Anchorage-Independent Growth of Fibroblasts That Express a Truncated IGF-I Receptor
The purpose of this investigation was to study signaling by an insulin-like growth factor I receptor (IGF-I R) that lacks the extracellular portion of the receptor. We transfected IGF-I R-negative mouse embryo fibroblasts with a truncated IGF-I R consisting of only the transmembrane and cytoplasmic...
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| Veröffentlicht in: | Biochemical and biophysical research communications 2001-08, Vol.286 (3), p.472-477 |
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| creator | Himmelmann, Barbara Terry, Cheryl Dey, Bhakta R. Lopaczynski, Wlodzimierz Nissley, Peter |
| description | The purpose of this investigation was to study signaling by an insulin-like growth factor I receptor (IGF-I R) that lacks the extracellular portion of the receptor. We transfected IGF-I R-negative mouse embryo fibroblasts with a truncated IGF-I R consisting of only the transmembrane and cytoplasmic part of the β subunit. Proliferation as assessed by counting cells was the same for vector only transfectants and the truncated receptor transfectants in defined medium containing EGF and PDGF. In contrast, anchorage-independent growth as measured by colony formation in soft agar was markedly increased for the truncated IGF-I R transfectants compared to the vector transfectants. MAP-kinase activity in the truncated IGF-I R transfectants was not higher than in the vector transfectants; however, PI 3-kinase activity was significantly higher in the IGF-I R transfectants. These results provide evidence that an IGF-I receptor consisting of only the transmembrane and cytoplasmic domain of the β subunit can signal pathways leading to anchorage-independent growth. |
| doi_str_mv | 10.1006/bbrc.2001.5417 |
| format | Article |
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We transfected IGF-I R-negative mouse embryo fibroblasts with a truncated IGF-I R consisting of only the transmembrane and cytoplasmic part of the β subunit. Proliferation as assessed by counting cells was the same for vector only transfectants and the truncated receptor transfectants in defined medium containing EGF and PDGF. In contrast, anchorage-independent growth as measured by colony formation in soft agar was markedly increased for the truncated IGF-I R transfectants compared to the vector transfectants. MAP-kinase activity in the truncated IGF-I R transfectants was not higher than in the vector transfectants; however, PI 3-kinase activity was significantly higher in the IGF-I R transfectants. These results provide evidence that an IGF-I receptor consisting of only the transmembrane and cytoplasmic domain of the β subunit can signal pathways leading to anchorage-independent growth.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.2001.5417</identifier><identifier>PMID: 11511082</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>anchorage-independent growth ; Animals ; Cell Division ; Cells, Cultured ; Culture Media, Serum-Free ; EGF ; Epidermal Growth Factor - pharmacology ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; IGF-I receptor ; MAP kinase ; Mice ; Mice, Knockout ; Mitogen-Activated Protein Kinase 1 - metabolism ; PDGF ; Phosphatidylinositol 3-Kinases - metabolism ; PI3-kinase ; Platelet-Derived Growth Factor - pharmacology ; Receptor, IGF Type 1 - genetics ; Receptor, IGF Type 1 - metabolism ; Sequence Deletion ; Signal Transduction ; Transfection</subject><ispartof>Biochemical and biophysical research communications, 2001-08, Vol.286 (3), p.472-477</ispartof><rights>2001 Academic Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c340t-16f2b2401837bfb7723b24aa308d429fb14256070a6005eeacbe82394307f7903</citedby><cites>FETCH-LOGICAL-c340t-16f2b2401837bfb7723b24aa308d429fb14256070a6005eeacbe82394307f7903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X01954178$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11511082$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Himmelmann, Barbara</creatorcontrib><creatorcontrib>Terry, Cheryl</creatorcontrib><creatorcontrib>Dey, Bhakta R.</creatorcontrib><creatorcontrib>Lopaczynski, Wlodzimierz</creatorcontrib><creatorcontrib>Nissley, Peter</creatorcontrib><title>Anchorage-Independent Growth of Fibroblasts That Express a Truncated IGF-I Receptor</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The purpose of this investigation was to study signaling by an insulin-like growth factor I receptor (IGF-I R) that lacks the extracellular portion of the receptor. We transfected IGF-I R-negative mouse embryo fibroblasts with a truncated IGF-I R consisting of only the transmembrane and cytoplasmic part of the β subunit. Proliferation as assessed by counting cells was the same for vector only transfectants and the truncated receptor transfectants in defined medium containing EGF and PDGF. In contrast, anchorage-independent growth as measured by colony formation in soft agar was markedly increased for the truncated IGF-I R transfectants compared to the vector transfectants. MAP-kinase activity in the truncated IGF-I R transfectants was not higher than in the vector transfectants; however, PI 3-kinase activity was significantly higher in the IGF-I R transfectants. These results provide evidence that an IGF-I receptor consisting of only the transmembrane and cytoplasmic domain of the β subunit can signal pathways leading to anchorage-independent growth.</description><subject>anchorage-independent growth</subject><subject>Animals</subject><subject>Cell Division</subject><subject>Cells, Cultured</subject><subject>Culture Media, Serum-Free</subject><subject>EGF</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>IGF-I receptor</subject><subject>MAP kinase</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>PDGF</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3-kinase</subject><subject>Platelet-Derived Growth Factor - pharmacology</subject><subject>Receptor, IGF Type 1 - genetics</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Sequence Deletion</subject><subject>Signal Transduction</subject><subject>Transfection</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFrGzEQRkVJaFy31x6DTrmtM6Ndr3aPxsSOIVBIHMhNSNrZeoO92kjapv33kbGhp1xmGHjfB_MY-4kwQ4Dy1hhvZwIAZ_MC5Rc2QaghEwjFBZtAIjJR48sV-xbCa6KwKOuv7ApxjgiVmLCnRW93zuvflG36hgZKo4987d173HHX8lVnvDN7HWLg252O_O7v4CkErvnWj73VkRq-Wa-yDX8kS0N0_ju7bPU-0I_znrLn1d12eZ89_FpvlouHzOYFxAzLVhhRAFa5NK2RUuTp1DqHqilE3RosxLwECboEmBNpa6gSeV3kIFtZQz5lN6fewbu3kUJUhy5Y2u91T24MSiYXJUpM4OwEWu9C8NSqwXcH7f8pBHXUqI4a1VGjOmpMgetz82gO1PzHz94SUJ0ASv_96cirYDvqLTWdJxtV47rPuj8AVXh_aQ</recordid><startdate>20010824</startdate><enddate>20010824</enddate><creator>Himmelmann, Barbara</creator><creator>Terry, Cheryl</creator><creator>Dey, Bhakta R.</creator><creator>Lopaczynski, Wlodzimierz</creator><creator>Nissley, Peter</creator><general>Elsevier Inc</general><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>7X8</scope></search><sort><creationdate>20010824</creationdate><title>Anchorage-Independent Growth of Fibroblasts That Express a Truncated IGF-I Receptor</title><author>Himmelmann, Barbara ; Terry, Cheryl ; Dey, Bhakta R. ; Lopaczynski, Wlodzimierz ; Nissley, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c340t-16f2b2401837bfb7723b24aa308d429fb14256070a6005eeacbe82394307f7903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>anchorage-independent growth</topic><topic>Animals</topic><topic>Cell Division</topic><topic>Cells, Cultured</topic><topic>Culture Media, Serum-Free</topic><topic>EGF</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>IGF-I receptor</topic><topic>MAP kinase</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>PDGF</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3-kinase</topic><topic>Platelet-Derived Growth Factor - pharmacology</topic><topic>Receptor, IGF Type 1 - genetics</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Sequence Deletion</topic><topic>Signal Transduction</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Himmelmann, Barbara</creatorcontrib><creatorcontrib>Terry, Cheryl</creatorcontrib><creatorcontrib>Dey, Bhakta R.</creatorcontrib><creatorcontrib>Lopaczynski, Wlodzimierz</creatorcontrib><creatorcontrib>Nissley, Peter</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Himmelmann, Barbara</au><au>Terry, Cheryl</au><au>Dey, Bhakta R.</au><au>Lopaczynski, Wlodzimierz</au><au>Nissley, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anchorage-Independent Growth of Fibroblasts That Express a Truncated IGF-I Receptor</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2001-08-24</date><risdate>2001</risdate><volume>286</volume><issue>3</issue><spage>472</spage><epage>477</epage><pages>472-477</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The purpose of this investigation was to study signaling by an insulin-like growth factor I receptor (IGF-I R) that lacks the extracellular portion of the receptor. We transfected IGF-I R-negative mouse embryo fibroblasts with a truncated IGF-I R consisting of only the transmembrane and cytoplasmic part of the β subunit. Proliferation as assessed by counting cells was the same for vector only transfectants and the truncated receptor transfectants in defined medium containing EGF and PDGF. In contrast, anchorage-independent growth as measured by colony formation in soft agar was markedly increased for the truncated IGF-I R transfectants compared to the vector transfectants. MAP-kinase activity in the truncated IGF-I R transfectants was not higher than in the vector transfectants; however, PI 3-kinase activity was significantly higher in the IGF-I R transfectants. These results provide evidence that an IGF-I receptor consisting of only the transmembrane and cytoplasmic domain of the β subunit can signal pathways leading to anchorage-independent growth.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11511082</pmid><doi>10.1006/bbrc.2001.5417</doi><tpages>6</tpages></addata></record> |
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| subjects | anchorage-independent growth Animals Cell Division Cells, Cultured Culture Media, Serum-Free EGF Epidermal Growth Factor - pharmacology Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism IGF-I receptor MAP kinase Mice Mice, Knockout Mitogen-Activated Protein Kinase 1 - metabolism PDGF Phosphatidylinositol 3-Kinases - metabolism PI3-kinase Platelet-Derived Growth Factor - pharmacology Receptor, IGF Type 1 - genetics Receptor, IGF Type 1 - metabolism Sequence Deletion Signal Transduction Transfection |
| title | Anchorage-Independent Growth of Fibroblasts That Express a Truncated IGF-I Receptor |
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