><term>Trabectedin</term><term>Tumor Cells, Cultured</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Cellules cancéreuses en culture</term><term>Génome fongique</term><term>Humains</term><term>Relation structure-activité</term><term>Stress oxydatif</term><term>Séquençage par oligonucléotides en batterie</term><term>Trabectédine</term><term>Tétrahydroisoquinoléines</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Saframycin A (SafA) is a natural product that inhibits human cancer cell proliferation. Its synthetic analog, QAD, is a more potent inhibitor of these cells. SafA does not affect wild-type yeast, but it does inhibit growth of the strain CCY333 (DeltaPDR1/PDR3/ERG6) (IC50 = 0.9 microM). QAD is also a more effective inhibitor of CCY333 growth (IC50 = 0.4 microM). Transcription profiling of SafA- and QAD-treated CCY333 cultures showed that both drugs generated nearly identical profiles, with altered expression levels (> or =2-fold) of more than 240 genes. Both agents induced the overexpression of genes involved in glycolysis, oxidative stress, and protein degradation and repressed genes encoding histones, biosynthetic enzymes, and the cellular import machinery. Significantly, neither drug affected the expression of known DNA-damage repair genes, as might have been expected if their primary mechanism of action involved the covalent modification of DNA.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12031667</PMID><DateCompleted><Year>2002</Year><Month>10</Month><Day>16</Day></DateCompleted><DateRevised><Year>2019</Year><Month>10</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1074-5521</ISSN><JournalIssue CitedMedium="Print"><Volume>9</Volume><Issue>5</Issue><PubDate><Year>2002</Year><Month>May</Month></PubDate></JournalIssue><Title>Chemistry & biology</Title><ISOAbbreviation>Chem Biol</ISOAbbreviation></Journal><ArticleTitle>Transcriptional response pathways in a yeast strain sensitive to saframycin a and a more potent analog: evidence for a common basis of activity.</ArticleTitle><Pagination><MedlinePgn>607-18</MedlinePgn></Pagination><Abstract><AbstractText>Saframycin A (SafA) is a natural product that inhibits human cancer cell proliferation. Its synthetic analog, QAD, is a more potent inhibitor of these cells. SafA does not affect wild-type yeast, but it does inhibit growth of the strain CCY333 (DeltaPDR1/PDR3/ERG6) (IC50 = 0.9 microM). QAD is also a more effective inhibitor of CCY333 growth (IC50 = 0.4 microM). Transcription profiling of SafA- and QAD-treated CCY333 cultures showed that both drugs generated nearly identical profiles, with altered expression levels (> or =2-fold) of more than 240 genes. Both agents induced the overexpression of genes involved in glycolysis, oxidative stress, and protein degradation and repressed genes encoding histones, biosynthetic enzymes, and the cellular import machinery. Significantly, neither drug affected the expression of known DNA-damage repair genes, as might have been expected if their primary mechanism of action involved the covalent modification of DNA.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Plowright</LastName><ForeName>Alleyn T</ForeName><Initials>AT</Initials><AffiliationInfo><Affiliation>Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schaus</LastName><ForeName>Scott E</ForeName><Initials>SE</Initials></Author><Author ValidYN="Y"><LastName>Myers</LastName><ForeName>Andrew G</ForeName><Initials>AG</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Chem Biol</MedlineTA><NlmUniqueID>9500160</NlmUniqueID><ISSNLinking>1074-5521</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004271">DNA, Fungal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004149">Dioxoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005227">Fatty Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007546">Isoquinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011804">Quinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016681" MajorTopicYN="N">Genome, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007546" MajorTopicYN="N">Isoquinolines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011804" MajorTopicYN="N">Quinolines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013329" MajorTopicYN="N">Structure-Activity Relationship</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D044005" MajorTopicYN="N">Tetrahydroisoquinolines</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000077606" MajorTopicYN="N">Trabectedin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>5</Month><Day>29</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>10</Month><Day>17</Day><Hour>4</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>5</Month><Day>29</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">12031667</ArticleId><ArticleId IdType="pii">S1074552102001370</ArticleId><ArticleId IdType="doi">10.1016/s1074-5521(02)00137-0</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region><settlement><li>Cambridge (Massachusetts)</li></settlement><orgName><li>Université Harvard</li></orgName></list><tree><noCountry><name sortKey="Myers, Andrew G" sort="Myers, Andrew G" uniqKey="Myers A" first="Andrew G" last="Myers">Andrew G. Myers</name><name sortKey="Schaus, Scott E" sort="Schaus, Scott E" uniqKey="Schaus S" first="Scott E" last="Schaus">Scott E. Schaus</name></noCountry><country name="États-Unis"><region name="Massachusetts"><name sortKey="Plowright, Alleyn T" sort="Plowright, Alleyn T" uniqKey="Plowright A" first="Alleyn T" last="Plowright">Alleyn T. Plowright</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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