A chemical genomics approach toward understanding the global functions of the target of rapamycin protein (TOR).
Identifieur interne : 001A44 ( Main/Exploration ); précédent : 001A43; suivant : 001A45A chemical genomics approach toward understanding the global functions of the target of rapamycin protein (TOR).
Auteurs : T F Chan [États-Unis] ; J. Carvalho ; L. Riles ; X F ZhengSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2000.
Descripteurs français
- KwdFr :
- Génomique (MeSH), Humains (MeSH), Microtubules (physiologie), Phosphatidylinositol 3-kinases (MeSH), Phosphotransferases (Alcohol Group Acceptor) (génétique), Phosphotransferases (Alcohol Group Acceptor) (métabolisme), Protein kinases (génétique), Protein kinases (métabolisme), Protéines de Saccharomyces cerevisiae (MeSH), Protéines du cycle cellulaire (MeSH), Protéines fongiques (génétique), Protéines fongiques (métabolisme), Protéines ribosomiques (génétique), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Sirolimus (pharmacologie), Sérine-thréonine kinases TOR (MeSH), Tests de sensibilité microbienne (MeSH), Transcription génétique (MeSH), Ubiquitines (physiologie), Vacuoles (physiologie).
- MESH :
- croissance et développement : Saccharomyces cerevisiae.
- effets des médicaments et des substances chimiques : Saccharomyces cerevisiae.
- génétique : Phosphotransferases (Alcohol Group Acceptor), Protein kinases, Protéines fongiques, Protéines ribosomiques, Saccharomyces cerevisiae.
- métabolisme : Phosphotransferases (Alcohol Group Acceptor), Protein kinases, Protéines fongiques.
- pharmacologie : Sirolimus.
- physiologie : Microtubules, Ubiquitines, Vacuoles.
- Génomique, Humains, Phosphatidylinositol 3-kinases, Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire, Régulation de l'expression des gènes fongiques, Sérine-thréonine kinases TOR, Tests de sensibilité microbienne, Transcription génétique.
English descriptors
- KwdEn :
- Cell Cycle Proteins (MeSH), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Expression Regulation, Fungal (MeSH), Genomics (MeSH), Humans (MeSH), Microbial Sensitivity Tests (MeSH), Microtubules (physiology), Phosphatidylinositol 3-Kinases (MeSH), Phosphotransferases (Alcohol Group Acceptor) (genetics), Phosphotransferases (Alcohol Group Acceptor) (metabolism), Protein Kinases (genetics), Protein Kinases (metabolism), Ribosomal Proteins (genetics), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae Proteins (MeSH), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (MeSH), Transcription, Genetic (MeSH), Ubiquitins (physiology), Vacuoles (physiology).
- MESH :
- chemical , genetics : Fungal Proteins, Phosphotransferases (Alcohol Group Acceptor), Protein Kinases, Ribosomal Proteins.
- chemical , metabolism : Fungal Proteins, Phosphotransferases (Alcohol Group Acceptor), Protein Kinases.
- chemical , pharmacology : Sirolimus.
- chemical , physiology : Ubiquitins.
- chemical : Cell Cycle Proteins, Phosphatidylinositol 3-Kinases, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases.
- drug effects : Saccharomyces cerevisiae.
- genetics : Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- physiology : Microtubules, Vacuoles.
- Gene Expression Regulation, Fungal, Genomics, Humans, Microbial Sensitivity Tests, Transcription, Genetic.
Abstract
The target of rapamycin protein (TOR) is a highly conserved ataxia telangiectasia-related protein kinase essential for cell growth. Emerging evidence indicates that TOR signaling is highly complex and is involved in a variety of cellular processes. To understand its general functions, we took a chemical genomics approach to explore the genetic interaction between TOR and other yeast genes on a genomic scale. In this study, the rapamycin sensitivity of individual deletion mutants generated by the Saccharomyces Genome Deletion Project was systematically measured. Our results provide a global view of the rapamycin-sensitive functions of TOR. In contrast to conventional genetic analysis, this approach offers a simple and thorough analysis of genetic interaction on a genomic scale and measures genetic interaction at different possible levels. It can be used to study the functions of other drug targets and to identify novel protein components of a conserved core biological process such as DNA damage checkpoint/repair that is interfered with by a cell-permeable chemical compound.
DOI: 10.1073/pnas.240444197
PubMed: 11078525
PubMed Central: PMC27207
Affiliations:
- États-Unis
- Missouri (État)
- Saint-Louis (Missouri)
- École de médecine (Université Washington de Saint-Louis)
Links toward previous steps (curation, corpus...)
Le document en format XML
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Emerging evidence indicates that TOR signaling is highly complex and is involved in a variety of cellular processes. To understand its general functions, we took a chemical genomics approach to explore the genetic interaction between TOR and other yeast genes on a genomic scale. In this study, the rapamycin sensitivity of individual deletion mutants generated by the Saccharomyces Genome Deletion Project was systematically measured. Our results provide a global view of the rapamycin-sensitive functions of TOR. In contrast to conventional genetic analysis, this approach offers a simple and thorough analysis of genetic interaction on a genomic scale and measures genetic interaction at different possible levels. It can be used to study the functions of other drug targets and to identify novel protein components of a conserved core biological process such as DNA damage checkpoint/repair that is interfered with by a cell-permeable chemical compound.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11078525</PMID><DateCompleted><Year>2001</Year><Month>05</Month><Day>24</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0027-8424</ISSN><JournalIssue CitedMedium="Print"><Volume>97</Volume><Issue>24</Issue><PubDate><Year>2000</Year><Month>Nov</Month><Day>21</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 chemical genomics approach toward understanding the global functions of the target of rapamycin protein (TOR).</ArticleTitle><Pagination><MedlinePgn>13227-32</MedlinePgn></Pagination><Abstract><AbstractText>The target of rapamycin protein (TOR) is a highly conserved ataxia telangiectasia-related protein kinase essential for cell growth. Emerging evidence indicates that TOR signaling is highly complex and is involved in a variety of cellular processes. To understand its general functions, we took a chemical genomics approach to explore the genetic interaction between TOR and other yeast genes on a genomic scale. In this study, the rapamycin sensitivity of individual deletion mutants generated by the Saccharomyces Genome Deletion Project was systematically measured. Our results provide a global view of the rapamycin-sensitive functions of TOR. In contrast to conventional genetic analysis, this approach offers a simple and thorough analysis of genetic interaction on a genomic scale and measures genetic interaction at different possible levels. It can be used to study the functions of other drug targets and to identify novel protein components of a conserved core biological process such as DNA damage checkpoint/repair that is interfered with by a cell-permeable chemical compound.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chan</LastName><ForeName>T F</ForeName><Initials>TF</Initials><AffiliationInfo><Affiliation>Departments of Pathology and Immunology and Genetics, Washington University School of Medicine, St. Louis, MO 63110, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carvalho</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Riles</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>X F</ForeName><Initials>XF</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal 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Carvalho</name><name sortKey="Riles, L" sort="Riles, L" uniqKey="Riles L" first="L" last="Riles">L. Riles</name><name sortKey="Zheng, X F" sort="Zheng, X F" uniqKey="Zheng X" first="X F" last="Zheng">X F Zheng</name></noCountry><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Chan, T F" sort="Chan, T F" uniqKey="Chan T" first="T F" last="Chan">T F Chan</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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