Toward unraveling the complexity of simple epithelial keratins in human disease
Simple epithelial keratins (SEKs) are found primarily in single-layered simple epithelia and include keratin 7 (K7), K8, K18-K20, and K23. Genetically engineered mice that lack SEKs or overexpress mutant SEKs have helped illuminate several keratin functions and served as important disease models. In...
Gespeichert in:
| Veröffentlicht in: | The Journal of clinical investigation 2009-07, Vol.119 (7), p.1794-1805 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1805 |
|---|---|
| container_issue | 7 |
| container_start_page | 1794 |
| container_title | The Journal of clinical investigation |
| container_volume | 119 |
| creator | Omary, M Bishr Ku, Nam-On Strnad, Pavel Hanada, Shinichiro |
| description | Simple epithelial keratins (SEKs) are found primarily in single-layered simple epithelia and include keratin 7 (K7), K8, K18-K20, and K23. Genetically engineered mice that lack SEKs or overexpress mutant SEKs have helped illuminate several keratin functions and served as important disease models. Insight into the contribution of SEKs to human disease has indicated that K8 and K18 are the major constituents of Mallory-Denk bodies, hepatic inclusions associated with several liver diseases, and are essential for inclusion formation. Furthermore, mutations in the genes encoding K8, K18, and K19 predispose individuals to a variety of liver diseases. Hence, as we discuss here, the SEK cytoskeleton is involved in the orchestration of several important cellular functions and contributes to the pathogenesis of human liver disease. |
| doi_str_mv | 10.1172/jci37762 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2701867</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A213084876</galeid><sourcerecordid>A213084876</sourcerecordid><originalsourceid>FETCH-LOGICAL-c639t-fdeac033c95deb4386c7bd09f152fb5526f1213b0c163f4536086c666ac0c5583</originalsourceid><addsrcrecordid>eNqN0ktv1DAQAOAIgehSkPgFyOJQwSHFj9hOLkjVisdWlVaCwtVynEnixbGXOCntv8dlV9CtekA5JLa_GWsmk2UvCT4lRNJ3G2OZlII-yhaE8zIvKSsfZwuMKckrycqj7FmMG4xJUfDiaXZEKl7K9LnI1pfhlx4bNPtRX4GzvkNTD8iEYevg2k43KLQo2tsVgq1NZ85qh37AqCfrI7Ie9fOgPWpsBB3hefak1S7Ci_37OPv28cPl8nN-sf60Wp5d5EawasrbBrTBjJmKN1AXrBRG1g2uWsJpW3NORUsoYTU2RLC24EzgRIQQKcqkCtlx9n6XdzvXAzQG_DRqp7ajHfR4o4K26vDE21514UpRiUkpZEpwsk8whp8zxEkNNhpwTnsIc1RCFqIgBU3w9T24CfPoU3GKYswlp5IllO9Qpx0o69uQLjUd-NQnFzy0Nm2fpYpwWZRSJH_6gE9PA4M1Dwa8PQhIZoLrqdNzjGr19cv_2_X3Q3tyx_ag3dTH4ObJBh8P4ZsdNGOIcYT2b68JVrdDqM6Xqz9DmOiru__mH9xPHfsNhunUig</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>200575273</pqid></control><display><type>article</type><title>Toward unraveling the complexity of simple epithelial keratins in human disease</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Omary, M Bishr ; Ku, Nam-On ; Strnad, Pavel ; Hanada, Shinichiro</creator><creatorcontrib>Omary, M Bishr ; Ku, Nam-On ; Strnad, Pavel ; Hanada, Shinichiro</creatorcontrib><description>Simple epithelial keratins (SEKs) are found primarily in single-layered simple epithelia and include keratin 7 (K7), K8, K18-K20, and K23. Genetically engineered mice that lack SEKs or overexpress mutant SEKs have helped illuminate several keratin functions and served as important disease models. Insight into the contribution of SEKs to human disease has indicated that K8 and K18 are the major constituents of Mallory-Denk bodies, hepatic inclusions associated with several liver diseases, and are essential for inclusion formation. Furthermore, mutations in the genes encoding K8, K18, and K19 predispose individuals to a variety of liver diseases. Hence, as we discuss here, the SEK cytoskeleton is involved in the orchestration of several important cellular functions and contributes to the pathogenesis of human liver disease.</description><identifier>ISSN: 0021-9738</identifier><identifier>EISSN: 1558-8238</identifier><identifier>DOI: 10.1172/jci37762</identifier><identifier>PMID: 19587454</identifier><language>eng</language><publisher>United States: American Society for Clinical Investigation</publisher><subject>Animals ; Antigens ; Apoptosis ; Biomarkers, Tumor ; Biomedical research ; Gene mutations ; Genetic aspects ; Genotype & phenotype ; Health aspects ; Humans ; Inflammatory bowel disease ; Keratin ; Keratins - analysis ; Keratins - chemistry ; Keratins - genetics ; Keratins - physiology ; Liver diseases ; Liver Diseases - etiology ; Mice ; Mice, Transgenic ; Mutation ; Neoplasm Metastasis ; Neoplasms, Glandular and Epithelial - diagnosis ; Neoplasms, Glandular and Epithelial - therapy ; Phosphorylation ; Physiological aspects ; Proteins ; Proteins - physiology ; Review Series ; Risk factors</subject><ispartof>The Journal of clinical investigation, 2009-07, Vol.119 (7), p.1794-1805</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-fdeac033c95deb4386c7bd09f152fb5526f1213b0c163f4536086c666ac0c5583</citedby><cites>FETCH-LOGICAL-c639t-fdeac033c95deb4386c7bd09f152fb5526f1213b0c163f4536086c666ac0c5583</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/PMC2701867/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701867/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19587454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Omary, M Bishr</creatorcontrib><creatorcontrib>Ku, Nam-On</creatorcontrib><creatorcontrib>Strnad, Pavel</creatorcontrib><creatorcontrib>Hanada, Shinichiro</creatorcontrib><title>Toward unraveling the complexity of simple epithelial keratins in human disease</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Simple epithelial keratins (SEKs) are found primarily in single-layered simple epithelia and include keratin 7 (K7), K8, K18-K20, and K23. Genetically engineered mice that lack SEKs or overexpress mutant SEKs have helped illuminate several keratin functions and served as important disease models. Insight into the contribution of SEKs to human disease has indicated that K8 and K18 are the major constituents of Mallory-Denk bodies, hepatic inclusions associated with several liver diseases, and are essential for inclusion formation. Furthermore, mutations in the genes encoding K8, K18, and K19 predispose individuals to a variety of liver diseases. Hence, as we discuss here, the SEK cytoskeleton is involved in the orchestration of several important cellular functions and contributes to the pathogenesis of human liver disease.</description><subject>Animals</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Biomarkers, Tumor</subject><subject>Biomedical research</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Genotype & phenotype</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammatory bowel disease</subject><subject>Keratin</subject><subject>Keratins - analysis</subject><subject>Keratins - chemistry</subject><subject>Keratins - genetics</subject><subject>Keratins - physiology</subject><subject>Liver diseases</subject><subject>Liver Diseases - etiology</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Mutation</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasms, Glandular and Epithelial - diagnosis</subject><subject>Neoplasms, Glandular and Epithelial - therapy</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Proteins - physiology</subject><subject>Review Series</subject><subject>Risk factors</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>eNqN0ktv1DAQAOAIgehSkPgFyOJQwSHFj9hOLkjVisdWlVaCwtVynEnixbGXOCntv8dlV9CtekA5JLa_GWsmk2UvCT4lRNJ3G2OZlII-yhaE8zIvKSsfZwuMKckrycqj7FmMG4xJUfDiaXZEKl7K9LnI1pfhlx4bNPtRX4GzvkNTD8iEYevg2k43KLQo2tsVgq1NZ85qh37AqCfrI7Ie9fOgPWpsBB3hefak1S7Ci_37OPv28cPl8nN-sf60Wp5d5EawasrbBrTBjJmKN1AXrBRG1g2uWsJpW3NORUsoYTU2RLC24EzgRIQQKcqkCtlx9n6XdzvXAzQG_DRqp7ajHfR4o4K26vDE21514UpRiUkpZEpwsk8whp8zxEkNNhpwTnsIc1RCFqIgBU3w9T24CfPoU3GKYswlp5IllO9Qpx0o69uQLjUd-NQnFzy0Nm2fpYpwWZRSJH_6gE9PA4M1Dwa8PQhIZoLrqdNzjGr19cv_2_X3Q3tyx_ag3dTH4ObJBh8P4ZsdNGOIcYT2b68JVrdDqM6Xqz9DmOiru__mH9xPHfsNhunUig</recordid><startdate>200907</startdate><enddate>200907</enddate><creator>Omary, M Bishr</creator><creator>Ku, Nam-On</creator><creator>Strnad, Pavel</creator><creator>Hanada, Shinichiro</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>Toward unraveling the complexity of simple epithelial keratins in human disease</title><author>Omary, M Bishr ; Ku, Nam-On ; Strnad, Pavel ; Hanada, Shinichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c639t-fdeac033c95deb4386c7bd09f152fb5526f1213b0c163f4536086c666ac0c5583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Biomarkers, Tumor</topic><topic>Biomedical research</topic><topic>Gene mutations</topic><topic>Genetic aspects</topic><topic>Genotype & phenotype</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Inflammatory bowel disease</topic><topic>Keratin</topic><topic>Keratins - analysis</topic><topic>Keratins - chemistry</topic><topic>Keratins - genetics</topic><topic>Keratins - physiology</topic><topic>Liver diseases</topic><topic>Liver Diseases - etiology</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Mutation</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasms, Glandular and Epithelial - diagnosis</topic><topic>Neoplasms, Glandular and Epithelial - therapy</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Proteins - physiology</topic><topic>Review Series</topic><topic>Risk factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Omary, M Bishr</creatorcontrib><creatorcontrib>Ku, Nam-On</creatorcontrib><creatorcontrib>Strnad, Pavel</creatorcontrib><creatorcontrib>Hanada, Shinichiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Omary, M Bishr</au><au>Ku, Nam-On</au><au>Strnad, Pavel</au><au>Hanada, Shinichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Toward unraveling the complexity of simple epithelial keratins in human disease</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>2009-07</date><risdate>2009</risdate><volume>119</volume><issue>7</issue><spage>1794</spage><epage>1805</epage><pages>1794-1805</pages><issn>0021-9738</issn><eissn>1558-8238</eissn><abstract>Simple epithelial keratins (SEKs) are found primarily in single-layered simple epithelia and include keratin 7 (K7), K8, K18-K20, and K23. Genetically engineered mice that lack SEKs or overexpress mutant SEKs have helped illuminate several keratin functions and served as important disease models. Insight into the contribution of SEKs to human disease has indicated that K8 and K18 are the major constituents of Mallory-Denk bodies, hepatic inclusions associated with several liver diseases, and are essential for inclusion formation. Furthermore, mutations in the genes encoding K8, K18, and K19 predispose individuals to a variety of liver diseases. Hence, as we discuss here, the SEK cytoskeleton is involved in the orchestration of several important cellular functions and contributes to the pathogenesis of human liver disease.</abstract><cop>United States</cop><pub>American Society for Clinical Investigation</pub><pmid>19587454</pmid><doi>10.1172/jci37762</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9738 |
| ispartof | The Journal of clinical investigation, 2009-07, Vol.119 (7), p.1794-1805 |
| issn | 0021-9738 1558-8238 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2701867 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Antigens Apoptosis Biomarkers, Tumor Biomedical research Gene mutations Genetic aspects Genotype & phenotype Health aspects Humans Inflammatory bowel disease Keratin Keratins - analysis Keratins - chemistry Keratins - genetics Keratins - physiology Liver diseases Liver Diseases - etiology Mice Mice, Transgenic Mutation Neoplasm Metastasis Neoplasms, Glandular and Epithelial - diagnosis Neoplasms, Glandular and Epithelial - therapy Phosphorylation Physiological aspects Proteins Proteins - physiology Review Series Risk factors |
| title | Toward unraveling the complexity of simple epithelial keratins in human disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-16T14%3A30%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Toward%20unraveling%20the%20complexity%20of%20simple%20epithelial%20keratins%20in%20human%20disease&rft.jtitle=The%20Journal%20of%20clinical%20investigation&rft.au=Omary,%20M%20Bishr&rft.date=2009-07&rft.volume=119&rft.issue=7&rft.spage=1794&rft.epage=1805&rft.pages=1794-1805&rft.issn=0021-9738&rft.eissn=1558-8238&rft_id=info:doi/10.1172/jci37762&rft_dat=%3Cgale_pubme%3EA213084876%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=200575273&rft_id=info:pmid/19587454&rft_galeid=A213084876&rfr_iscdi=true |