Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis
Glucocorticoid-induced tumor necrosis factor receptor (GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes,...
Gespeichert in:
| Veröffentlicht in: | The Journal of biological chemistry 2005-11, Vol.280 (45), p.37725-37731 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 37731 |
|---|---|
| container_issue | 45 |
| container_start_page | 37725 |
| container_title | The Journal of biological chemistry |
| container_volume | 280 |
| creator | Wang, Jian Devgan, Vikram Corrado, Marcella Prabhu, Nita S. El-Deiry, Wafik S. Riccardi, Carlo Pandolfi, Pier Paolo Missero, Caterina Dotto, G. Paolo |
| description | Glucocorticoid-induced tumor necrosis factor receptor (GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes, and that it is under negative transcriptional control of p21Cip1/WAF1, independently from the cell cycle. Although GITR expression is higher in p21-deficient keratinocytes and skin, it is down-modulated with differentiation and in response to UVB. The combined analysis of keratinocytes with increased GITR expression versus normal keratinocytes and skin of mice with a disruption of the GITR gene indicates that this protein protects keratinocytes from UVB-induced apoptosis both in vitro and in vivo. |
| doi_str_mv | 10.1074/jbc.M507976200 |
| format | Article |
| fullrecord | <record><control><sourceid>elsevier_pubme</sourceid><recordid>TN_cdi_pubmed_primary_16155000</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0021925820592326</els_id><sourcerecordid>S0021925820592326</sourcerecordid><originalsourceid>FETCH-LOGICAL-e1320-e7b38585abe1e566e64fe63d8927fd429ac12a5b72a07d006973c87116f327273</originalsourceid><addsrcrecordid>eNpFUU1vEzEQtRAVDS1XjsgHrtt67PV69xhFpFSkRULpx83y2rOJq2S9sh1Qfw9_FFcBOpeZkd6beTOPkI_ALoCp-vKptxc3kqlONZyxN2QGrBWVkPD4lswY41B1XLan5H1KT6xE3cE7cgoNSFm6Gfl9tTvYYEPM3gbvKj-6g0VH14d9iPQWbQzJJ7o0Npf-B1qcXorrRA2dOCz8BJcP8yXQdTRjstFP2YfR7OjaxA1mugjjgDH6cVPIZVI2o0UaBvoNo8l-DPY5Y6I50Lt7uvKbbf4vYT6FsqtwzsnJYHYJP_zNZ-Ru-WW9-Fqtvl9dL-arCkFwVqHqRStbaXoElE2DTT1gI1zbcTW4mnfGAjeyV9ww5RhrOiVsqwCaQXDFlTgjn45zp0O_R6en6PcmPut_3yqAz0fAtgj95SPq3ge7xb3mLdO11EIpLgusPcKwiP3pMepkPZa7XaHYrF3wGph-8U8X__Srf-IPGn2MgA</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Wang, Jian ; Devgan, Vikram ; Corrado, Marcella ; Prabhu, Nita S. ; El-Deiry, Wafik S. ; Riccardi, Carlo ; Pandolfi, Pier Paolo ; Missero, Caterina ; Dotto, G. Paolo</creator><creatorcontrib>Wang, Jian ; Devgan, Vikram ; Corrado, Marcella ; Prabhu, Nita S. ; El-Deiry, Wafik S. ; Riccardi, Carlo ; Pandolfi, Pier Paolo ; Missero, Caterina ; Dotto, G. Paolo</creatorcontrib><description>Glucocorticoid-induced tumor necrosis factor receptor (GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes, and that it is under negative transcriptional control of p21Cip1/WAF1, independently from the cell cycle. Although GITR expression is higher in p21-deficient keratinocytes and skin, it is down-modulated with differentiation and in response to UVB. The combined analysis of keratinocytes with increased GITR expression versus normal keratinocytes and skin of mice with a disruption of the GITR gene indicates that this protein protects keratinocytes from UVB-induced apoptosis both in vitro and in vivo.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M507976200</identifier><identifier>PMID: 16155000</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis - radiation effects ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p21 - genetics ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Epidermal Cells ; Epidermis - metabolism ; Epidermis - radiation effects ; Female ; Gene Deletion ; Glucocorticoid-Induced TNFR-Related Protein ; Glucocorticoids - pharmacology ; Keratinocytes - cytology ; Keratinocytes - radiation effects ; Mice ; Receptors, Nerve Growth Factor - metabolism ; Receptors, Tumor Necrosis Factor - metabolism ; Transcription, Genetic ; Ultraviolet Rays</subject><ispartof>The Journal of biological chemistry, 2005-11, Vol.280 (45), p.37725-37731</ispartof><rights>2005 © 2005 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16155000$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Devgan, Vikram</creatorcontrib><creatorcontrib>Corrado, Marcella</creatorcontrib><creatorcontrib>Prabhu, Nita S.</creatorcontrib><creatorcontrib>El-Deiry, Wafik S.</creatorcontrib><creatorcontrib>Riccardi, Carlo</creatorcontrib><creatorcontrib>Pandolfi, Pier Paolo</creatorcontrib><creatorcontrib>Missero, Caterina</creatorcontrib><creatorcontrib>Dotto, G. Paolo</creatorcontrib><title>Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Glucocorticoid-induced tumor necrosis factor receptor (GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes, and that it is under negative transcriptional control of p21Cip1/WAF1, independently from the cell cycle. Although GITR expression is higher in p21-deficient keratinocytes and skin, it is down-modulated with differentiation and in response to UVB. The combined analysis of keratinocytes with increased GITR expression versus normal keratinocytes and skin of mice with a disruption of the GITR gene indicates that this protein protects keratinocytes from UVB-induced apoptosis both in vitro and in vivo.</description><subject>Animals</subject><subject>Apoptosis - radiation effects</subject><subject>Cells, Cultured</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - genetics</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</subject><subject>Epidermal Cells</subject><subject>Epidermis - metabolism</subject><subject>Epidermis - radiation effects</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Glucocorticoid-Induced TNFR-Related Protein</subject><subject>Glucocorticoids - pharmacology</subject><subject>Keratinocytes - cytology</subject><subject>Keratinocytes - radiation effects</subject><subject>Mice</subject><subject>Receptors, Nerve Growth Factor - metabolism</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Transcription, Genetic</subject><subject>Ultraviolet Rays</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUU1vEzEQtRAVDS1XjsgHrtt67PV69xhFpFSkRULpx83y2rOJq2S9sh1Qfw9_FFcBOpeZkd6beTOPkI_ALoCp-vKptxc3kqlONZyxN2QGrBWVkPD4lswY41B1XLan5H1KT6xE3cE7cgoNSFm6Gfl9tTvYYEPM3gbvKj-6g0VH14d9iPQWbQzJJ7o0Npf-B1qcXorrRA2dOCz8BJcP8yXQdTRjstFP2YfR7OjaxA1mugjjgDH6cVPIZVI2o0UaBvoNo8l-DPY5Y6I50Lt7uvKbbf4vYT6FsqtwzsnJYHYJP_zNZ-Ru-WW9-Fqtvl9dL-arCkFwVqHqRStbaXoElE2DTT1gI1zbcTW4mnfGAjeyV9ww5RhrOiVsqwCaQXDFlTgjn45zp0O_R6en6PcmPut_3yqAz0fAtgj95SPq3ge7xb3mLdO11EIpLgusPcKwiP3pMepkPZa7XaHYrF3wGph-8U8X__Srf-IPGn2MgA</recordid><startdate>20051111</startdate><enddate>20051111</enddate><creator>Wang, Jian</creator><creator>Devgan, Vikram</creator><creator>Corrado, Marcella</creator><creator>Prabhu, Nita S.</creator><creator>El-Deiry, Wafik S.</creator><creator>Riccardi, Carlo</creator><creator>Pandolfi, Pier Paolo</creator><creator>Missero, Caterina</creator><creator>Dotto, G. Paolo</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</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></search><sort><creationdate>20051111</creationdate><title>Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis</title><author>Wang, Jian ; Devgan, Vikram ; Corrado, Marcella ; Prabhu, Nita S. ; El-Deiry, Wafik S. ; Riccardi, Carlo ; Pandolfi, Pier Paolo ; Missero, Caterina ; Dotto, G. Paolo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e1320-e7b38585abe1e566e64fe63d8927fd429ac12a5b72a07d006973c87116f327273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis - radiation effects</topic><topic>Cells, Cultured</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - genetics</topic><topic>Cyclin-Dependent Kinase Inhibitor p21 - metabolism</topic><topic>Epidermal Cells</topic><topic>Epidermis - metabolism</topic><topic>Epidermis - radiation effects</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Glucocorticoid-Induced TNFR-Related Protein</topic><topic>Glucocorticoids - pharmacology</topic><topic>Keratinocytes - cytology</topic><topic>Keratinocytes - radiation effects</topic><topic>Mice</topic><topic>Receptors, Nerve Growth Factor - metabolism</topic><topic>Receptors, Tumor Necrosis Factor - metabolism</topic><topic>Transcription, Genetic</topic><topic>Ultraviolet Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Devgan, Vikram</creatorcontrib><creatorcontrib>Corrado, Marcella</creatorcontrib><creatorcontrib>Prabhu, Nita S.</creatorcontrib><creatorcontrib>El-Deiry, Wafik S.</creatorcontrib><creatorcontrib>Riccardi, Carlo</creatorcontrib><creatorcontrib>Pandolfi, Pier Paolo</creatorcontrib><creatorcontrib>Missero, Caterina</creatorcontrib><creatorcontrib>Dotto, G. Paolo</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><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Jian</au><au>Devgan, Vikram</au><au>Corrado, Marcella</au><au>Prabhu, Nita S.</au><au>El-Deiry, Wafik S.</au><au>Riccardi, Carlo</au><au>Pandolfi, Pier Paolo</au><au>Missero, Caterina</au><au>Dotto, G. Paolo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2005-11-11</date><risdate>2005</risdate><volume>280</volume><issue>45</issue><spage>37725</spage><epage>37731</epage><pages>37725-37731</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Glucocorticoid-induced tumor necrosis factor receptor (GITR) is a member of the tumor necrosis factor receptor superfamily, is expressed in T lymphocytes, and exerts an anti-apoptotic function in these cells. We reported that GITR is also highly expressed in the skin, specifically in keratinocytes, and that it is under negative transcriptional control of p21Cip1/WAF1, independently from the cell cycle. Although GITR expression is higher in p21-deficient keratinocytes and skin, it is down-modulated with differentiation and in response to UVB. The combined analysis of keratinocytes with increased GITR expression versus normal keratinocytes and skin of mice with a disruption of the GITR gene indicates that this protein protects keratinocytes from UVB-induced apoptosis both in vitro and in vivo.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16155000</pmid><doi>10.1074/jbc.M507976200</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9258 |
| ispartof | The Journal of biological chemistry, 2005-11, Vol.280 (45), p.37725-37731 |
| issn | 0021-9258 1083-351X |
| language | eng |
| recordid | cdi_pubmed_primary_16155000 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Apoptosis - radiation effects Cells, Cultured Cyclin-Dependent Kinase Inhibitor p21 - genetics Cyclin-Dependent Kinase Inhibitor p21 - metabolism Epidermal Cells Epidermis - metabolism Epidermis - radiation effects Female Gene Deletion Glucocorticoid-Induced TNFR-Related Protein Glucocorticoids - pharmacology Keratinocytes - cytology Keratinocytes - radiation effects Mice Receptors, Nerve Growth Factor - metabolism Receptors, Tumor Necrosis Factor - metabolism Transcription, Genetic Ultraviolet Rays |
| title | Glucocorticoid-induced Tumor Necrosis Factor Receptor Is a p21Cip1/WAF1 Transcriptional Target Conferring Resistance of Keratinocytes to UV Light-induced Apoptosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-12T15%3A45%3A49IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-elsevier_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Glucocorticoid-induced%20Tumor%20Necrosis%20Factor%20Receptor%20Is%20a%20p21Cip1/WAF1%20Transcriptional%20Target%20Conferring%20Resistance%20of%20Keratinocytes%20to%20UV%20Light-induced%20Apoptosis&rft.jtitle=The%20Journal%20of%20biological%20chemistry&rft.au=Wang,%20Jian&rft.date=2005-11-11&rft.volume=280&rft.issue=45&rft.spage=37725&rft.epage=37731&rft.pages=37725-37731&rft.issn=0021-9258&rft.eissn=1083-351X&rft_id=info:doi/10.1074/jbc.M507976200&rft_dat=%3Celsevier_pubme%3ES0021925820592326%3C/elsevier_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/16155000&rft_els_id=S0021925820592326&rfr_iscdi=true |