Dysfunctions of neuronal and glial intermediate filaments in disease
Intermediate filaments (IFs) are abundant structures found in most eukaryotic cells, including those in the nervous system. In the CNS, the primary components of neuronal IFs are alpha-internexin and the neurofilament triplet proteins. In the peripheral nervous system, a fifth neuronal IF protein kn...
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description | Intermediate filaments (IFs) are abundant structures found in most eukaryotic cells, including those in the nervous system. In the CNS, the primary components of neuronal IFs are alpha-internexin and the neurofilament triplet proteins. In the peripheral nervous system, a fifth neuronal IF protein known as peripherin is also present. IFs in astrocytes are primarily composed of glial fibrillary acidic protein (GFAP), although vimentin is also expressed in immature astrocytes and some mature astrocytes. In this Review, we focus on the IFs of glial cells (primarily GFAP) and neurons as well as their relationship to different neurodegenerative diseases. |
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In the CNS, the primary components of neuronal IFs are alpha-internexin and the neurofilament triplet proteins. In the peripheral nervous system, a fifth neuronal IF protein known as peripherin is also present. IFs in astrocytes are primarily composed of glial fibrillary acidic protein (GFAP), although vimentin is also expressed in immature astrocytes and some mature astrocytes. In this Review, we focus on the IFs of glial cells (primarily GFAP) and neurons as well as their relationship to different neurodegenerative diseases.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/jci38003</identifier><identifier>PMID: 19587456</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Alexander Disease - etiology ; Amino acids ; Amyotrophic Lateral Sclerosis - etiology ; Animals ; Astrocytes - physiology ; Biomedical research ; Charcot-Marie-Tooth Disease - etiology ; Cytomegalovirus Infections - etiology ; Cytoskeletal Proteins - physiology ; Degeneration ; Disease ; Glial Fibrillary Acidic Protein - cerebrospinal fluid ; Glial Fibrillary Acidic Protein - physiology ; Humans ; Intermediate filament proteins ; Intermediate Filaments - physiology ; Kinases ; Molecular weight ; Mutation ; Nervous system ; Neurodegenerative Diseases - etiology ; Neurofilament Proteins - genetics ; Neuroglia - physiology ; Neurons ; Neurons - physiology ; Physiological aspects ; Protein Tyrosine Phosphatases, Non-Receptor - genetics ; Proteins ; Review Series</subject><ispartof>The Journal of clinical investigation, 2009-07, Vol.119 (7), p.1814-1824</ispartof><rights>COPYRIGHT 2009 American Society for Clinical Investigation</rights><rights>Copyright American Society for Clinical Investigation Jul 2009</rights><rights>Copyright © 2009, American Society for Clinical Investigation</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c639t-98b7d8268d9485aa8f5ed8f3f305d035fbf9cde9f3d59c81522778e9da3755503</citedby><cites>FETCH-LOGICAL-c639t-98b7d8268d9485aa8f5ed8f3f305d035fbf9cde9f3d59c81522778e9da3755503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701870/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701870/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19587456$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liem, Ronald K H</creatorcontrib><creatorcontrib>Messing, Albee</creatorcontrib><title>Dysfunctions of neuronal and glial intermediate filaments in disease</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Intermediate filaments (IFs) are abundant structures found in most eukaryotic cells, including those in the nervous system. In the CNS, the primary components of neuronal IFs are alpha-internexin and the neurofilament triplet proteins. In the peripheral nervous system, a fifth neuronal IF protein known as peripherin is also present. IFs in astrocytes are primarily composed of glial fibrillary acidic protein (GFAP), although vimentin is also expressed in immature astrocytes and some mature astrocytes. In this Review, we focus on the IFs of glial cells (primarily GFAP) and neurons as well as their relationship to different neurodegenerative diseases.</description><subject>Alexander Disease - etiology</subject><subject>Amino acids</subject><subject>Amyotrophic Lateral Sclerosis - etiology</subject><subject>Animals</subject><subject>Astrocytes - physiology</subject><subject>Biomedical research</subject><subject>Charcot-Marie-Tooth Disease - etiology</subject><subject>Cytomegalovirus Infections - etiology</subject><subject>Cytoskeletal Proteins - physiology</subject><subject>Degeneration</subject><subject>Disease</subject><subject>Glial Fibrillary Acidic Protein - cerebrospinal fluid</subject><subject>Glial Fibrillary Acidic Protein - physiology</subject><subject>Humans</subject><subject>Intermediate filament proteins</subject><subject>Intermediate Filaments - physiology</subject><subject>Kinases</subject><subject>Molecular weight</subject><subject>Mutation</subject><subject>Nervous system</subject><subject>Neurodegenerative Diseases - etiology</subject><subject>Neurofilament Proteins - genetics</subject><subject>Neuroglia - physiology</subject><subject>Neurons</subject><subject>Neurons - physiology</subject><subject>Physiological aspects</subject><subject>Protein Tyrosine Phosphatases, Non-Receptor - genetics</subject><subject>Proteins</subject><subject>Review Series</subject><issn>0021-9738</issn><issn>1558-8238</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkl1rHCEUhqW0NJu00F9Qhl6E9GJSHcdRbwph048tgUC_bsXV46yLq-k4U5p_Xze7tNmSi-KFos95z-H1RegFweeE8ObN2ngqMKaP0IwwJmrRUPEYzTBuSC05FUfoOOc1xqRtWfsUHRHJBG9ZN0OXl7fZTdGMPsVcJVdFmIYUdah0tFUffDn5OMKwAev1CJXzQW8gjrlcV9Zn0BmeoSdOhwzP9_sJ-vb-3df5x_rq-sNifnFVm47KsZZiya1oOmFlK5jWwjGwwlFHMbOYMrd00liQjlomjSCsaTgXIK2mnDGG6Ql6u9O9mZZlHlPGGHRQN4Pf6OFWJe3V4Uv0K9Wnn6rhmAi-FTjdCwzpxwR5VBufDYSgI6Qpq463HSOsLeCrf8B1moZiS1YNxh3BTG6hegf1OoDy0aXS1PQQofROEYpVoC4aQrFoBReFP3-AL8vCxpsHC14fFBRmhF9jr6ec1eLL5_9nr78fsqf32BXoMK5yCtNdCA7Bsx1ohpTzAO6P1wSrbfLUp_niLnkFfXn_b_6C-6jR3-dz0Hg</recordid><startdate>200907</startdate><enddate>200907</enddate><creator>Liem, Ronald K H</creator><creator>Messing, Albee</creator><general>American Society for Clinical Investigation</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>S0X</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200907</creationdate><title>Dysfunctions of neuronal and glial intermediate filaments in disease</title><author>Liem, Ronald K H ; 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subjects | Alexander Disease - etiology Amino acids Amyotrophic Lateral Sclerosis - etiology Animals Astrocytes - physiology Biomedical research Charcot-Marie-Tooth Disease - etiology Cytomegalovirus Infections - etiology Cytoskeletal Proteins - physiology Degeneration Disease Glial Fibrillary Acidic Protein - cerebrospinal fluid Glial Fibrillary Acidic Protein - physiology Humans Intermediate filament proteins Intermediate Filaments - physiology Kinases Molecular weight Mutation Nervous system Neurodegenerative Diseases - etiology Neurofilament Proteins - genetics Neuroglia - physiology Neurons Neurons - physiology Physiological aspects Protein Tyrosine Phosphatases, Non-Receptor - genetics Proteins Review Series |
title | Dysfunctions of neuronal and glial intermediate filaments in disease |
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