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Regulation of CFTR expression and function during differentiation of intestinal epithelial cells
CFTR, the protein defective in cystic fibrosis is regulated during differentiation of intestinal epithelial cells. The undifferentiated cells (Caco‐2 and HT‐29) show a lower level of CFTR mRNA, while a 10‐fold increase is seen in differentiated cells. These differences correlate well with those of o...
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Published in: | The EMBO journal 1992-07, Vol.11 (7), p.2487-2494 |
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creator | Sood, R. Bear, C. Auerbach, W. Reyes, E. Jensen, T. Kartner, N. Riordan, J.R. Buchwald, M. |
description | CFTR, the protein defective in cystic fibrosis is regulated during differentiation of intestinal epithelial cells. The undifferentiated cells (Caco‐2 and HT‐29) show a lower level of CFTR mRNA, while a 10‐fold increase is seen in differentiated cells. These differences correlate well with those of other intestinal‐specific genes, including sucrase‐isomaltase, villin and alpha 1‐antitrypsin, indicating that the regulation is cell specific. In Caco‐2 cells the increase in CFTR mRNA cannot be accounted for by increased transcription of the gene. These data indicate that CFTR mRNA stabilizing factor(s) might be present in differentiated cells. The higher levels of CFTR mRNA in differentiated cells are accompanied by decreased protein levels, indicating, as well, involvement of translational control in the regulation of CFTR in these cells. Finally, fully differentiated cells show lowered levels of cyclic AMP‐activated C1‐ transport, the characteristic function of CFTR. Thus, CFTR function in differentiated cells is modulated by a complex interaction of regulatory elements. Caco‐2 and HT‐29 cells provide a suitable in vitro system in which to study the mechanism of regulation of CFTR. |
doi_str_mv | 10.1002/j.1460-2075.1992.tb05313.x |
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The undifferentiated cells (Caco‐2 and HT‐29) show a lower level of CFTR mRNA, while a 10‐fold increase is seen in differentiated cells. These differences correlate well with those of other intestinal‐specific genes, including sucrase‐isomaltase, villin and alpha 1‐antitrypsin, indicating that the regulation is cell specific. In Caco‐2 cells the increase in CFTR mRNA cannot be accounted for by increased transcription of the gene. These data indicate that CFTR mRNA stabilizing factor(s) might be present in differentiated cells. The higher levels of CFTR mRNA in differentiated cells are accompanied by decreased protein levels, indicating, as well, involvement of translational control in the regulation of CFTR in these cells. Finally, fully differentiated cells show lowered levels of cyclic AMP‐activated C1‐ transport, the characteristic function of CFTR. Thus, CFTR function in differentiated cells is modulated by a complex interaction of regulatory elements. Caco‐2 and HT‐29 cells provide a suitable in vitro system in which to study the mechanism of regulation of CFTR.</description><identifier>ISSN: 0261-4189</identifier><identifier>EISSN: 1460-2075</identifier><identifier>DOI: 10.1002/j.1460-2075.1992.tb05313.x</identifier><identifier>PMID: 1378393</identifier><identifier>CODEN: EMJODG</identifier><language>eng</language><publisher>London: Nature Publishing Group</publisher><subject>Biological and medical sciences ; Blotting, Western ; Carrier Proteins - genetics ; Cell Differentiation ; cells ; Colon - cytology ; Colon - metabolism ; cystic fibrosis ; Cystic Fibrosis - metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator ; differentiation ; Epithelial Cells ; Epithelium - metabolism ; expression ; function ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression Regulation ; intestine ; Iodine Radioisotopes - metabolism ; Membrane Proteins - genetics ; Microfilament Proteins - genetics ; Molecular and cellular biology ; Molecular genetics ; regulation ; RNA, Messenger - metabolism ; Transcription, Genetic ; transmembrane conductance regulator ; Tumor Cells, Cultured</subject><ispartof>The EMBO journal, 1992-07, Vol.11 (7), p.2487-2494</ispartof><rights>1992 European Molecular Biology Organization</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5383-80a3dc0082b344798e9ea7303ea781ce5f474331b626d87662fad3a4d521bce13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC556723/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC556723/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5359543$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1378393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sood, R.</creatorcontrib><creatorcontrib>Bear, C.</creatorcontrib><creatorcontrib>Auerbach, W.</creatorcontrib><creatorcontrib>Reyes, E.</creatorcontrib><creatorcontrib>Jensen, T.</creatorcontrib><creatorcontrib>Kartner, N.</creatorcontrib><creatorcontrib>Riordan, J.R.</creatorcontrib><creatorcontrib>Buchwald, M.</creatorcontrib><title>Regulation of CFTR expression and function during differentiation of intestinal epithelial cells</title><title>The EMBO journal</title><addtitle>EMBO J</addtitle><description>CFTR, the protein defective in cystic fibrosis is regulated during differentiation of intestinal epithelial cells. The undifferentiated cells (Caco‐2 and HT‐29) show a lower level of CFTR mRNA, while a 10‐fold increase is seen in differentiated cells. These differences correlate well with those of other intestinal‐specific genes, including sucrase‐isomaltase, villin and alpha 1‐antitrypsin, indicating that the regulation is cell specific. In Caco‐2 cells the increase in CFTR mRNA cannot be accounted for by increased transcription of the gene. These data indicate that CFTR mRNA stabilizing factor(s) might be present in differentiated cells. The higher levels of CFTR mRNA in differentiated cells are accompanied by decreased protein levels, indicating, as well, involvement of translational control in the regulation of CFTR in these cells. Finally, fully differentiated cells show lowered levels of cyclic AMP‐activated C1‐ transport, the characteristic function of CFTR. Thus, CFTR function in differentiated cells is modulated by a complex interaction of regulatory elements. Caco‐2 and HT‐29 cells provide a suitable in vitro system in which to study the mechanism of regulation of CFTR.</description><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Carrier Proteins - genetics</subject><subject>Cell Differentiation</subject><subject>cells</subject><subject>Colon - cytology</subject><subject>Colon - metabolism</subject><subject>cystic fibrosis</subject><subject>Cystic Fibrosis - metabolism</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator</subject><subject>differentiation</subject><subject>Epithelial Cells</subject><subject>Epithelium - metabolism</subject><subject>expression</subject><subject>function</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>intestine</subject><subject>Iodine Radioisotopes - metabolism</subject><subject>Membrane Proteins - genetics</subject><subject>Microfilament Proteins - genetics</subject><subject>Molecular and cellular biology</subject><subject>Molecular genetics</subject><subject>regulation</subject><subject>RNA, Messenger - metabolism</subject><subject>Transcription, Genetic</subject><subject>transmembrane conductance regulator</subject><subject>Tumor Cells, Cultured</subject><issn>0261-4189</issn><issn>1460-2075</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><recordid>eNqVUV1rFDEUDaLUbfUnCIOIbzPmc5IIPtSl9YOKUOpzzGSSbZZsZk1m7Pbfm-kuqz6JL_decs4J53AAeIlggyDEb9YNoi2sMeSsQVLiZuwgI4g0u0dgcYQegwXELaopEvIpOM15DSFkgqMTcIIIF0SSBfh-bVdT0KMfYjW4anl5c13Z3TbZnOcnHfvKTdE84P2UfFxVvXfOJhtHf5T5ONo8-qhDZbd-vLXBl9PYEPIz8MTpkO3zwz4D3y4vbpYf66uvHz4tz69qw4ggtYCa9AZCgTtCKZfCSqs5gaRMgYxljnJKCOpa3PaCty12uiea9gyjzlhEzsC7_b_bqdvY3hR_SQe1TX6j070atFd_I9HfqtXwUzHWckyK_vVBn4YfU0mjNj7PCXS0w5RV8cKhbOk_iajFJRCXhfh2TzRpyDlZdzSDoJp7VGs1l6XmstTcozr0qHZF_OLPOL-l--IK_uqA62x0cElH4_ORxgiTjM608z3tzgd7_x8G1MWX958fbvILCoK84Q</recordid><startdate>199207</startdate><enddate>199207</enddate><creator>Sood, R.</creator><creator>Bear, C.</creator><creator>Auerbach, W.</creator><creator>Reyes, E.</creator><creator>Jensen, T.</creator><creator>Kartner, N.</creator><creator>Riordan, J.R.</creator><creator>Buchwald, M.</creator><general>Nature Publishing Group</general><scope>IQODW</scope><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>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>199207</creationdate><title>Regulation of CFTR expression and function during differentiation of intestinal epithelial cells</title><author>Sood, R. ; Bear, C. ; Auerbach, W. ; Reyes, E. ; Jensen, T. ; Kartner, N. ; Riordan, J.R. ; Buchwald, M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5383-80a3dc0082b344798e9ea7303ea781ce5f474331b626d87662fad3a4d521bce13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Carrier Proteins - genetics</topic><topic>Cell Differentiation</topic><topic>cells</topic><topic>Colon - cytology</topic><topic>Colon - metabolism</topic><topic>cystic fibrosis</topic><topic>Cystic Fibrosis - metabolism</topic><topic>Cystic Fibrosis Transmembrane Conductance Regulator</topic><topic>differentiation</topic><topic>Epithelial Cells</topic><topic>Epithelium - metabolism</topic><topic>expression</topic><topic>function</topic><topic>Fundamental and applied biological sciences. 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The undifferentiated cells (Caco‐2 and HT‐29) show a lower level of CFTR mRNA, while a 10‐fold increase is seen in differentiated cells. These differences correlate well with those of other intestinal‐specific genes, including sucrase‐isomaltase, villin and alpha 1‐antitrypsin, indicating that the regulation is cell specific. In Caco‐2 cells the increase in CFTR mRNA cannot be accounted for by increased transcription of the gene. These data indicate that CFTR mRNA stabilizing factor(s) might be present in differentiated cells. The higher levels of CFTR mRNA in differentiated cells are accompanied by decreased protein levels, indicating, as well, involvement of translational control in the regulation of CFTR in these cells. Finally, fully differentiated cells show lowered levels of cyclic AMP‐activated C1‐ transport, the characteristic function of CFTR. Thus, CFTR function in differentiated cells is modulated by a complex interaction of regulatory elements. 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subjects | Biological and medical sciences Blotting, Western Carrier Proteins - genetics Cell Differentiation cells Colon - cytology Colon - metabolism cystic fibrosis Cystic Fibrosis - metabolism Cystic Fibrosis Transmembrane Conductance Regulator differentiation Epithelial Cells Epithelium - metabolism expression function Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation intestine Iodine Radioisotopes - metabolism Membrane Proteins - genetics Microfilament Proteins - genetics Molecular and cellular biology Molecular genetics regulation RNA, Messenger - metabolism Transcription, Genetic transmembrane conductance regulator Tumor Cells, Cultured |
title | Regulation of CFTR expression and function during differentiation of intestinal epithelial cells |
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