RapamycinFungusV1, Main, Exploration, bibRecord, 001670

The Rheb switch 2 segment is critical for signaling to target of rapamycin complex 1.

Identifieur interne : 001670 ( Main/Exploration ); précédent : 001669; suivant : 001671

The Rheb switch 2 segment is critical for signaling to target of rapamycin complex 1.

Auteurs : Xiaomeng Long [États-Unis] ; Yenshou Lin ; Sara Ortiz-Vega ; Susann Busch ; Joseph Avruch

Source :

The Journal of biological chemistry [ 0021-9258 ] ; 2007.

RBID : pubmed:17470430

Descripteurs français

KwdFr :
- Animaux (MeSH), Données de séquences moléculaires (MeSH), Guanosine triphosphate (métabolisme), Humains (MeSH), Lignée cellulaire (MeSH), Mutation (MeSH), Neuropeptides (composition chimique), Neuropeptides (physiologie), Peptides (composition chimique), Protein kinases (métabolisme), Protéine homologue de Ras enrichie dans le cerveau (MeSH), Protéines G monomériques (composition chimique), Protéines G monomériques (métabolisme), Protéines G monomériques (physiologie), Schizosaccharomyces (métabolisme), Similitude de séquences d'acides aminés (MeSH), Séquence d'acides aminés (MeSH), Sérine-thréonine kinases TOR (MeSH), Transduction du signal (MeSH), Transfection (MeSH).
MESH :
- composition chimique : Neuropeptides, Peptides, Protéines G monomériques.
- métabolisme : Guanosine triphosphate, Protein kinases, Protéines G monomériques, Schizosaccharomyces.
- physiologie : Neuropeptides, Protéines G monomériques.
- Animaux, Données de séquences moléculaires, Humains, Lignée cellulaire, Mutation, Protéine homologue de Ras enrichie dans le cerveau, Similitude de séquences d'acides aminés, Séquence d'acides aminés, Sérine-thréonine kinases TOR, Transduction du signal, Transfection.

English descriptors

KwdEn :
- Amino Acid Sequence (MeSH), Animals (MeSH), Cell Line (MeSH), Guanosine Triphosphate (metabolism), Humans (MeSH), Molecular Sequence Data (MeSH), Monomeric GTP-Binding Proteins (chemistry), Monomeric GTP-Binding Proteins (metabolism), Monomeric GTP-Binding Proteins (physiology), Mutation (MeSH), Neuropeptides (chemistry), Neuropeptides (physiology), Peptides (chemistry), Protein Kinases (metabolism), Ras Homolog Enriched in Brain Protein (MeSH), Schizosaccharomyces (metabolism), Sequence Homology, Amino Acid (MeSH), Signal Transduction (MeSH), TOR Serine-Threonine Kinases (MeSH), Transfection (MeSH).
MESH :
- chemical , chemistry : Monomeric GTP-Binding Proteins, Neuropeptides, Peptides.
- chemical , metabolism : Guanosine Triphosphate, Monomeric GTP-Binding Proteins, Protein Kinases.
- chemical , physiology : Monomeric GTP-Binding Proteins, Neuropeptides.
- metabolism : Schizosaccharomyces.
- Amino Acid Sequence, Animals, Cell Line, Humans, Molecular Sequence Data, Mutation, Ras Homolog Enriched in Brain Protein, Sequence Homology, Amino Acid, Signal Transduction, TOR Serine-Threonine Kinases, Transfection.

Abstract

The small GTPase Rheb is a positive upstream regulator of the target of rapamycin (TOR) complex 1 in mammalian cells and can bind directly to TOR complex 1. To identify the regions of the Rheb surface most critical for signaling to TOR complex 1, we created a set of 26 mutants wherein clusters of 1-5 putative solvent-exposed residues were changed to alanine, ultimately changing 65 residues distributed over the entire Rheb surface. The signaling function of these mutants was assessed by their ability, in comparison to wild type Rheb, to restore the phosphorylation of S6K1(Thr389) when expressed transiently in amino acid-deprived 293T cells. The major finding is that two mutants situated in the Rheb switch 2 segment, Y67A/I69A and I76A/D77A, exhibit a near total loss of function, whereas extensive replacement of the switch 1 segment and other surface residues with alanines causes relatively little disturbance of Rheb rescue of S6K1 from amino acid withdrawal. This is surprising in view of the minimal impact of guanyl nucleotide on Rheb switch 2 configuration. The loss of function Rheb switch 2 mutants are well expressed and exhibit partial agonist function in amino acid-replete cells. They are unimpaired in their ability to bind GTP or mammalian (m)TOR in vivo or in vitro, and the mTOR polypeptides retrieved with these inactive Rheb mutants exhibit kinase activity in vitro comparable with mTOR bound to wild type Rheb. We conclude that Rheb signaling to mTOR in vivo requires a Rheb switch 2-dependent interaction with an element other than the three known polypeptide components of TOR complex 1.

DOI: 10.1074/jbc.M610736200
PubMed: 17470430
PubMed Central: PMC3205911

Affiliations:

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

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The small GTPase Rheb is a positive upstream regulator of the target of rapamycin (TOR) complex 1 in mammalian cells and can bind directly to TOR complex 1. To identify the regions of the Rheb surface most critical for signaling to TOR complex 1, we created a set of 26 mutants wherein clusters of 1-5 putative solvent-exposed residues were changed to alanine, ultimately changing 65 residues distributed over the entire Rheb surface. The signaling function of these mutants was assessed by their ability, in comparison to wild type Rheb, to restore the phosphorylation of S6K1(Thr389) when expressed transiently in amino acid-deprived 293T cells. The major finding is that two mutants situated in the Rheb switch 2 segment, Y67A/I69A and I76A/D77A, exhibit a near total loss of function, whereas extensive replacement of the switch 1 segment and other surface residues with alanines causes relatively little disturbance of Rheb rescue of S6K1 from amino acid withdrawal. This is surprising in view of the minimal impact of guanyl nucleotide on Rheb switch 2 configuration. The loss of function Rheb switch 2 mutants are well expressed and exhibit partial agonist function in amino acid-replete cells. They are unimpaired in their ability to bind GTP or mammalian (m)TOR in vivo or in vitro, and the mTOR polypeptides retrieved with these inactive Rheb mutants exhibit kinase activity in vitro comparable with mTOR bound to wild type Rheb. We conclude that Rheb signaling to mTOR in vivo requires a Rheb switch 2-dependent interaction with an element other than the three known polypeptide components of TOR complex 1.</div>
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<Abstract><AbstractText>The small GTPase Rheb is a positive upstream regulator of the target of rapamycin (TOR) complex 1 in mammalian cells and can bind directly to TOR complex 1. To identify the regions of the Rheb surface most critical for signaling to TOR complex 1, we created a set of 26 mutants wherein clusters of 1-5 putative solvent-exposed residues were changed to alanine, ultimately changing 65 residues distributed over the entire Rheb surface. The signaling function of these mutants was assessed by their ability, in comparison to wild type Rheb, to restore the phosphorylation of S6K1(Thr389) when expressed transiently in amino acid-deprived 293T cells. The major finding is that two mutants situated in the Rheb switch 2 segment, Y67A/I69A and I76A/D77A, exhibit a near total loss of function, whereas extensive replacement of the switch 1 segment and other surface residues with alanines causes relatively little disturbance of Rheb rescue of S6K1 from amino acid withdrawal. This is surprising in view of the minimal impact of guanyl nucleotide on Rheb switch 2 configuration. The loss of function Rheb switch 2 mutants are well expressed and exhibit partial agonist function in amino acid-replete cells. They are unimpaired in their ability to bind GTP or mammalian (m)TOR in vivo or in vitro, and the mTOR polypeptides retrieved with these inactive Rheb mutants exhibit kinase activity in vitro comparable with mTOR bound to wild type Rheb. We conclude that Rheb signaling to mTOR in vivo requires a Rheb switch 2-dependent interaction with an element other than the three known polypeptide components of TOR complex 1.</AbstractText>
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	Serveur d'exploration sur la rapamycine et les champignons
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Serveur d'exploration sur la rapamycine et les champignons

The Rheb switch 2 segment is critical for signaling to target of rapamycin complex 1.

The Rheb switch 2 segment is critical for signaling to target of rapamycin complex 1.

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