CtBP2 contributes to malignant development of human esophageal squamous cell carcinoma by regulation of p16INK4A
C‐terminal binding protein‐2 (CtBP2), as a transcriptional co‐repressor, has been shown to mediate the repression of p16INK4A, a tumor suppressor gene product, in primary human cells. Here we aimed to investigate how the correlation between CtBP2 and p16INK4A influenced the development of esophageal...
Gespeichert in:
| Veröffentlicht in: | Journal of cellular biochemistry 2013-06, Vol.114 (6), p.1343-1354 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1354 |
|---|---|
| container_issue | 6 |
| container_start_page | 1343 |
| container_title | Journal of cellular biochemistry |
| container_volume | 114 |
| creator | Guan, Chengqi Shi, Hui Wang, Huijie Zhang, Jianguo Ni, Wenkai Chen, Buyou Hou, Sicong Yang, Xiaojing Shen, Aiguo Ni, Runzhou |
| description | C‐terminal binding protein‐2 (CtBP2), as a transcriptional co‐repressor, has been shown to mediate the repression of p16INK4A, a tumor suppressor gene product, in primary human cells. Here we aimed to investigate how the correlation between CtBP2 and p16INK4A influenced the development of esophageal squamous cell carcinoma (ESCC). Immunohistochemistry of ESCC tissue sections indicated that the CtBP2 and p16INK4A expressions were inversely correlated to each other with a linear regression coefficient of −0.747 (P |
| doi_str_mv | 10.1002/jcb.24475 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_1328545750</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1328545750</sourcerecordid><originalsourceid>FETCH-LOGICAL-i2475-10731cc6d19be1ba9e1e956ca308b76fb2f84dea230a6a2d589d513e93154c943</originalsourceid><addsrcrecordid>eNpdkU9v1DAQxS0EokvhwBdAlrhwSeu_cXxsV3QpVKUHEFIv1sSZ3XpJ4jROgP32eLulB04z0vze6M08Qt5ydsIZE6dbX58IpYx-RhacWVOoUqnnZMGMZIWQXByRVyltGWPWSvGSHAkptJZWLMiwnM5vBPWxn8ZQzxMmOkXaQRs2PfQTbfAXtnHoMPdxTe_mDnqKKQ53sEFoabqfoYtzoh7blnoYfehjB7Te0RE3cwtTiP1eOfDy8vqLOntNXqyhTfjmsR6T7xcfvy0_FVdfV5fLs6siiHxIwbN37n3ZcFsjr8EiR6tLD5JVtSnXtVhXqkEQkkEJotGVbTSXaCXXylslj8mHw95hjPczpsl1Ie1NQo_Zr-NSVFppo1lG3_-HbuM89tndnjLcqIrpTL17pOa6w8YNY-hg3Ll_v8zA6QH4HVrcPc05c_uQXA7JPYTkPi_PH5qsKA6KkCb886SA8acrjczkj-uVM7crfXFrpLuRfwE1JpHy</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1327174805</pqid></control><display><type>article</type><title>CtBP2 contributes to malignant development of human esophageal squamous cell carcinoma by regulation of p16INK4A</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Guan, Chengqi ; Shi, Hui ; Wang, Huijie ; Zhang, Jianguo ; Ni, Wenkai ; Chen, Buyou ; Hou, Sicong ; Yang, Xiaojing ; Shen, Aiguo ; Ni, Runzhou</creator><creatorcontrib>Guan, Chengqi ; Shi, Hui ; Wang, Huijie ; Zhang, Jianguo ; Ni, Wenkai ; Chen, Buyou ; Hou, Sicong ; Yang, Xiaojing ; Shen, Aiguo ; Ni, Runzhou</creatorcontrib><description>C‐terminal binding protein‐2 (CtBP2), as a transcriptional co‐repressor, has been shown to mediate the repression of p16INK4A, a tumor suppressor gene product, in primary human cells. Here we aimed to investigate how the correlation between CtBP2 and p16INK4A influenced the development of esophageal squamous cell carcinoma (ESCC). Immunohistochemistry of ESCC tissue sections indicated that the CtBP2 and p16INK4A expressions were inversely correlated to each other with a linear regression coefficient of −0.747 (P < 0.05), and Western blot analysis revealed that CtBP2 was higher expressed in tumorous tissues than in adjacent non‐tumorous tissues. Either CtBP2 or p16INK4A expression was significantly related to histological differentiation (P = 0.016 or 0.001) and to the expression of Ki‐67, a proliferating marker (P = 0.006 or 0.02), and patients with higher CtBP2 and lower p16INK4A expressions had shorter overall survival. We also observed that CtBP2 modulated the cell proliferation and cell cycle in ECA109 cells, an ESCC cell line, by inhibiting p16INK4A. Overexpression or knockdown of CtBP2 in ECA109 cells was found to inhibit or activate the mRNA or protein expression of p16INK4A, which in turn altered the cell proliferation and cell cycle in ECA109 cells, as measured by flow cytometry and cell count assay. Additionally, after ECA109 cells silenced for CtBP2 were treated with cisplatin (an anti‐ESCC agent), the p16INK4A expression was up‐regulated, and the cell apoptosis was promoted, thus confirming the repression of p16INK4A by CtBP2. Collectively, all results suggested that CtBP2 might contribute to the progression of ESCC through a negative transcriptional regulation of p16INK4A. J. Cell. Biochem. 114: 1343–1354, 2013. © 2013 Wiley Periodicals, Inc.</description><identifier>ISSN: 0730-2312</identifier><identifier>EISSN: 1097-4644</identifier><identifier>DOI: 10.1002/jcb.24475</identifier><identifier>PMID: 23255392</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Alcohol Oxidoreductases - physiology ; Antineoplastic Agents - pharmacology ; C-TERMINAL BINDING PROTEIN 2 (CtBP2) ; Carcinogenesis - genetics ; Carcinogenesis - metabolism ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - mortality ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin - pharmacology ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - metabolism ; Esophageal Neoplasms - mortality ; Esophageal Squamous Cell Carcinoma ; ESOPHAGEAL SQUAMOUS CELL CARCINOMA (ESCC) ; Female ; Gene Expression ; Gene Expression Regulation, Neoplastic ; Humans ; Kaplan-Meier Estimate ; Male ; MALIGNANT DEVELOPMENT ; Middle Aged ; Nerve Tissue Proteins - physiology ; p16INK4A ; Prognosis</subject><ispartof>Journal of cellular biochemistry, 2013-06, Vol.114 (6), p.1343-1354</ispartof><rights>Copyright © 2013 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcb.24475$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcb.24475$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23255392$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guan, Chengqi</creatorcontrib><creatorcontrib>Shi, Hui</creatorcontrib><creatorcontrib>Wang, Huijie</creatorcontrib><creatorcontrib>Zhang, Jianguo</creatorcontrib><creatorcontrib>Ni, Wenkai</creatorcontrib><creatorcontrib>Chen, Buyou</creatorcontrib><creatorcontrib>Hou, Sicong</creatorcontrib><creatorcontrib>Yang, Xiaojing</creatorcontrib><creatorcontrib>Shen, Aiguo</creatorcontrib><creatorcontrib>Ni, Runzhou</creatorcontrib><title>CtBP2 contributes to malignant development of human esophageal squamous cell carcinoma by regulation of p16INK4A</title><title>Journal of cellular biochemistry</title><addtitle>J. Cell. Biochem</addtitle><description>C‐terminal binding protein‐2 (CtBP2), as a transcriptional co‐repressor, has been shown to mediate the repression of p16INK4A, a tumor suppressor gene product, in primary human cells. Here we aimed to investigate how the correlation between CtBP2 and p16INK4A influenced the development of esophageal squamous cell carcinoma (ESCC). Immunohistochemistry of ESCC tissue sections indicated that the CtBP2 and p16INK4A expressions were inversely correlated to each other with a linear regression coefficient of −0.747 (P < 0.05), and Western blot analysis revealed that CtBP2 was higher expressed in tumorous tissues than in adjacent non‐tumorous tissues. Either CtBP2 or p16INK4A expression was significantly related to histological differentiation (P = 0.016 or 0.001) and to the expression of Ki‐67, a proliferating marker (P = 0.006 or 0.02), and patients with higher CtBP2 and lower p16INK4A expressions had shorter overall survival. We also observed that CtBP2 modulated the cell proliferation and cell cycle in ECA109 cells, an ESCC cell line, by inhibiting p16INK4A. Overexpression or knockdown of CtBP2 in ECA109 cells was found to inhibit or activate the mRNA or protein expression of p16INK4A, which in turn altered the cell proliferation and cell cycle in ECA109 cells, as measured by flow cytometry and cell count assay. Additionally, after ECA109 cells silenced for CtBP2 were treated with cisplatin (an anti‐ESCC agent), the p16INK4A expression was up‐regulated, and the cell apoptosis was promoted, thus confirming the repression of p16INK4A by CtBP2. Collectively, all results suggested that CtBP2 might contribute to the progression of ESCC through a negative transcriptional regulation of p16INK4A. J. Cell. Biochem. 114: 1343–1354, 2013. © 2013 Wiley Periodicals, Inc.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alcohol Oxidoreductases - physiology</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>C-TERMINAL BINDING PROTEIN 2 (CtBP2)</subject><subject>Carcinogenesis - genetics</subject><subject>Carcinogenesis - metabolism</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - mortality</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cisplatin - pharmacology</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - metabolism</subject><subject>Esophageal Neoplasms - mortality</subject><subject>Esophageal Squamous Cell Carcinoma</subject><subject>ESOPHAGEAL SQUAMOUS CELL CARCINOMA (ESCC)</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Kaplan-Meier Estimate</subject><subject>Male</subject><subject>MALIGNANT DEVELOPMENT</subject><subject>Middle Aged</subject><subject>Nerve Tissue Proteins - physiology</subject><subject>p16INK4A</subject><subject>Prognosis</subject><issn>0730-2312</issn><issn>1097-4644</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU9v1DAQxS0EokvhwBdAlrhwSeu_cXxsV3QpVKUHEFIv1sSZ3XpJ4jROgP32eLulB04z0vze6M08Qt5ydsIZE6dbX58IpYx-RhacWVOoUqnnZMGMZIWQXByRVyltGWPWSvGSHAkptJZWLMiwnM5vBPWxn8ZQzxMmOkXaQRs2PfQTbfAXtnHoMPdxTe_mDnqKKQ53sEFoabqfoYtzoh7blnoYfehjB7Te0RE3cwtTiP1eOfDy8vqLOntNXqyhTfjmsR6T7xcfvy0_FVdfV5fLs6siiHxIwbN37n3ZcFsjr8EiR6tLD5JVtSnXtVhXqkEQkkEJotGVbTSXaCXXylslj8mHw95hjPczpsl1Ie1NQo_Zr-NSVFppo1lG3_-HbuM89tndnjLcqIrpTL17pOa6w8YNY-hg3Ll_v8zA6QH4HVrcPc05c_uQXA7JPYTkPi_PH5qsKA6KkCb886SA8acrjczkj-uVM7crfXFrpLuRfwE1JpHy</recordid><startdate>201306</startdate><enddate>201306</enddate><creator>Guan, Chengqi</creator><creator>Shi, Hui</creator><creator>Wang, Huijie</creator><creator>Zhang, Jianguo</creator><creator>Ni, Wenkai</creator><creator>Chen, Buyou</creator><creator>Hou, Sicong</creator><creator>Yang, Xiaojing</creator><creator>Shen, Aiguo</creator><creator>Ni, Runzhou</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201306</creationdate><title>CtBP2 contributes to malignant development of human esophageal squamous cell carcinoma by regulation of p16INK4A</title><author>Guan, Chengqi ; Shi, Hui ; Wang, Huijie ; Zhang, Jianguo ; Ni, Wenkai ; Chen, Buyou ; Hou, Sicong ; Yang, Xiaojing ; Shen, Aiguo ; Ni, Runzhou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2475-10731cc6d19be1ba9e1e956ca308b76fb2f84dea230a6a2d589d513e93154c943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alcohol Oxidoreductases - physiology</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>C-TERMINAL BINDING PROTEIN 2 (CtBP2)</topic><topic>Carcinogenesis - genetics</topic><topic>Carcinogenesis - metabolism</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - mortality</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cisplatin - pharmacology</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - metabolism</topic><topic>Esophageal Neoplasms - mortality</topic><topic>Esophageal Squamous Cell Carcinoma</topic><topic>ESOPHAGEAL SQUAMOUS CELL CARCINOMA (ESCC)</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Kaplan-Meier Estimate</topic><topic>Male</topic><topic>MALIGNANT DEVELOPMENT</topic><topic>Middle Aged</topic><topic>Nerve Tissue Proteins - physiology</topic><topic>p16INK4A</topic><topic>Prognosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guan, Chengqi</creatorcontrib><creatorcontrib>Shi, Hui</creatorcontrib><creatorcontrib>Wang, Huijie</creatorcontrib><creatorcontrib>Zhang, Jianguo</creatorcontrib><creatorcontrib>Ni, Wenkai</creatorcontrib><creatorcontrib>Chen, Buyou</creatorcontrib><creatorcontrib>Hou, Sicong</creatorcontrib><creatorcontrib>Yang, Xiaojing</creatorcontrib><creatorcontrib>Shen, Aiguo</creatorcontrib><creatorcontrib>Ni, Runzhou</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guan, Chengqi</au><au>Shi, Hui</au><au>Wang, Huijie</au><au>Zhang, Jianguo</au><au>Ni, Wenkai</au><au>Chen, Buyou</au><au>Hou, Sicong</au><au>Yang, Xiaojing</au><au>Shen, Aiguo</au><au>Ni, Runzhou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CtBP2 contributes to malignant development of human esophageal squamous cell carcinoma by regulation of p16INK4A</atitle><jtitle>Journal of cellular biochemistry</jtitle><addtitle>J. Cell. Biochem</addtitle><date>2013-06</date><risdate>2013</risdate><volume>114</volume><issue>6</issue><spage>1343</spage><epage>1354</epage><pages>1343-1354</pages><issn>0730-2312</issn><eissn>1097-4644</eissn><abstract>C‐terminal binding protein‐2 (CtBP2), as a transcriptional co‐repressor, has been shown to mediate the repression of p16INK4A, a tumor suppressor gene product, in primary human cells. Here we aimed to investigate how the correlation between CtBP2 and p16INK4A influenced the development of esophageal squamous cell carcinoma (ESCC). Immunohistochemistry of ESCC tissue sections indicated that the CtBP2 and p16INK4A expressions were inversely correlated to each other with a linear regression coefficient of −0.747 (P < 0.05), and Western blot analysis revealed that CtBP2 was higher expressed in tumorous tissues than in adjacent non‐tumorous tissues. Either CtBP2 or p16INK4A expression was significantly related to histological differentiation (P = 0.016 or 0.001) and to the expression of Ki‐67, a proliferating marker (P = 0.006 or 0.02), and patients with higher CtBP2 and lower p16INK4A expressions had shorter overall survival. We also observed that CtBP2 modulated the cell proliferation and cell cycle in ECA109 cells, an ESCC cell line, by inhibiting p16INK4A. Overexpression or knockdown of CtBP2 in ECA109 cells was found to inhibit or activate the mRNA or protein expression of p16INK4A, which in turn altered the cell proliferation and cell cycle in ECA109 cells, as measured by flow cytometry and cell count assay. Additionally, after ECA109 cells silenced for CtBP2 were treated with cisplatin (an anti‐ESCC agent), the p16INK4A expression was up‐regulated, and the cell apoptosis was promoted, thus confirming the repression of p16INK4A by CtBP2. Collectively, all results suggested that CtBP2 might contribute to the progression of ESCC through a negative transcriptional regulation of p16INK4A. J. Cell. Biochem. 114: 1343–1354, 2013. © 2013 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>23255392</pmid><doi>10.1002/jcb.24475</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0730-2312 |
| ispartof | Journal of cellular biochemistry, 2013-06, Vol.114 (6), p.1343-1354 |
| issn | 0730-2312 1097-4644 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1328545750 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Adult Aged Aged, 80 and over Alcohol Oxidoreductases - physiology Antineoplastic Agents - pharmacology C-TERMINAL BINDING PROTEIN 2 (CtBP2) Carcinogenesis - genetics Carcinogenesis - metabolism Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - mortality Cell Line, Tumor Cell Proliferation Cisplatin - pharmacology Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p16 - metabolism Esophageal Neoplasms - genetics Esophageal Neoplasms - metabolism Esophageal Neoplasms - mortality Esophageal Squamous Cell Carcinoma ESOPHAGEAL SQUAMOUS CELL CARCINOMA (ESCC) Female Gene Expression Gene Expression Regulation, Neoplastic Humans Kaplan-Meier Estimate Male MALIGNANT DEVELOPMENT Middle Aged Nerve Tissue Proteins - physiology p16INK4A Prognosis |
| title | CtBP2 contributes to malignant development of human esophageal squamous cell carcinoma by regulation of p16INK4A |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T15%3A27%3A38IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CtBP2%20contributes%20to%20malignant%20development%20of%20human%20esophageal%20squamous%20cell%20carcinoma%20by%20regulation%20of%20p16INK4A&rft.jtitle=Journal%20of%20cellular%20biochemistry&rft.au=Guan,%20Chengqi&rft.date=2013-06&rft.volume=114&rft.issue=6&rft.spage=1343&rft.epage=1354&rft.pages=1343-1354&rft.issn=0730-2312&rft.eissn=1097-4644&rft_id=info:doi/10.1002/jcb.24475&rft_dat=%3Cproquest_pubme%3E1328545750%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1327174805&rft_id=info:pmid/23255392&rfr_iscdi=true |