RapamycinFungusV1, Main, Exploration, bibRecord, 001A30

TOR signaling regulates microtubule structure and function.

Identifieur interne : 001A30 ( Main/Exploration ); précédent : 001A29; suivant : 001A31

TOR signaling regulates microtubule structure and function.

Auteurs : J H Choi [États-Unis] ; N R Adames ; T F Chan ; C. Zeng ; J A Cooper ; X F Zheng

Source :

Current biology : CB [ 0960-9822 ] ; 2000.

RBID : pubmed:10899009

Descripteurs français

KwdFr :
- Appareil du fuseau (effets des médicaments et des substances chimiques), Humains (MeSH), Microtubules (effets des médicaments et des substances chimiques), Microtubules (physiologie), Mutation (MeSH), Protéines fongiques (physiologie), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (physiologie), Sirolimus (pharmacologie), Transduction du signal (MeSH).
MESH :
- effets des médicaments et des substances chimiques : Appareil du fuseau, Microtubules, Saccharomyces cerevisiae.
- génétique : Saccharomyces cerevisiae.
- pharmacologie : Sirolimus.
- physiologie : Microtubules, Protéines fongiques, Saccharomyces cerevisiae.
- Humains, Mutation, Transduction du signal.

English descriptors

KwdEn :
- Fungal Proteins (physiology), Humans (MeSH), Microtubules (drug effects), Microtubules (physiology), Mutation (MeSH), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (physiology), Signal Transduction (MeSH), Sirolimus (pharmacology), Spindle Apparatus (drug effects).
MESH :
- chemical , pharmacology : Sirolimus.
- chemical , physiology : Fungal Proteins.
- drug effects : Microtubules, Saccharomyces cerevisiae, Spindle Apparatus.
- genetics : Saccharomyces cerevisiae.
- physiology : Microtubules, Saccharomyces cerevisiae.
- Humans, Mutation, Signal Transduction.

Abstract

The functional diversity and structural heterogeneity of microtubules are largely determined by microtubule-associated proteins (MAPs) [1] [2]. Bik1p (bilateral karyogamy defect protein) is one of the MAPs required for microtubule assembly, stability and function in cell processes such as karyogamy and nuclear migration and positioning in the yeast Saccharomyces cerevisiae [3]. The macrocyclic immunosuppressive antibiotic rapamycin, complexed with its binding protein FKBP12, binds to and inhibits the target of rapamycin protein (TOR) in yeast [4] [5]. We report here that TOR physically interacts with Bik1p, the yeast homolog of human CLIP-170/Restin [6] [7]. Inhibition of TOR by rapamycin significantly affects microtubule assembly, elongation and stability. This function of TOR is independent of new protein synthesis. Rapamycin also causes defects in spindle orientation, nuclear movement and positioning, karyogamy and chromosomal stability, defects also found in the bikDelta mutant. Our data suggest a role for TOR signaling in regulating microtubule stability and function, possibly through Bik1p.

DOI: 10.1016/s0960-9822(00)00599-6
PubMed: 10899009

Affiliations:

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Le document en format XML

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<term>Humans (MeSH)</term>
<term>Microtubules (drug effects)</term>
<term>Microtubules (physiology)</term>
<term>Mutation (MeSH)</term>
<term>Saccharomyces cerevisiae (drug effects)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (physiology)</term>
<term>Signal Transduction (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
<term>Spindle Apparatus (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Appareil du fuseau (effets des médicaments et des substances chimiques)</term>
<term>Humains (MeSH)</term>
<term>Microtubules (effets des médicaments et des substances chimiques)</term>
<term>Microtubules (physiologie)</term>
<term>Mutation (MeSH)</term>
<term>Protéines fongiques (physiologie)</term>
<term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (physiologie)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Transduction du signal (MeSH)</term>
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<term>Saccharomyces cerevisiae</term>
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<term>Mutation</term>
<term>Signal Transduction</term>
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<term>Mutation</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">The functional diversity and structural heterogeneity of microtubules are largely determined by microtubule-associated proteins (MAPs) [1] [2]. Bik1p (bilateral karyogamy defect protein) is one of the MAPs required for microtubule assembly, stability and function in cell processes such as karyogamy and nuclear migration and positioning in the yeast Saccharomyces cerevisiae [3]. The macrocyclic immunosuppressive antibiotic rapamycin, complexed with its binding protein FKBP12, binds to and inhibits the target of rapamycin protein (TOR) in yeast [4] [5]. We report here that TOR physically interacts with Bik1p, the yeast homolog of human CLIP-170/Restin [6] [7]. Inhibition of TOR by rapamycin significantly affects microtubule assembly, elongation and stability. This function of TOR is independent of new protein synthesis. Rapamycin also causes defects in spindle orientation, nuclear movement and positioning, karyogamy and chromosomal stability, defects also found in the bikDelta mutant. Our data suggest a role for TOR signaling in regulating microtubule stability and function, possibly through Bik1p.</div>
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<Month>07</Month>
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<Abstract><AbstractText>The functional diversity and structural heterogeneity of microtubules are largely determined by microtubule-associated proteins (MAPs) [1] [2]. Bik1p (bilateral karyogamy defect protein) is one of the MAPs required for microtubule assembly, stability and function in cell processes such as karyogamy and nuclear migration and positioning in the yeast Saccharomyces cerevisiae [3]. The macrocyclic immunosuppressive antibiotic rapamycin, complexed with its binding protein FKBP12, binds to and inhibits the target of rapamycin protein (TOR) in yeast [4] [5]. We report here that TOR physically interacts with Bik1p, the yeast homolog of human CLIP-170/Restin [6] [7]. Inhibition of TOR by rapamycin significantly affects microtubule assembly, elongation and stability. This function of TOR is independent of new protein synthesis. Rapamycin also causes defects in spindle orientation, nuclear movement and positioning, karyogamy and chromosomal stability, defects also found in the bikDelta mutant. Our data suggest a role for TOR signaling in regulating microtubule stability and function, possibly through Bik1p.</AbstractText>
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TOR signaling regulates microtubule structure and function.

TOR signaling regulates microtubule structure and function.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki