A single heteromeric receptor complex is sufficient to mediate biological effects of transforming growth factor-beta ligands
Transforming growth factor beta (TGF-beta), a multifunctional cytokine that regulates a variety of biological functions, signals through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane serine-threonine kinase, was cloned based on its...
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| Veröffentlicht in: | The Journal of biological chemistry 1994-05, Vol.269 (21), p.14861-14864 |
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| container_issue | 21 |
| container_start_page | 14861 |
| container_title | The Journal of biological chemistry |
| container_volume | 269 |
| creator | BASSING, C. H HOWE, D. J SEGARINI, P. R DONAHOE, P. K XIAO-FAN WANG |
| description | Transforming growth factor beta (TGF-beta), a multifunctional cytokine that regulates a variety of biological functions, signals
through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane
serine-threonine kinase, was cloned based on its ability to directly bind TGF-beta. Recently, a number of candidate type I
TGF-beta receptors have been isolated. Although only one of these transmembrane kinases (R4) has been shown to mediate TGF-beta-dependent
gene activation, others bind TGF-beta when overexpressed in COS cells. Consequently, it has been postulated that the diversity
of TGF-beta responses is generated through the association of distinct type I receptors with the type II TGF-beta receptor,
thus creating receptor complexes of differential signaling capacities. In contrast to this model, we demonstrate that stable
expression of only the R4 type I TGF-beta receptor in a mutant cell line lacking endogenous type I TGF-beta receptor was able
to complex with the endogenous type II TGF-beta receptor and restore the effects of TGF-beta on inhibition of cell proliferation
and activation of specific genes, regardless of which of the three mammalian isoforms of TGF-beta was used as the ligand.
Therefore, R4 acts as a fully functional type I TGF-beta receptor, and the differential effects of TGF-beta are likely mediated
by a single receptor complex consisting of R4 and the type II receptor. |
| doi_str_mv | 10.1016/S0021-9258(17)36543-2 |
| format | Article |
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through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane
serine-threonine kinase, was cloned based on its ability to directly bind TGF-beta. Recently, a number of candidate type I
TGF-beta receptors have been isolated. Although only one of these transmembrane kinases (R4) has been shown to mediate TGF-beta-dependent
gene activation, others bind TGF-beta when overexpressed in COS cells. Consequently, it has been postulated that the diversity
of TGF-beta responses is generated through the association of distinct type I receptors with the type II TGF-beta receptor,
thus creating receptor complexes of differential signaling capacities. In contrast to this model, we demonstrate that stable
expression of only the R4 type I TGF-beta receptor in a mutant cell line lacking endogenous type I TGF-beta receptor was able
to complex with the endogenous type II TGF-beta receptor and restore the effects of TGF-beta on inhibition of cell proliferation
and activation of specific genes, regardless of which of the three mammalian isoforms of TGF-beta was used as the ligand.
Therefore, R4 acts as a fully functional type I TGF-beta receptor, and the differential effects of TGF-beta are likely mediated
by a single receptor complex consisting of R4 and the type II receptor.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1016/S0021-9258(17)36543-2</identifier><identifier>PMID: 8195115</identifier><identifier>CODEN: JBCHA3</identifier><language>eng</language><publisher>Bethesda, MD: American Society for Biochemistry and Molecular Biology</publisher><subject>Animals ; Biological and medical sciences ; Cell Line ; Cell receptors ; Cell structures and functions ; Fundamental and applied biological sciences. Psychology ; Hormone receptors. Growth factor receptors. Cytokine receptors. Prostaglandin receptors ; Ligands ; Mink ; Molecular and cellular biology ; Receptors, Transforming Growth Factor beta - metabolism ; Transforming Growth Factor beta - metabolism</subject><ispartof>The Journal of biological chemistry, 1994-05, Vol.269 (21), p.14861-14864</ispartof><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-5ae15b9279140355d28241c981e02b4cec6ba0c752fcbacd0072aa5847628c483</citedby><cites>FETCH-LOGICAL-c440t-5ae15b9279140355d28241c981e02b4cec6ba0c752fcbacd0072aa5847628c483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4207635$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8195115$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BASSING, C. H</creatorcontrib><creatorcontrib>HOWE, D. J</creatorcontrib><creatorcontrib>SEGARINI, P. R</creatorcontrib><creatorcontrib>DONAHOE, P. K</creatorcontrib><creatorcontrib>XIAO-FAN WANG</creatorcontrib><title>A single heteromeric receptor complex is sufficient to mediate biological effects of transforming growth factor-beta ligands</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Transforming growth factor beta (TGF-beta), a multifunctional cytokine that regulates a variety of biological functions, signals
through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane
serine-threonine kinase, was cloned based on its ability to directly bind TGF-beta. Recently, a number of candidate type I
TGF-beta receptors have been isolated. Although only one of these transmembrane kinases (R4) has been shown to mediate TGF-beta-dependent
gene activation, others bind TGF-beta when overexpressed in COS cells. Consequently, it has been postulated that the diversity
of TGF-beta responses is generated through the association of distinct type I receptors with the type II TGF-beta receptor,
thus creating receptor complexes of differential signaling capacities. In contrast to this model, we demonstrate that stable
expression of only the R4 type I TGF-beta receptor in a mutant cell line lacking endogenous type I TGF-beta receptor was able
to complex with the endogenous type II TGF-beta receptor and restore the effects of TGF-beta on inhibition of cell proliferation
and activation of specific genes, regardless of which of the three mammalian isoforms of TGF-beta was used as the ligand.
Therefore, R4 acts as a fully functional type I TGF-beta receptor, and the differential effects of TGF-beta are likely mediated
by a single receptor complex consisting of R4 and the type II receptor.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Line</subject><subject>Cell receptors</subject><subject>Cell structures and functions</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hormone receptors. Growth factor receptors. Cytokine receptors. Prostaglandin receptors</subject><subject>Ligands</subject><subject>Mink</subject><subject>Molecular and cellular biology</subject><subject>Receptors, Transforming Growth Factor beta - metabolism</subject><subject>Transforming Growth Factor beta - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2LFDEQhoMo6-zqT1jIQUQPral0PrqPy7K6woIHFbyFdKbSHenujEmGVfDHm9kdBm_mkkM99Ra8DyGXwN4BA_X-C2Mcmp7L7g3ot62Som34E7IB1rVNK-H7U7I5Ic_Jec4_WH2ihzNy1kEvAeSG_LmiOazjjHTCgikumIKjCR3uSkzUxWU34y8aMs1774MLuBZaIl1wG2xBOoQ4xzE4O1P0Hl3JNHpakl2zj2mp0XRM8b5M1FtXE5sBi6VzGO26zS_IM2_njC-P_wX59uHm6_Vtc_f546frq7vGCcFKIy2CHHquexCslXLLOy7A9R0g44Nw6NRgmdOSezdYt2VMc2tlJ7TinRNde0FeP-buUvy5x1zMErLDebYrxn02WkngTKj_gqC00JrxCspH0KWYc0JvdiksNv02wMxBj3nQYw7dG9DmQY857F0eD-yHWuFp6-ijzl8d5zbXTn3t0YV8wgRnWrX_YFMYp_uQ0FQPbsLFcNWbehdEp6D9C8SopTQ</recordid><startdate>19940527</startdate><enddate>19940527</enddate><creator>BASSING, C. H</creator><creator>HOWE, D. J</creator><creator>SEGARINI, P. R</creator><creator>DONAHOE, P. K</creator><creator>XIAO-FAN WANG</creator><general>American Society for Biochemistry and Molecular Biology</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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19940527</creationdate><title>A single heteromeric receptor complex is sufficient to mediate biological effects of transforming growth factor-beta ligands</title><author>BASSING, C. H ; HOWE, D. J ; SEGARINI, P. R ; DONAHOE, P. K ; XIAO-FAN WANG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-5ae15b9279140355d28241c981e02b4cec6ba0c752fcbacd0072aa5847628c483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Line</topic><topic>Cell receptors</topic><topic>Cell structures and functions</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hormone receptors. Growth factor receptors. Cytokine receptors. Prostaglandin receptors</topic><topic>Ligands</topic><topic>Mink</topic><topic>Molecular and cellular biology</topic><topic>Receptors, Transforming Growth Factor beta - metabolism</topic><topic>Transforming Growth Factor beta - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BASSING, C. H</creatorcontrib><creatorcontrib>HOWE, D. J</creatorcontrib><creatorcontrib>SEGARINI, P. R</creatorcontrib><creatorcontrib>DONAHOE, P. K</creatorcontrib><creatorcontrib>XIAO-FAN WANG</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</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>BASSING, C. H</au><au>HOWE, D. J</au><au>SEGARINI, P. R</au><au>DONAHOE, P. K</au><au>XIAO-FAN WANG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A single heteromeric receptor complex is sufficient to mediate biological effects of transforming growth factor-beta ligands</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1994-05-27</date><risdate>1994</risdate><volume>269</volume><issue>21</issue><spage>14861</spage><epage>14864</epage><pages>14861-14864</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><coden>JBCHA3</coden><abstract>Transforming growth factor beta (TGF-beta), a multifunctional cytokine that regulates a variety of biological functions, signals
through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane
serine-threonine kinase, was cloned based on its ability to directly bind TGF-beta. Recently, a number of candidate type I
TGF-beta receptors have been isolated. Although only one of these transmembrane kinases (R4) has been shown to mediate TGF-beta-dependent
gene activation, others bind TGF-beta when overexpressed in COS cells. Consequently, it has been postulated that the diversity
of TGF-beta responses is generated through the association of distinct type I receptors with the type II TGF-beta receptor,
thus creating receptor complexes of differential signaling capacities. In contrast to this model, we demonstrate that stable
expression of only the R4 type I TGF-beta receptor in a mutant cell line lacking endogenous type I TGF-beta receptor was able
to complex with the endogenous type II TGF-beta receptor and restore the effects of TGF-beta on inhibition of cell proliferation
and activation of specific genes, regardless of which of the three mammalian isoforms of TGF-beta was used as the ligand.
Therefore, R4 acts as a fully functional type I TGF-beta receptor, and the differential effects of TGF-beta are likely mediated
by a single receptor complex consisting of R4 and the type II receptor.</abstract><cop>Bethesda, MD</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>8195115</pmid><doi>10.1016/S0021-9258(17)36543-2</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of biological chemistry, 1994-05, Vol.269 (21), p.14861-14864 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library |
| subjects | Animals Biological and medical sciences Cell Line Cell receptors Cell structures and functions Fundamental and applied biological sciences. Psychology Hormone receptors. Growth factor receptors. Cytokine receptors. Prostaglandin receptors Ligands Mink Molecular and cellular biology Receptors, Transforming Growth Factor beta - metabolism Transforming Growth Factor beta - metabolism |
| title | A single heteromeric receptor complex is sufficient to mediate biological effects of transforming growth factor-beta ligands |
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