RapamycinFungusV1, Main, Exploration, bibRecord, 000A87

Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.

Identifieur interne : 000A87 ( Main/Exploration ); précédent : 000A86; suivant : 000A88

Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.

Auteurs : Anu Chaudhary [États-Unis] ; Mara Leite [États-Unis] ; Bridget R. Kulasekara [États-Unis] ; Melissa A. Altura [États-Unis] ; Cassandra Ogahara [États-Unis] ; Eli Weiss [États-Unis] ; Wenqing Fu [États-Unis] ; Marie-Pierre Blanc [États-Unis] ; Michael O'Keeffe [États-Unis] ; Cox Terhorst [États-Unis] ; Joshua M. Akey [États-Unis] ; Samuel I. Miller [États-Unis]

Source :

Current biology : CB [ 1879-0445 ] ; 2016.

RBID : pubmed:27345162

Descripteurs français

English descriptors

KwdEn :
- Autophagy (genetics), Beclin-1 (metabolism), Class III Phosphatidylinositol 3-Kinases (metabolism), Gene Expression (MeSH), Genome-Wide Association Study (MeSH), Humans (MeSH), Signaling Lymphocytic Activation Molecule Family (genetics), Signaling Lymphocytic Activation Molecule Family (metabolism).
MESH :
- chemical , genetics : Signaling Lymphocytic Activation Molecule Family.
- chemical , metabolism : Beclin-1, Class III Phosphatidylinositol 3-Kinases, Signaling Lymphocytic Activation Molecule Family.
- genetics : Autophagy.
- Gene Expression, Genome-Wide Association Study, Humans.

Abstract

Mutations in genes encoding autophagy proteins have been associated with human autoimmune diseases, suggesting that diversity in autophagy responses could be associated with disease susceptibility or severity. A cellular genome-wide association study (GWAS) screen was performed to explore normal human diversity in responses to rapamycin, a microbial product that induces autophagy. Cells from several human populations demonstrated variability in expression of a cell surface receptor, CD244 (SlamF4, 2B4), that correlated with changes in rapamycin-induced autophagy. High expression of CD244 and receptor activation with its endogenous ligand CD48 inhibited starvation- and rapamycin-induced autophagy by promoting association of CD244 with the autophagy complex proteins Vps34 and Beclin-1. The association of CD244 with this complex reduced Vps34 lipid kinase activity. Lack of CD244 is associated with auto-antibody production in mice, and lower expression of human CD244 has previously been implicated in severity of human rheumatoid arthritis and systemic lupus erythematosus, indicating that increased autophagy as a result of low levels of CD244 may alter disease outcomes.

DOI: 10.1016/j.cub.2016.05.003
PubMed: 27345162

Affiliations:

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

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Le document en format XML

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<author><name sortKey="Blanc, Marie Pierre" sort="Blanc, Marie Pierre" uniqKey="Blanc M" first="Marie-Pierre" last="Blanc">Marie-Pierre Blanc</name>
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<author><name sortKey="Blanc, Marie Pierre" sort="Blanc, Marie Pierre" uniqKey="Blanc M" first="Marie-Pierre" last="Blanc">Marie-Pierre Blanc</name>
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<author><name sortKey="Terhorst, Cox" sort="Terhorst, Cox" uniqKey="Terhorst C" first="Cox" last="Terhorst">Cox Terhorst</name>
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<author><name sortKey="Akey, Joshua M" sort="Akey, Joshua M" uniqKey="Akey J" first="Joshua M" last="Akey">Joshua M. Akey</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (genetics)</term>
<term>Beclin-1 (metabolism)</term>
<term>Class III Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Gene Expression (MeSH)</term>
<term>Genome-Wide Association Study (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Signaling Lymphocytic Activation Molecule Family (genetics)</term>
<term>Signaling Lymphocytic Activation Molecule Family (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie (génétique)</term>
<term>Bécline-1 (métabolisme)</term>
<term>Expression des gènes (MeSH)</term>
<term>Famille des molécules de signalisation de l'activation des lymphocytes (génétique)</term>
<term>Famille des molécules de signalisation de l'activation des lymphocytes (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Phosphatidylinositol 3-kinases de classe III (métabolisme)</term>
<term>Étude d'association pangénomique (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Signaling Lymphocytic Activation Molecule Family</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term>
<term>Class III Phosphatidylinositol 3-Kinases</term>
<term>Signaling Lymphocytic Activation Molecule Family</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autophagy</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Autophagie</term>
<term>Famille des molécules de signalisation de l'activation des lymphocytes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Bécline-1</term>
<term>Famille des molécules de signalisation de l'activation des lymphocytes</term>
<term>Phosphatidylinositol 3-kinases de classe III</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Gene Expression</term>
<term>Genome-Wide Association Study</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Expression des gènes</term>
<term>Humains</term>
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<front><div type="abstract" xml:lang="en">Mutations in genes encoding autophagy proteins have been associated with human autoimmune diseases, suggesting that diversity in autophagy responses could be associated with disease susceptibility or severity. A cellular genome-wide association study (GWAS) screen was performed to explore normal human diversity in responses to rapamycin, a microbial product that induces autophagy. Cells from several human populations demonstrated variability in expression of a cell surface receptor, CD244 (SlamF4, 2B4), that correlated with changes in rapamycin-induced autophagy. High expression of CD244 and receptor activation with its endogenous ligand CD48 inhibited starvation- and rapamycin-induced autophagy by promoting association of CD244 with the autophagy complex proteins Vps34 and Beclin-1. The association of CD244 with this complex reduced Vps34 lipid kinase activity. Lack of CD244 is associated with auto-antibody production in mice, and lower expression of human CD244 has previously been implicated in severity of human rheumatoid arthritis and systemic lupus erythematosus, indicating that increased autophagy as a result of low levels of CD244 may alter disease outcomes.</div>
</front>
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<Month>12</Month>
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<ArticleTitle>Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.</ArticleTitle>
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<Abstract><AbstractText>Mutations in genes encoding autophagy proteins have been associated with human autoimmune diseases, suggesting that diversity in autophagy responses could be associated with disease susceptibility or severity. A cellular genome-wide association study (GWAS) screen was performed to explore normal human diversity in responses to rapamycin, a microbial product that induces autophagy. Cells from several human populations demonstrated variability in expression of a cell surface receptor, CD244 (SlamF4, 2B4), that correlated with changes in rapamycin-induced autophagy. High expression of CD244 and receptor activation with its endogenous ligand CD48 inhibited starvation- and rapamycin-induced autophagy by promoting association of CD244 with the autophagy complex proteins Vps34 and Beclin-1. The association of CD244 with this complex reduced Vps34 lipid kinase activity. Lack of CD244 is associated with auto-antibody production in mice, and lower expression of human CD244 has previously been implicated in severity of human rheumatoid arthritis and systemic lupus erythematosus, indicating that increased autophagy as a result of low levels of CD244 may alter disease outcomes.</AbstractText>
<CopyrightInformation>Copyright © 2016 Elsevier Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Chaudhary</LastName>
<ForeName>Anu</ForeName>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Leite</LastName>
<ForeName>Mara</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Microbiology, University of Washington, Seattle, WA 98195, USA.</Affiliation>
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<AffiliationInfo><Affiliation>Department of Microbiology, University of Washington, Seattle, WA 98195, USA; Department of Immunology, University of Washington, Seattle, WA 98195, USA; Department of Medicine, University of Washington, Seattle, WA 98195, USA; Department of Genome Sciences, University of Washington, Seattle, WA 98195, USA. Electronic address: millersi@uw.edu.</Affiliation>
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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

Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.

Human Diversity in a Cell Surface Receptor that Inhibits Autophagy.

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