Critical Function for SIP, a Ubiquitin E3 Ligase Component of the β-Catenin Degradation Pathway, for Thymocyte Development and G1 Checkpoint
β-catenin has been implicated in thymocyte development because of its function as a coactivator of Tcf/LEF-family transcription factors. Previously, we discovered a novel pathway for p53-induced β-catenin degradation through a ubiquitin E3 ligase complex involving Siah1, SIP (CacyBP), Skp1, and Ebi....
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2006, Vol.24 (1), p.29-39 |
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| creator | Fukushima, Toru Zapata, Juan M. Singha, Netai C. Thomas, Michael Kress, Christina L. Krajewska, Maryla Krajewski, Stan Ronai, Ze'ev Reed, John C. Matsuzawa, Shu-ichi |
| description | β-catenin has been implicated in thymocyte development because of its function as a coactivator of Tcf/LEF-family transcription factors. Previously, we discovered a novel pathway for p53-induced β-catenin degradation through a ubiquitin E3 ligase complex involving Siah1, SIP (CacyBP), Skp1, and Ebi. To gain insights into the physiological relevance of this new degradation pathway in vivo, we generated mutant mice lacking SIP. We demonstrate here that
SIP
−/− thymocytes have an impaired pre-TCR checkpoint with failure of
TCRβ gene rearrangement and increased apoptosis, resulting in reduced cellularity of the thymus. Moreover, the degradation of β-catenin in response to DNA damage is significantly impaired in
SIP
−/− cells.
SIP
−/− embryonic fibroblasts show a growth-rate increase resulting from defects in G1 arrest. Thus, the β-catenin degradation pathway mediated by SIP defines an essential checkpoint for thymocyte development and cell-cycle progression. |
| doi_str_mv | 10.1016/j.immuni.2005.12.002 |
| format | Article |
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SIP
−/− thymocytes have an impaired pre-TCR checkpoint with failure of
TCRβ gene rearrangement and increased apoptosis, resulting in reduced cellularity of the thymus. Moreover, the degradation of β-catenin in response to DNA damage is significantly impaired in
SIP
−/− cells.
SIP
−/− embryonic fibroblasts show a growth-rate increase resulting from defects in G1 arrest. Thus, the β-catenin degradation pathway mediated by SIP defines an essential checkpoint for thymocyte development and cell-cycle progression.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/j.immuni.2005.12.002</identifier><identifier>PMID: 16413921</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Apoptosis ; beta Catenin - metabolism ; Calcium-Binding Proteins - deficiency ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - physiology ; Cell Proliferation ; G1 Phase - genetics ; Gamma Rays ; Mice ; Mice, Mutant Strains ; Morphogenesis ; Organ Size ; Receptors, Antigen, T-Cell - metabolism ; Spleen - cytology ; Spleen - growth & development ; T-Lymphocytes - cytology ; T-Lymphocytes - enzymology ; Thymus Gland - cytology ; Thymus Gland - growth & development ; Thymus Gland - radiation effects ; Ubiquitin-Protein Ligases - genetics ; Ubiquitin-Protein Ligases - physiology ; Ultraviolet Rays</subject><ispartof>Immunity (Cambridge, Mass.), 2006, Vol.24 (1), p.29-39</ispartof><rights>2006 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-7178858cb4fc49f7836e3b4ca32d45ad5ee11b6eacfd870d0524378731b153583</citedby><cites>FETCH-LOGICAL-c437t-7178858cb4fc49f7836e3b4ca32d45ad5ee11b6eacfd870d0524378731b153583</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1074761305004103$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16413921$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fukushima, Toru</creatorcontrib><creatorcontrib>Zapata, Juan M.</creatorcontrib><creatorcontrib>Singha, Netai C.</creatorcontrib><creatorcontrib>Thomas, Michael</creatorcontrib><creatorcontrib>Kress, Christina L.</creatorcontrib><creatorcontrib>Krajewska, Maryla</creatorcontrib><creatorcontrib>Krajewski, Stan</creatorcontrib><creatorcontrib>Ronai, Ze'ev</creatorcontrib><creatorcontrib>Reed, John C.</creatorcontrib><creatorcontrib>Matsuzawa, Shu-ichi</creatorcontrib><title>Critical Function for SIP, a Ubiquitin E3 Ligase Component of the β-Catenin Degradation Pathway, for Thymocyte Development and G1 Checkpoint</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>β-catenin has been implicated in thymocyte development because of its function as a coactivator of Tcf/LEF-family transcription factors. Previously, we discovered a novel pathway for p53-induced β-catenin degradation through a ubiquitin E3 ligase complex involving Siah1, SIP (CacyBP), Skp1, and Ebi. To gain insights into the physiological relevance of this new degradation pathway in vivo, we generated mutant mice lacking SIP. We demonstrate here that
SIP
−/− thymocytes have an impaired pre-TCR checkpoint with failure of
TCRβ gene rearrangement and increased apoptosis, resulting in reduced cellularity of the thymus. Moreover, the degradation of β-catenin in response to DNA damage is significantly impaired in
SIP
−/− cells.
SIP
−/− embryonic fibroblasts show a growth-rate increase resulting from defects in G1 arrest. Thus, the β-catenin degradation pathway mediated by SIP defines an essential checkpoint for thymocyte development and cell-cycle progression.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>beta Catenin - metabolism</subject><subject>Calcium-Binding Proteins - deficiency</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - physiology</subject><subject>Cell Proliferation</subject><subject>G1 Phase - genetics</subject><subject>Gamma Rays</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Morphogenesis</subject><subject>Organ Size</subject><subject>Receptors, Antigen, T-Cell - metabolism</subject><subject>Spleen - cytology</subject><subject>Spleen - growth & development</subject><subject>T-Lymphocytes - cytology</subject><subject>T-Lymphocytes - enzymology</subject><subject>Thymus Gland - cytology</subject><subject>Thymus Gland - growth & development</subject><subject>Thymus Gland - radiation effects</subject><subject>Ubiquitin-Protein Ligases - genetics</subject><subject>Ubiquitin-Protein Ligases - physiology</subject><subject>Ultraviolet Rays</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhiMEoqXwBgj5xKkJntiJkwsSCm2ptBKVaM-W40y6XhJ7aztF-xC8DA_CM-HtrsQNTh7J3_-NNH-WvQVaAIX6w6Yw87xYU5SUVgWUBaXls-wUaCtyDg19vp8Fz0UN7CR7FcKGUuBVS19mJ1BzYG0Jp9nPzptotJrI5WJ1NM6S0Xny7frmnChy15uHJf1bcsHIytyrgKRz89ZZtJG4kcQ1kt-_8k5FtIn6jPdeDepJc6Pi-ofanT_5bte72eldxIQ84uS2816g7ECugHRr1N-3ztj4Onsxqingm-N7lt1dXtx2X_LV16vr7tMq15yJmAsQTVM1uuej5u0oGlYj67lWrBx4pYYKEaCvUelxaAQdaFWmXCMY9FCxqmFn2fuDd-vdw4IhytkEjdOkLLolSEHrpk3X-y8IoiwrVrYJ5AdQexeCx1FuvZmV30mgct-X3MhDX3Lfl4RSpr5S7N3Rv_QzDn9Dx4IS8PEAYDrHo0EvgzZoNQ7Go45ycObfG_4ALdypEw</recordid><startdate>2006</startdate><enddate>2006</enddate><creator>Fukushima, Toru</creator><creator>Zapata, Juan M.</creator><creator>Singha, Netai C.</creator><creator>Thomas, Michael</creator><creator>Kress, Christina L.</creator><creator>Krajewska, Maryla</creator><creator>Krajewski, Stan</creator><creator>Ronai, Ze'ev</creator><creator>Reed, John C.</creator><creator>Matsuzawa, Shu-ichi</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>2006</creationdate><title>Critical Function for SIP, a Ubiquitin E3 Ligase Component of the β-Catenin Degradation Pathway, for Thymocyte Development and G1 Checkpoint</title><author>Fukushima, Toru ; Zapata, Juan M. ; Singha, Netai C. ; Thomas, Michael ; Kress, Christina L. ; Krajewska, Maryla ; Krajewski, Stan ; Ronai, Ze'ev ; Reed, John C. ; Matsuzawa, Shu-ichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-7178858cb4fc49f7836e3b4ca32d45ad5ee11b6eacfd870d0524378731b153583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>beta Catenin - metabolism</topic><topic>Calcium-Binding Proteins - deficiency</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - physiology</topic><topic>Cell Proliferation</topic><topic>G1 Phase - genetics</topic><topic>Gamma Rays</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Morphogenesis</topic><topic>Organ Size</topic><topic>Receptors, Antigen, T-Cell - metabolism</topic><topic>Spleen - cytology</topic><topic>Spleen - growth & development</topic><topic>T-Lymphocytes - cytology</topic><topic>T-Lymphocytes - enzymology</topic><topic>Thymus Gland - cytology</topic><topic>Thymus Gland - growth & development</topic><topic>Thymus Gland - radiation effects</topic><topic>Ubiquitin-Protein Ligases - genetics</topic><topic>Ubiquitin-Protein Ligases - physiology</topic><topic>Ultraviolet Rays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fukushima, Toru</creatorcontrib><creatorcontrib>Zapata, Juan M.</creatorcontrib><creatorcontrib>Singha, Netai C.</creatorcontrib><creatorcontrib>Thomas, Michael</creatorcontrib><creatorcontrib>Kress, Christina L.</creatorcontrib><creatorcontrib>Krajewska, Maryla</creatorcontrib><creatorcontrib>Krajewski, Stan</creatorcontrib><creatorcontrib>Ronai, Ze'ev</creatorcontrib><creatorcontrib>Reed, John C.</creatorcontrib><creatorcontrib>Matsuzawa, Shu-ichi</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fukushima, Toru</au><au>Zapata, Juan M.</au><au>Singha, Netai C.</au><au>Thomas, Michael</au><au>Kress, Christina L.</au><au>Krajewska, Maryla</au><au>Krajewski, Stan</au><au>Ronai, Ze'ev</au><au>Reed, John C.</au><au>Matsuzawa, Shu-ichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Critical Function for SIP, a Ubiquitin E3 Ligase Component of the β-Catenin Degradation Pathway, for Thymocyte Development and G1 Checkpoint</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><addtitle>Immunity</addtitle><date>2006</date><risdate>2006</risdate><volume>24</volume><issue>1</issue><spage>29</spage><epage>39</epage><pages>29-39</pages><issn>1074-7613</issn><eissn>1097-4180</eissn><abstract>β-catenin has been implicated in thymocyte development because of its function as a coactivator of Tcf/LEF-family transcription factors. 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SIP
−/− thymocytes have an impaired pre-TCR checkpoint with failure of
TCRβ gene rearrangement and increased apoptosis, resulting in reduced cellularity of the thymus. Moreover, the degradation of β-catenin in response to DNA damage is significantly impaired in
SIP
−/− cells.
SIP
−/− embryonic fibroblasts show a growth-rate increase resulting from defects in G1 arrest. Thus, the β-catenin degradation pathway mediated by SIP defines an essential checkpoint for thymocyte development and cell-cycle progression.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16413921</pmid><doi>10.1016/j.immuni.2005.12.002</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Immunity (Cambridge, Mass.), 2006, Vol.24 (1), p.29-39 |
| issn | 1074-7613 1097-4180 |
| language | eng |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Apoptosis beta Catenin - metabolism Calcium-Binding Proteins - deficiency Calcium-Binding Proteins - genetics Calcium-Binding Proteins - physiology Cell Proliferation G1 Phase - genetics Gamma Rays Mice Mice, Mutant Strains Morphogenesis Organ Size Receptors, Antigen, T-Cell - metabolism Spleen - cytology Spleen - growth & development T-Lymphocytes - cytology T-Lymphocytes - enzymology Thymus Gland - cytology Thymus Gland - growth & development Thymus Gland - radiation effects Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - physiology Ultraviolet Rays |
| title | Critical Function for SIP, a Ubiquitin E3 Ligase Component of the β-Catenin Degradation Pathway, for Thymocyte Development and G1 Checkpoint |
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