Smad-mediated transcription is required for transforming growth factor-beta 1-induced p57(Kip2) proteolysis in osteoblastic cells
Cyclin-dependent kinase inhibitory proteins (CKIs) are negative regulators of the cell cycle. Of all CKIs, only p57(Kip2) plays an essential role(s) that other CKIs cannot compensate for in embryonic development. Recently, we found that p57(Kip2) is degraded through the ubiquitin-proteasome pathway...
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Veröffentlicht in: | The Journal of biological chemistry 2001-04, Vol.276 (14), p.10700-10705 |
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creator | Nishimori, S Tanaka, Y Chiba, T Fujii, M Imamura, T Miyazono, K Ogasawara, T Kawaguchi, H Igarashi, T Fujita, T Tanaka, K Toyoshima, H |
description | Cyclin-dependent kinase inhibitory proteins (CKIs) are negative regulators of the cell cycle. Of all CKIs, only p57(Kip2) plays an essential role(s) that other CKIs cannot compensate for in embryonic development. Recently, we found that p57(Kip2) is degraded through the ubiquitin-proteasome pathway in osteoblastic cells stimulated to proliferation by transforming growth factor (TGF)-beta1 (Urano, T., Yashiroda, H., Muraoka, M., Tanaka, K., Hosoi, T., Inoue, S., Ouchi, Y., and Toyoshima, H. (1999) J. Biol. Chem. 274, 12197-12200). We report here that TGF-beta1-induced p57(Kip2) proteolysis is mediated through transcription by the Smad pathway. When the constitutively active form of the TGF-beta type I receptor ALK-5(TD) was ectopically expressed in osteoblastic cells, p57(Kip2) that had been accumulated by serum starvation causing the cell-cycle arrest was rapidly degraded in a manner analogous to TGF-beta1 stimulation. Moreover, Smad2 or Smad3 with Smad4 enhanced the proteolytic pathway of p57(Kip2). The degradation of p57(Kip2) evoked by TGF-beta1 was blocked by forced expression of an inhibitory Smad called Smad7 or by the addition of actinomycin D or alpha-amanitin. These results indicate that accelerated degradation of p57(Kip2) by TGF-beta1/Smad signaling is mediated through a newly synthesized factor(s) that modifies p57(Kip2) or the ubiquitin-proteasome pathway. |
doi_str_mv | 10.1074/jbc.M007499200 |
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Of all CKIs, only p57(Kip2) plays an essential role(s) that other CKIs cannot compensate for in embryonic development. Recently, we found that p57(Kip2) is degraded through the ubiquitin-proteasome pathway in osteoblastic cells stimulated to proliferation by transforming growth factor (TGF)-beta1 (Urano, T., Yashiroda, H., Muraoka, M., Tanaka, K., Hosoi, T., Inoue, S., Ouchi, Y., and Toyoshima, H. (1999) J. Biol. Chem. 274, 12197-12200). We report here that TGF-beta1-induced p57(Kip2) proteolysis is mediated through transcription by the Smad pathway. When the constitutively active form of the TGF-beta type I receptor ALK-5(TD) was ectopically expressed in osteoblastic cells, p57(Kip2) that had been accumulated by serum starvation causing the cell-cycle arrest was rapidly degraded in a manner analogous to TGF-beta1 stimulation. Moreover, Smad2 or Smad3 with Smad4 enhanced the proteolytic pathway of p57(Kip2). The degradation of p57(Kip2) evoked by TGF-beta1 was blocked by forced expression of an inhibitory Smad called Smad7 or by the addition of actinomycin D or alpha-amanitin. These results indicate that accelerated degradation of p57(Kip2) by TGF-beta1/Smad signaling is mediated through a newly synthesized factor(s) that modifies p57(Kip2) or the ubiquitin-proteasome pathway.</description><identifier>ISSN: 0021-9258</identifier><identifier>DOI: 10.1074/jbc.M007499200</identifier><identifier>PMID: 11152674</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p57 ; Cyclin-Dependent Kinases - metabolism ; Mice ; Nuclear Proteins - metabolism ; Osteoblasts - metabolism ; Signal Transduction - drug effects ; Transforming Growth Factor beta - metabolism ; Transforming Growth Factor beta - pharmacology</subject><ispartof>The Journal of biological chemistry, 2001-04, Vol.276 (14), p.10700-10705</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11152674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishimori, S</creatorcontrib><creatorcontrib>Tanaka, Y</creatorcontrib><creatorcontrib>Chiba, T</creatorcontrib><creatorcontrib>Fujii, M</creatorcontrib><creatorcontrib>Imamura, T</creatorcontrib><creatorcontrib>Miyazono, K</creatorcontrib><creatorcontrib>Ogasawara, T</creatorcontrib><creatorcontrib>Kawaguchi, H</creatorcontrib><creatorcontrib>Igarashi, T</creatorcontrib><creatorcontrib>Fujita, T</creatorcontrib><creatorcontrib>Tanaka, K</creatorcontrib><creatorcontrib>Toyoshima, H</creatorcontrib><title>Smad-mediated transcription is required for transforming growth factor-beta 1-induced p57(Kip2) proteolysis in osteoblastic cells</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Cyclin-dependent kinase inhibitory proteins (CKIs) are negative regulators of the cell cycle. Of all CKIs, only p57(Kip2) plays an essential role(s) that other CKIs cannot compensate for in embryonic development. Recently, we found that p57(Kip2) is degraded through the ubiquitin-proteasome pathway in osteoblastic cells stimulated to proliferation by transforming growth factor (TGF)-beta1 (Urano, T., Yashiroda, H., Muraoka, M., Tanaka, K., Hosoi, T., Inoue, S., Ouchi, Y., and Toyoshima, H. (1999) J. Biol. Chem. 274, 12197-12200). We report here that TGF-beta1-induced p57(Kip2) proteolysis is mediated through transcription by the Smad pathway. When the constitutively active form of the TGF-beta type I receptor ALK-5(TD) was ectopically expressed in osteoblastic cells, p57(Kip2) that had been accumulated by serum starvation causing the cell-cycle arrest was rapidly degraded in a manner analogous to TGF-beta1 stimulation. Moreover, Smad2 or Smad3 with Smad4 enhanced the proteolytic pathway of p57(Kip2). The degradation of p57(Kip2) evoked by TGF-beta1 was blocked by forced expression of an inhibitory Smad called Smad7 or by the addition of actinomycin D or alpha-amanitin. These results indicate that accelerated degradation of p57(Kip2) by TGF-beta1/Smad signaling is mediated through a newly synthesized factor(s) that modifies p57(Kip2) or the ubiquitin-proteasome pathway.</description><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Cyclin-Dependent Kinase Inhibitor p57</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Mice</subject><subject>Nuclear Proteins - metabolism</subject><subject>Osteoblasts - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Transforming Growth Factor beta - pharmacology</subject><issn>0021-9258</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1UD1PwzAU9ACipbAyIk8IhhTbdeJ4RBVfoogBmKPn2Cmukji1HaGO_HOMWt7y7nSn0-kQuqBkTongtxtVz19JQlIyQo7QlBBGM8nycoJOQ9iQdFzSEzShlOasEHyKft470FlntIVoNI4e-lB7O0TremwD9mY7Wp-Uxvm9mkBn-zVee_cdv3ADdXQ-UyYCppnt9Vgn95CL6xc7sBs8eBeNa3chhdkeu5CYaiFEW-PatG04Q8cNtMGcH_4MfT7cfyyfstXb4_PybpUNdCFjprTiKjeaNLpkJSiAmoCQWhtFoWR5QUWTcy6FNlAQxQkoLUBKwUtaclMuZuhqn5sabUcTYtXZ8NcAeuPGUAlBqCgIScbLg3FUaZhq8LYDv6v-R1v8AiBhb8s</recordid><startdate>20010406</startdate><enddate>20010406</enddate><creator>Nishimori, S</creator><creator>Tanaka, Y</creator><creator>Chiba, T</creator><creator>Fujii, M</creator><creator>Imamura, T</creator><creator>Miyazono, K</creator><creator>Ogasawara, T</creator><creator>Kawaguchi, H</creator><creator>Igarashi, T</creator><creator>Fujita, T</creator><creator>Tanaka, K</creator><creator>Toyoshima, H</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20010406</creationdate><title>Smad-mediated transcription is required for transforming growth factor-beta 1-induced p57(Kip2) proteolysis in osteoblastic cells</title><author>Nishimori, S ; Tanaka, Y ; Chiba, T ; Fujii, M ; Imamura, T ; Miyazono, K ; Ogasawara, T ; Kawaguchi, H ; Igarashi, T ; Fujita, T ; Tanaka, K ; Toyoshima, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p139t-bdb4b5ed0fd828abaac0a79ddeb1a825617f54497dea60b40abd7a99748184e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Cyclin-Dependent Kinase Inhibitor p57</topic><topic>Cyclin-Dependent Kinases - metabolism</topic><topic>Mice</topic><topic>Nuclear Proteins - metabolism</topic><topic>Osteoblasts - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Transforming Growth Factor beta - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishimori, S</creatorcontrib><creatorcontrib>Tanaka, Y</creatorcontrib><creatorcontrib>Chiba, T</creatorcontrib><creatorcontrib>Fujii, M</creatorcontrib><creatorcontrib>Imamura, T</creatorcontrib><creatorcontrib>Miyazono, K</creatorcontrib><creatorcontrib>Ogasawara, T</creatorcontrib><creatorcontrib>Kawaguchi, H</creatorcontrib><creatorcontrib>Igarashi, T</creatorcontrib><creatorcontrib>Fujita, T</creatorcontrib><creatorcontrib>Tanaka, K</creatorcontrib><creatorcontrib>Toyoshima, H</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishimori, S</au><au>Tanaka, Y</au><au>Chiba, T</au><au>Fujii, M</au><au>Imamura, T</au><au>Miyazono, K</au><au>Ogasawara, T</au><au>Kawaguchi, H</au><au>Igarashi, T</au><au>Fujita, T</au><au>Tanaka, K</au><au>Toyoshima, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Smad-mediated transcription is required for transforming growth factor-beta 1-induced p57(Kip2) proteolysis in osteoblastic cells</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2001-04-06</date><risdate>2001</risdate><volume>276</volume><issue>14</issue><spage>10700</spage><epage>10705</epage><pages>10700-10705</pages><issn>0021-9258</issn><abstract>Cyclin-dependent kinase inhibitory proteins (CKIs) are negative regulators of the cell cycle. Of all CKIs, only p57(Kip2) plays an essential role(s) that other CKIs cannot compensate for in embryonic development. Recently, we found that p57(Kip2) is degraded through the ubiquitin-proteasome pathway in osteoblastic cells stimulated to proliferation by transforming growth factor (TGF)-beta1 (Urano, T., Yashiroda, H., Muraoka, M., Tanaka, K., Hosoi, T., Inoue, S., Ouchi, Y., and Toyoshima, H. (1999) J. Biol. Chem. 274, 12197-12200). We report here that TGF-beta1-induced p57(Kip2) proteolysis is mediated through transcription by the Smad pathway. When the constitutively active form of the TGF-beta type I receptor ALK-5(TD) was ectopically expressed in osteoblastic cells, p57(Kip2) that had been accumulated by serum starvation causing the cell-cycle arrest was rapidly degraded in a manner analogous to TGF-beta1 stimulation. Moreover, Smad2 or Smad3 with Smad4 enhanced the proteolytic pathway of p57(Kip2). The degradation of p57(Kip2) evoked by TGF-beta1 was blocked by forced expression of an inhibitory Smad called Smad7 or by the addition of actinomycin D or alpha-amanitin. These results indicate that accelerated degradation of p57(Kip2) by TGF-beta1/Smad signaling is mediated through a newly synthesized factor(s) that modifies p57(Kip2) or the ubiquitin-proteasome pathway.</abstract><cop>United States</cop><pmid>11152674</pmid><doi>10.1074/jbc.M007499200</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cells, Cultured Cyclin-Dependent Kinase Inhibitor p57 Cyclin-Dependent Kinases - metabolism Mice Nuclear Proteins - metabolism Osteoblasts - metabolism Signal Transduction - drug effects Transforming Growth Factor beta - metabolism Transforming Growth Factor beta - pharmacology |
title | Smad-mediated transcription is required for transforming growth factor-beta 1-induced p57(Kip2) proteolysis in osteoblastic cells |
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