ChloroquineV1, France, Analysis, bibRecord, 000229

Autophagy modulation as a potential therapeutic target for diverse diseases

Identifieur interne : 000229 ( France/Analysis ); précédent : 000228; suivant : 000230

Autophagy modulation as a potential therapeutic target for diverse diseases

Auteurs : David C. Rubinsztein [Royaume-Uni] ; Patrice Codogno [France] ; Beth Levine [États-Unis]

Source :

Nature Reviews Drug Discovery [ 1474-1776 ] ; 2012-09.

RBID : ISTEX:32FD5CD49AA6E68C452BCC94E3DF157227A9BC54

Abstract

Autophagy is an essential, conserved lysosomal degradation pathway that controls the quality of the cytoplasm by eliminating protein aggregates and damaged organelles. It begins when double-membraned autophagosomes engulf portions of the cytoplasm, which is followed by fusion of these vesicles with lysosomes and degradation of the autophagic contents. In addition to its vital homeostatic role, this degradation pathway is involved in various human disorders, including metabolic conditions, neurodegenerative diseases, cancers and infectious diseases. This article provides an overview of the mechanisms and regulation of autophagy, the role of this pathway in disease and strategies for therapeutic modulation.

Url:

https://api.istex.fr/ark:/67375/GT4-26JJ9W0B-4/fulltext.pdf

DOI: 10.1038/nrd3802

Affiliations:

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

to stream Istex, to step Corpus: 000449
to stream Istex, to step Curation: 000449
to stream Istex, to step Checkpoint: 000434
to stream Main, to step Merge: 001426
to stream Main, to step Curation: 001425
to stream Main, to step Exploration: 001425
to stream France, to step Extraction: 000229

Links to Exploration step

ISTEX:32FD5CD49AA6E68C452BCC94E3DF157227A9BC54

Le document en format XML

<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Autophagy modulation as a potential therapeutic target for diverse diseases</title>
<author><name sortKey="Rubinsztein, David C" sort="Rubinsztein, David C" uniqKey="Rubinsztein D" first="David C." last="Rubinsztein">David C. Rubinsztein</name>
</author>
<author><name sortKey="Codogno, Patrice" sort="Codogno, Patrice" uniqKey="Codogno P" first="Patrice" last="Codogno">Patrice Codogno</name>
</author>
<author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:32FD5CD49AA6E68C452BCC94E3DF157227A9BC54</idno>
<date when="2012" year="2012">2012</date>
<idno type="doi">10.1038/nrd3802</idno>
<idno type="url">https://api.istex.fr/ark:/67375/GT4-26JJ9W0B-4/fulltext.pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000449</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000449</idno>
<idno type="wicri:Area/Istex/Curation">000449</idno>
<idno type="wicri:Area/Istex/Checkpoint">000434</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">000434</idno>
<idno type="wicri:doubleKey">1474-1776:2012:Rubinsztein D:autophagy:modulation:as</idno>
<idno type="wicri:Area/Main/Merge">001426</idno>
<idno type="wicri:Area/Main/Curation">001425</idno>
<idno type="wicri:Area/Main/Exploration">001425</idno>
<idno type="wicri:Area/France/Extraction">000229</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Autophagy modulation as a potential therapeutic target for diverse diseases</title>
<author><name sortKey="Rubinsztein, David C" sort="Rubinsztein, David C" uniqKey="Rubinsztein D" first="David C." last="Rubinsztein">David C. Rubinsztein</name>
<affiliation wicri:level="4"><country xml:lang="fr" wicri:curation="lc">Royaume-Uni</country>
<wicri:regionArea>Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Wellcome Trust/MRC Building, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY</wicri:regionArea>
<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
</placeName>
</affiliation>
<affiliation></affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">Royaume-Uni</country>
</affiliation>
</author>
<author><name sortKey="Codogno, Patrice" sort="Codogno, Patrice" uniqKey="Codogno P" first="Patrice" last="Codogno">Patrice Codogno</name>
<affiliation wicri:level="3"><country xml:lang="fr">France</country>
<wicri:regionArea>Faculté de Pharmacie, Institut National de la Santé et de la Recherche Médicale (INSERM) UMR984, Université Paris-Sud 11, 5 rue Jean-Baptiste Clément, 92296 Châtenay-Malabry</wicri:regionArea>
<placeName><region type="region" nuts="2">Île-de-France</region>
<settlement type="city">Châtenay-Malabry</settlement>
</placeName>
</affiliation>
<affiliation></affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">France</country>
</affiliation>
</author>
<author><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
<affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">États-Unis</country>
<wicri:regionArea>Departments of Internal Medicine and Microbiology, Center for Autophagy Research, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390</wicri:regionArea>
<wicri:noRegion>Texas 75390</wicri:noRegion>
</affiliation>
<affiliation></affiliation>
<affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j" type="main">Nature Reviews Drug Discovery</title>
<idno type="ISSN">1474-1776</idno>
<idno type="eISSN">1474-1784</idno>
<imprint><publisher>Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.</publisher>
<date when="2012-09">2012-09</date>
<biblScope unit="vol">11</biblScope>
<biblScope unit="issue">9</biblScope>
<biblScope unit="page" from="709">709</biblScope>
<biblScope unit="page" to="730">730</biblScope>
<date type="Copyright" when="2012">2012</date>
</imprint>
<idno type="ISSN">1474-1776</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">1474-1776</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="eng">Autophagy is an essential, conserved lysosomal degradation pathway that controls the quality of the cytoplasm by eliminating protein aggregates and damaged organelles. It begins when double-membraned autophagosomes engulf portions of the cytoplasm, which is followed by fusion of these vesicles with lysosomes and degradation of the autophagic contents. In addition to its vital homeostatic role, this degradation pathway is involved in various human disorders, including metabolic conditions, neurodegenerative diseases, cancers and infectious diseases. This article provides an overview of the mechanisms and regulation of autophagy, the role of this pathway in disease and strategies for therapeutic modulation.</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
<li>Royaume-Uni</li>
<li>États-Unis</li>
</country>
<region><li>Angleterre</li>
<li>Angleterre de l'Est</li>
<li>Île-de-France</li>
</region>
<settlement><li>Cambridge</li>
<li>Châtenay-Malabry</li>
</settlement>
<orgName><li>Université de Cambridge</li>
</orgName>
</list>
<tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Rubinsztein, David C" sort="Rubinsztein, David C" uniqKey="Rubinsztein D" first="David C." last="Rubinsztein">David C. Rubinsztein</name>
</region>
<name sortKey="Rubinsztein, David C" sort="Rubinsztein, David C" uniqKey="Rubinsztein D" first="David C." last="Rubinsztein">David C. Rubinsztein</name>
</country>
<country name="France"><region name="Île-de-France"><name sortKey="Codogno, Patrice" sort="Codogno, Patrice" uniqKey="Codogno P" first="Patrice" last="Codogno">Patrice Codogno</name>
</region>
<name sortKey="Codogno, Patrice" sort="Codogno, Patrice" uniqKey="Codogno P" first="Patrice" last="Codogno">Patrice Codogno</name>
</country>
<country name="États-Unis"><noRegion><name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
</noRegion>
<name sortKey="Levine, Beth" sort="Levine, Beth" uniqKey="Levine B" first="Beth" last="Levine">Beth Levine</name>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/France/Analysis

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000229 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/France/Analysis/biblio.hfd -nk 000229 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    France
   |étape=   Analysis
   |type=    RBID
   |clé=     ISTEX:32FD5CD49AA6E68C452BCC94E3DF157227A9BC54
   |texte=   Autophagy modulation as a potential therapeutic target for diverse diseases
}}

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021

	Serveur d'exploration Chloroquine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration Chloroquine

Autophagy modulation as a potential therapeutic target for diverse diseases

Autophagy modulation as a potential therapeutic target for diverse diseases

Source :

Abstract

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

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri