c-Jun Regulates Eyelid Closure and Skin Tumor Development through EGFR Signaling
To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated c-jun in the epidermis. Mice lacking c-jun in keratinocytes ( c-jun Δep) develop normal skin but express reduced levels of EGFR in the eyelids, leading to open eyes at birth, as observ...
Gespeichert in:
| Veröffentlicht in: | Developmental cell 2003-06, Vol.4 (6), p.879-889 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 889 |
|---|---|
| container_issue | 6 |
| container_start_page | 879 |
| container_title | Developmental cell |
| container_volume | 4 |
| creator | Zenz, Rainer Scheuch, Harald Martin, Paul Frank, Carsten Eferl, Robert Kenner, Lukas Sibilia, Maria Wagner, Erwin F |
| description | To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated
c-jun in the epidermis. Mice lacking
c-jun in keratinocytes (
c-jun
Δep) develop normal skin but express reduced levels of EGFR in the eyelids, leading to open eyes at birth, as observed in EGFR null mice. Primary keratinocytes from
c-jun
Δep mice proliferate poorly, show increased differentiation, and form prominent cortical actin bundles, most likely because of decreased expression of EGFR and its ligand HB-EGF. In the absence of c-Jun, tumor-prone K5-SOS-F transgenic mice develop smaller papillomas, with reduced expression of EGFR in basal keratinocytes. Thus, using three experimental systems, we show that EGFR and HB-EGF are regulated by c-Jun, which controls eyelid development, keratinocyte proliferation, and skin tumor formation. |
| doi_str_mv | 10.1016/S1534-5807(03)00161-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_18767477</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1534580703001618</els_id><sourcerecordid>18767477</sourcerecordid><originalsourceid>FETCH-LOGICAL-c491t-415aab5fe8618575176ca094b3a88aa6bb082142fa09528ba91be1686d3868d03</originalsourceid><addsrcrecordid>eNqFkEtPwzAMgCMEYmPwE0A5ITgUkrZp0xNCYxugSaBtnKO0dbtAHyNpJu3fkz0QRw6WLeuznXwIXVJyRwmN7ueUBaHHOIlvSHBLXIt6_Aj1KY-5Rxmjx67-RXrozJjPHcTJKepRP05c-H30nnmvtsEzKG0lOzB4tIFK5XhYtcZqwLLJ8fxLNXhh61bjJ1hD1a5qaDrcLXVryyUeTcYzPFdlIyvVlOfopJCVgYtDHqCP8WgxfPamb5OX4ePUy8KEdl5ImZQpK4C7J7GY0TjKJEnCNJCcSxmlKeE-Df3CNZnPU5nQFGjEozzgEc9JMEDX-70r3X5bMJ2olcmgqmQDrTXCeYjiMI4dyPZgpltjNBRipVUt9UZQIrYqxU6l2HoSJBA7S4K7uavDAZvWkP9NHdw54GEPgPvmWoEWJlPQZJArDVkn8lb9c-IHwY6B0Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18767477</pqid></control><display><type>article</type><title>c-Jun Regulates Eyelid Closure and Skin Tumor Development through EGFR Signaling</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><source>Cell Press Free Archives</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Zenz, Rainer ; Scheuch, Harald ; Martin, Paul ; Frank, Carsten ; Eferl, Robert ; Kenner, Lukas ; Sibilia, Maria ; Wagner, Erwin F</creator><creatorcontrib>Zenz, Rainer ; Scheuch, Harald ; Martin, Paul ; Frank, Carsten ; Eferl, Robert ; Kenner, Lukas ; Sibilia, Maria ; Wagner, Erwin F</creatorcontrib><description>To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated
c-jun in the epidermis. Mice lacking
c-jun in keratinocytes (
c-jun
Δep) develop normal skin but express reduced levels of EGFR in the eyelids, leading to open eyes at birth, as observed in EGFR null mice. Primary keratinocytes from
c-jun
Δep mice proliferate poorly, show increased differentiation, and form prominent cortical actin bundles, most likely because of decreased expression of EGFR and its ligand HB-EGF. In the absence of c-Jun, tumor-prone K5-SOS-F transgenic mice develop smaller papillomas, with reduced expression of EGFR in basal keratinocytes. Thus, using three experimental systems, we show that EGFR and HB-EGF are regulated by c-Jun, which controls eyelid development, keratinocyte proliferation, and skin tumor formation.</description><identifier>ISSN: 1534-5807</identifier><identifier>EISSN: 1878-1551</identifier><identifier>DOI: 10.1016/S1534-5807(03)00161-8</identifier><identifier>PMID: 12791272</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis - genetics ; Carcinogens - pharmacology ; Cell Division ; Epidermal Growth Factor - genetics ; Epidermal Growth Factor - metabolism ; Epidermis - cytology ; Epidermis - injuries ; Eyelids - abnormalities ; Eyelids - embryology ; Eyelids - metabolism ; Eyelids - ultrastructure ; Gene Expression Regulation, Developmental ; Gene Expression Regulation, Neoplastic ; Genes, jun ; Genetic Predisposition to Disease ; Heparin-binding EGF-like Growth Factor ; Intercellular Signaling Peptides and Proteins ; Mice ; Mice, Transgenic ; Models, Biological ; Papilloma - etiology ; Papilloma - metabolism ; Papilloma - pathology ; Receptor, Epidermal Growth Factor - genetics ; Receptor, Epidermal Growth Factor - metabolism ; Signal Transduction ; Skin Neoplasms - etiology ; Skin Neoplasms - metabolism ; Skin Neoplasms - pathology ; Tetradecanoylphorbol Acetate - pharmacology ; Transgenes</subject><ispartof>Developmental cell, 2003-06, Vol.4 (6), p.879-889</ispartof><rights>2003 Cell Press</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c491t-415aab5fe8618575176ca094b3a88aa6bb082142fa09528ba91be1686d3868d03</citedby><cites>FETCH-LOGICAL-c491t-415aab5fe8618575176ca094b3a88aa6bb082142fa09528ba91be1686d3868d03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S1534-5807(03)00161-8$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12791272$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zenz, Rainer</creatorcontrib><creatorcontrib>Scheuch, Harald</creatorcontrib><creatorcontrib>Martin, Paul</creatorcontrib><creatorcontrib>Frank, Carsten</creatorcontrib><creatorcontrib>Eferl, Robert</creatorcontrib><creatorcontrib>Kenner, Lukas</creatorcontrib><creatorcontrib>Sibilia, Maria</creatorcontrib><creatorcontrib>Wagner, Erwin F</creatorcontrib><title>c-Jun Regulates Eyelid Closure and Skin Tumor Development through EGFR Signaling</title><title>Developmental cell</title><addtitle>Dev Cell</addtitle><description>To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated
c-jun in the epidermis. Mice lacking
c-jun in keratinocytes (
c-jun
Δep) develop normal skin but express reduced levels of EGFR in the eyelids, leading to open eyes at birth, as observed in EGFR null mice. Primary keratinocytes from
c-jun
Δep mice proliferate poorly, show increased differentiation, and form prominent cortical actin bundles, most likely because of decreased expression of EGFR and its ligand HB-EGF. In the absence of c-Jun, tumor-prone K5-SOS-F transgenic mice develop smaller papillomas, with reduced expression of EGFR in basal keratinocytes. Thus, using three experimental systems, we show that EGFR and HB-EGF are regulated by c-Jun, which controls eyelid development, keratinocyte proliferation, and skin tumor formation.</description><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Carcinogens - pharmacology</subject><subject>Cell Division</subject><subject>Epidermal Growth Factor - genetics</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Epidermis - cytology</subject><subject>Epidermis - injuries</subject><subject>Eyelids - abnormalities</subject><subject>Eyelids - embryology</subject><subject>Eyelids - metabolism</subject><subject>Eyelids - ultrastructure</subject><subject>Gene Expression Regulation, Developmental</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, jun</subject><subject>Genetic Predisposition to Disease</subject><subject>Heparin-binding EGF-like Growth Factor</subject><subject>Intercellular Signaling Peptides and Proteins</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Models, Biological</subject><subject>Papilloma - etiology</subject><subject>Papilloma - metabolism</subject><subject>Papilloma - pathology</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Signal Transduction</subject><subject>Skin Neoplasms - etiology</subject><subject>Skin Neoplasms - metabolism</subject><subject>Skin Neoplasms - pathology</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Transgenes</subject><issn>1534-5807</issn><issn>1878-1551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtPwzAMgCMEYmPwE0A5ITgUkrZp0xNCYxugSaBtnKO0dbtAHyNpJu3fkz0QRw6WLeuznXwIXVJyRwmN7ueUBaHHOIlvSHBLXIt6_Aj1KY-5Rxmjx67-RXrozJjPHcTJKepRP05c-H30nnmvtsEzKG0lOzB4tIFK5XhYtcZqwLLJ8fxLNXhh61bjJ1hD1a5qaDrcLXVryyUeTcYzPFdlIyvVlOfopJCVgYtDHqCP8WgxfPamb5OX4ePUy8KEdl5ImZQpK4C7J7GY0TjKJEnCNJCcSxmlKeE-Df3CNZnPU5nQFGjEozzgEc9JMEDX-70r3X5bMJ2olcmgqmQDrTXCeYjiMI4dyPZgpltjNBRipVUt9UZQIrYqxU6l2HoSJBA7S4K7uavDAZvWkP9NHdw54GEPgPvmWoEWJlPQZJArDVkn8lb9c-IHwY6B0Q</recordid><startdate>20030601</startdate><enddate>20030601</enddate><creator>Zenz, Rainer</creator><creator>Scheuch, Harald</creator><creator>Martin, Paul</creator><creator>Frank, Carsten</creator><creator>Eferl, Robert</creator><creator>Kenner, Lukas</creator><creator>Sibilia, Maria</creator><creator>Wagner, Erwin F</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>P64</scope><scope>RC3</scope></search><sort><creationdate>20030601</creationdate><title>c-Jun Regulates Eyelid Closure and Skin Tumor Development through EGFR Signaling</title><author>Zenz, Rainer ; Scheuch, Harald ; Martin, Paul ; Frank, Carsten ; Eferl, Robert ; Kenner, Lukas ; Sibilia, Maria ; Wagner, Erwin F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c491t-415aab5fe8618575176ca094b3a88aa6bb082142fa09528ba91be1686d3868d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Carcinogens - pharmacology</topic><topic>Cell Division</topic><topic>Epidermal Growth Factor - genetics</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Epidermis - cytology</topic><topic>Epidermis - injuries</topic><topic>Eyelids - abnormalities</topic><topic>Eyelids - embryology</topic><topic>Eyelids - metabolism</topic><topic>Eyelids - ultrastructure</topic><topic>Gene Expression Regulation, Developmental</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, jun</topic><topic>Genetic Predisposition to Disease</topic><topic>Heparin-binding EGF-like Growth Factor</topic><topic>Intercellular Signaling Peptides and Proteins</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Models, Biological</topic><topic>Papilloma - etiology</topic><topic>Papilloma - metabolism</topic><topic>Papilloma - pathology</topic><topic>Receptor, Epidermal Growth Factor - genetics</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>Signal Transduction</topic><topic>Skin Neoplasms - etiology</topic><topic>Skin Neoplasms - metabolism</topic><topic>Skin Neoplasms - pathology</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Transgenes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zenz, Rainer</creatorcontrib><creatorcontrib>Scheuch, Harald</creatorcontrib><creatorcontrib>Martin, Paul</creatorcontrib><creatorcontrib>Frank, Carsten</creatorcontrib><creatorcontrib>Eferl, Robert</creatorcontrib><creatorcontrib>Kenner, Lukas</creatorcontrib><creatorcontrib>Sibilia, Maria</creatorcontrib><creatorcontrib>Wagner, Erwin F</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Developmental cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zenz, Rainer</au><au>Scheuch, Harald</au><au>Martin, Paul</au><au>Frank, Carsten</au><au>Eferl, Robert</au><au>Kenner, Lukas</au><au>Sibilia, Maria</au><au>Wagner, Erwin F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c-Jun Regulates Eyelid Closure and Skin Tumor Development through EGFR Signaling</atitle><jtitle>Developmental cell</jtitle><addtitle>Dev Cell</addtitle><date>2003-06-01</date><risdate>2003</risdate><volume>4</volume><issue>6</issue><spage>879</spage><epage>889</epage><pages>879-889</pages><issn>1534-5807</issn><eissn>1878-1551</eissn><abstract>To investigate the function of c-Jun during skin development and skin tumor formation, we conditionally inactivated
c-jun in the epidermis. Mice lacking
c-jun in keratinocytes (
c-jun
Δep) develop normal skin but express reduced levels of EGFR in the eyelids, leading to open eyes at birth, as observed in EGFR null mice. Primary keratinocytes from
c-jun
Δep mice proliferate poorly, show increased differentiation, and form prominent cortical actin bundles, most likely because of decreased expression of EGFR and its ligand HB-EGF. In the absence of c-Jun, tumor-prone K5-SOS-F transgenic mice develop smaller papillomas, with reduced expression of EGFR in basal keratinocytes. Thus, using three experimental systems, we show that EGFR and HB-EGF are regulated by c-Jun, which controls eyelid development, keratinocyte proliferation, and skin tumor formation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12791272</pmid><doi>10.1016/S1534-5807(03)00161-8</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1534-5807 |
| ispartof | Developmental cell, 2003-06, Vol.4 (6), p.879-889 |
| issn | 1534-5807 1878-1551 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_18767477 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete; Cell Press Free Archives; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Apoptosis - genetics Carcinogens - pharmacology Cell Division Epidermal Growth Factor - genetics Epidermal Growth Factor - metabolism Epidermis - cytology Epidermis - injuries Eyelids - abnormalities Eyelids - embryology Eyelids - metabolism Eyelids - ultrastructure Gene Expression Regulation, Developmental Gene Expression Regulation, Neoplastic Genes, jun Genetic Predisposition to Disease Heparin-binding EGF-like Growth Factor Intercellular Signaling Peptides and Proteins Mice Mice, Transgenic Models, Biological Papilloma - etiology Papilloma - metabolism Papilloma - pathology Receptor, Epidermal Growth Factor - genetics Receptor, Epidermal Growth Factor - metabolism Signal Transduction Skin Neoplasms - etiology Skin Neoplasms - metabolism Skin Neoplasms - pathology Tetradecanoylphorbol Acetate - pharmacology Transgenes |
| title | c-Jun Regulates Eyelid Closure and Skin Tumor Development through EGFR Signaling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-05T12%3A03%3A07IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=c-Jun%20Regulates%20Eyelid%20Closure%20and%20Skin%20Tumor%20Development%20through%20EGFR%20Signaling&rft.jtitle=Developmental%20cell&rft.au=Zenz,%20Rainer&rft.date=2003-06-01&rft.volume=4&rft.issue=6&rft.spage=879&rft.epage=889&rft.pages=879-889&rft.issn=1534-5807&rft.eissn=1878-1551&rft_id=info:doi/10.1016/S1534-5807(03)00161-8&rft_dat=%3Cproquest_cross%3E18767477%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=18767477&rft_id=info:pmid/12791272&rft_els_id=S1534580703001618&rfr_iscdi=true |