Endocytic membrane trafficking and neurodegenerative disease.
Identifieur interne : 000266 ( PubMed/Checkpoint ); précédent : 000265; suivant : 000267Endocytic membrane trafficking and neurodegenerative disease.
Auteurs : Andrea M A. Schreij [Canada] ; Edward A. Fon [Canada] ; Peter S. Mcpherson [Canada]Source :
- Cellular and molecular life sciences : CMLS [ 1420-9071 ] ; 2016.
English descriptors
- KwdEn :
- Amyotrophic Lateral Sclerosis (genetics), Autophagy (physiology), Clathrin-Coated Vesicles (metabolism), Endocytosis (genetics), Endocytosis (physiology), Humans, Lysosomes (metabolism), Multivesicular Bodies (metabolism), Parkinson Disease (genetics), Protein Transport (genetics), Protein Transport (physiology), Spastic Paraplegia, Hereditary (genetics).
- MESH :
- genetics : Amyotrophic Lateral Sclerosis, Endocytosis, Parkinson Disease, Protein Transport, Spastic Paraplegia, Hereditary.
- metabolism : Clathrin-Coated Vesicles, Lysosomes, Multivesicular Bodies.
- physiology : Autophagy, Endocytosis, Protein Transport.
- Humans.
Abstract
Neurodegenerative diseases are amongst the most devastating of human disorders. New technologies have led to a rapid increase in the identification of disease-related genes with an enhanced appreciation of the key roles played by genetics in the etiology of these disorders. Importantly, pinpointing the normal function of disease gene proteins leads to new understanding of the cellular machineries and pathways that are altered in the disease process. One such emerging pathway is membrane trafficking in the endosomal system. This key cellular process controls the localization and levels of a myriad of proteins and is thus critical for normal cell function. In this review we will focus on three neurodegenerative diseases; Parkinson disease, amyotrophic lateral sclerosis, and hereditary spastic paraplegias, for which a large number of newly discovered disease genes encode proteins that function in endosomal membrane trafficking. We will describe how alterations in these proteins affect endosomal function and speculate on the contributions of these disruptions to disease pathophysiology.
DOI: 10.1007/s00018-015-2105-x
PubMed: 26721251
Affiliations:
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Fon</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author><author><name sortKey="Mcpherson, Peter S" sort="Mcpherson, Peter S" uniqKey="Mcpherson P" first="Peter S" last="Mcpherson">Peter S. Mcpherson</name><affiliation wicri:level="4"><nlm:affiliation>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada. peter.mcpherson@mcgill.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author></analytic><series><title level="j">Cellular and molecular life sciences : CMLS</title><idno type="eISSN">1420-9071</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amyotrophic Lateral Sclerosis (genetics)</term><term>Autophagy (physiology)</term><term>Clathrin-Coated Vesicles (metabolism)</term><term>Endocytosis (genetics)</term><term>Endocytosis (physiology)</term><term>Humans</term><term>Lysosomes (metabolism)</term><term>Multivesicular Bodies (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Protein Transport (genetics)</term><term>Protein Transport (physiology)</term><term>Spastic Paraplegia, Hereditary (genetics)</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Endocytosis</term><term>Parkinson Disease</term><term>Protein Transport</term><term>Spastic Paraplegia, Hereditary</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Clathrin-Coated Vesicles</term><term>Lysosomes</term><term>Multivesicular Bodies</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Autophagy</term><term>Endocytosis</term><term>Protein Transport</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurodegenerative diseases are amongst the most devastating of human disorders. New technologies have led to a rapid increase in the identification of disease-related genes with an enhanced appreciation of the key roles played by genetics in the etiology of these disorders. Importantly, pinpointing the normal function of disease gene proteins leads to new understanding of the cellular machineries and pathways that are altered in the disease process. One such emerging pathway is membrane trafficking in the endosomal system. This key cellular process controls the localization and levels of a myriad of proteins and is thus critical for normal cell function. In this review we will focus on three neurodegenerative diseases; Parkinson disease, amyotrophic lateral sclerosis, and hereditary spastic paraplegias, for which a large number of newly discovered disease genes encode proteins that function in endosomal membrane trafficking. We will describe how alterations in these proteins affect endosomal function and speculate on the contributions of these disruptions to disease pathophysiology.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26721251</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>24</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>15</Day></DateCompleted><DateRevised><Year>2016</Year><Month>03</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1420-9071</ISSN><JournalIssue CitedMedium="Internet"><Volume>73</Volume><Issue>8</Issue><PubDate><Year>2016</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Cellular and molecular life sciences : CMLS</Title><ISOAbbreviation>Cell. Mol. Life Sci.</ISOAbbreviation></Journal><ArticleTitle>Endocytic membrane trafficking and neurodegenerative disease.</ArticleTitle><Pagination><MedlinePgn>1529-45</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00018-015-2105-x</ELocationID><Abstract><AbstractText>Neurodegenerative diseases are amongst the most devastating of human disorders. New technologies have led to a rapid increase in the identification of disease-related genes with an enhanced appreciation of the key roles played by genetics in the etiology of these disorders. Importantly, pinpointing the normal function of disease gene proteins leads to new understanding of the cellular machineries and pathways that are altered in the disease process. One such emerging pathway is membrane trafficking in the endosomal system. This key cellular process controls the localization and levels of a myriad of proteins and is thus critical for normal cell function. In this review we will focus on three neurodegenerative diseases; Parkinson disease, amyotrophic lateral sclerosis, and hereditary spastic paraplegias, for which a large number of newly discovered disease genes encode proteins that function in endosomal membrane trafficking. We will describe how alterations in these proteins affect endosomal function and speculate on the contributions of these disruptions to disease pathophysiology.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schreij</LastName><ForeName>Andrea M A</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fon</LastName><ForeName>Edward A</ForeName><Initials>EA</Initials><AffiliationInfo><Affiliation>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McPherson</LastName><ForeName>Peter S</ForeName><Initials>PS</Initials><AffiliationInfo><Affiliation>Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, H3A 2B4, Canada. peter.mcpherson@mcgill.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>12</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>Switzerland</Country><MedlineTA>Cell Mol Life Sci</MedlineTA><NlmUniqueID>9705402</NlmUniqueID><ISSNLinking>1420-682X</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000690" MajorTopicYN="N">Amyotrophic Lateral Sclerosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D022163" MajorTopicYN="N">Clathrin-Coated Vesicles</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004705" MajorTopicYN="N">Endocytosis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName><QualifierName UI="Q000378" 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PubStatus="pubmed"><Year>2016</Year><Month>1</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>8</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26721251</ArticleId><ArticleId IdType="doi">10.1007/s00018-015-2105-x</ArticleId><ArticleId IdType="pii">10.1007/s00018-015-2105-x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Québec</li></region><settlement><li>Montréal</li></settlement><orgName><li>Université McGill</li></orgName></list><tree><country name="Canada"><region name="Québec"><name sortKey="Schreij, Andrea M A" sort="Schreij, Andrea M A" uniqKey="Schreij A" first="Andrea M A" last="Schreij">Andrea M A. Schreij</name></region><name sortKey="Fon, Edward A" sort="Fon, Edward A" uniqKey="Fon E" first="Edward A" last="Fon">Edward A. Fon</name><name sortKey="Mcpherson, Peter S" sort="Mcpherson, Peter S" uniqKey="Mcpherson P" first="Peter S" last="Mcpherson">Peter S. Mcpherson</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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