The trk proto-oncogene rescues NGF responsiveness in mutant NGF-nonresponsive PC12 cell lines
The trk tyrosine kinase proto-oncogene product gp140 prototrk binds nerve growth factor (NGF) and is rapidly and selectively activated by this neurotrophic factor. To determine whether gp140 prototrk is involved in transducing a functional NGF signal, PC12 cell mutants (PC12nnr) deficient in high af...
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| Veröffentlicht in: | Cell 1991-09, Vol.66 (5), p.961-966 |
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| container_title | Cell |
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| creator | Loeb, David M. Maragos, Johnna Martin-Zanca, Dionisio Chao, Moses V. Parada, Luis F. Greene, Lloyd A. |
| description | The
trk tyrosine kinase proto-oncogene product gp140
prototrk binds nerve growth factor (NGF) and is rapidly and selectively activated by this neurotrophic factor. To determine whether gp140
prototrk is involved in transducing a functional NGF signal, PC12 cell mutants (PC12nnr) deficient in high affinity NGF binding and unresponsive to NGF were used. Northern analysis revealed that these mutant cells have greatly reduced levels of
trk expression. PC12nnr cultures were transiently transfected with expression vectors encoding the full-length rat
trk cDNA and assessed for responsiveness to NGF. Expression of exogenous
trk rescued the capacity for NGF-promoted neurite outgrowth, cellular hypertrophy, and serum-free survival by these cells. These results indicate that gp140
prototrk is necessary for functional NGF signal transduction. |
| doi_str_mv | 10.1016/0092-8674(91)90441-Z |
| format | Article |
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trk tyrosine kinase proto-oncogene product gp140
prototrk binds nerve growth factor (NGF) and is rapidly and selectively activated by this neurotrophic factor. To determine whether gp140
prototrk is involved in transducing a functional NGF signal, PC12 cell mutants (PC12nnr) deficient in high affinity NGF binding and unresponsive to NGF were used. Northern analysis revealed that these mutant cells have greatly reduced levels of
trk expression. PC12nnr cultures were transiently transfected with expression vectors encoding the full-length rat
trk cDNA and assessed for responsiveness to NGF. Expression of exogenous
trk rescued the capacity for NGF-promoted neurite outgrowth, cellular hypertrophy, and serum-free survival by these cells. These results indicate that gp140
prototrk is necessary for functional NGF signal transduction.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/0092-8674(91)90441-Z</identifier><identifier>PMID: 1653650</identifier><identifier>CODEN: CELLB5</identifier><language>eng</language><publisher>Cambridge, MA: Elsevier Inc</publisher><subject>Adrenal Gland Neoplasms - genetics ; Adrenal Gland Neoplasms - pathology ; Animals ; Biological and medical sciences ; Blotting, Northern ; Carbazoles - pharmacology ; Cell Differentiation ; Cell Division ; Cell physiology ; Cell Survival ; Fundamental and applied biological sciences. Psychology ; Gene Expression ; In Vitro Techniques ; Indole Alkaloids ; Molecular and cellular biology ; Nerve Growth Factors - physiology ; Pheochromocytoma - physiopathology ; Protein Kinase Inhibitors ; Protein-Tyrosine Kinases - physiology ; Proto-Oncogene Proteins - genetics ; Rats ; Receptor, trkA ; Receptors, Cell Surface - physiology ; Receptors, Nerve Growth Factor ; RNA, Messenger - genetics ; Signal Transduction ; Transfection ; Tumor Cells, Cultured</subject><ispartof>Cell, 1991-09, Vol.66 (5), p.961-966</ispartof><rights>1991</rights><rights>1992 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-2f27c3e4fd7fccf7d7fab2e28e976b0d3b6b2bc1c44623c4e992ce6c4911e1d43</citedby><cites>FETCH-LOGICAL-c332t-2f27c3e4fd7fccf7d7fab2e28e976b0d3b6b2bc1c44623c4e992ce6c4911e1d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0092-8674(91)90441-Z$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,46000</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=5015156$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1653650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Loeb, David M.</creatorcontrib><creatorcontrib>Maragos, Johnna</creatorcontrib><creatorcontrib>Martin-Zanca, Dionisio</creatorcontrib><creatorcontrib>Chao, Moses V.</creatorcontrib><creatorcontrib>Parada, Luis F.</creatorcontrib><creatorcontrib>Greene, Lloyd A.</creatorcontrib><title>The trk proto-oncogene rescues NGF responsiveness in mutant NGF-nonresponsive PC12 cell lines</title><title>Cell</title><addtitle>Cell</addtitle><description>The
trk tyrosine kinase proto-oncogene product gp140
prototrk binds nerve growth factor (NGF) and is rapidly and selectively activated by this neurotrophic factor. To determine whether gp140
prototrk is involved in transducing a functional NGF signal, PC12 cell mutants (PC12nnr) deficient in high affinity NGF binding and unresponsive to NGF were used. Northern analysis revealed that these mutant cells have greatly reduced levels of
trk expression. PC12nnr cultures were transiently transfected with expression vectors encoding the full-length rat
trk cDNA and assessed for responsiveness to NGF. Expression of exogenous
trk rescued the capacity for NGF-promoted neurite outgrowth, cellular hypertrophy, and serum-free survival by these cells. These results indicate that gp140
prototrk is necessary for functional NGF signal transduction.</description><subject>Adrenal Gland Neoplasms - genetics</subject><subject>Adrenal Gland Neoplasms - pathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Northern</subject><subject>Carbazoles - pharmacology</subject><subject>Cell Differentiation</subject><subject>Cell Division</subject><subject>Cell physiology</subject><subject>Cell Survival</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression</subject><subject>In Vitro Techniques</subject><subject>Indole Alkaloids</subject><subject>Molecular and cellular biology</subject><subject>Nerve Growth Factors - physiology</subject><subject>Pheochromocytoma - physiopathology</subject><subject>Protein Kinase Inhibitors</subject><subject>Protein-Tyrosine Kinases - physiology</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Rats</subject><subject>Receptor, trkA</subject><subject>Receptors, Cell Surface - physiology</subject><subject>Receptors, Nerve Growth Factor</subject><subject>RNA, Messenger - genetics</subject><subject>Signal Transduction</subject><subject>Transfection</subject><subject>Tumor Cells, Cultured</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEFrFDEUx4Mo7Vr9Bi3kIKKH0bwkk9lcCmWxVSi2h3opSJh586ZGZ5NtMlvw25txl_ampxf4_97jnx9jxyA-gADzUQgrq6Vp9DsL763QGqrbZ2wBwjaVhkY-Z4tH5JC9zPmnEGJZ1_UBOwBTK1OLBft-84P4lH7xTYpTrGLAeEeBeKKMW8r868X5_N7EkP1DCXLmPvD1dmrDNIdViOEp59crkBxpHPnoC_yKvRjaMdPr_Txi384_3aw-V5dXF19WZ5cVKiWnSg6yQUV66JsBcWjKaDtJckm2MZ3oVWc62SGg1kYq1GStRDKoLQBBr9URe7u7W35xX2pPbu3zXKMNFLfZNVIstdbqvyAYYbSyUEC9AzHFnBMNbpP8uk2_HQg363ezWze7dRbcX_3utqyd7O9vuzX1T0s73yV_s8_bjO04pDagz49YLaCG2hTsdIdRkfbgKbmMngJS7xPh5Pro_93jD9AxoXQ</recordid><startdate>19910906</startdate><enddate>19910906</enddate><creator>Loeb, David M.</creator><creator>Maragos, Johnna</creator><creator>Martin-Zanca, Dionisio</creator><creator>Chao, Moses V.</creator><creator>Parada, Luis F.</creator><creator>Greene, Lloyd A.</creator><general>Elsevier Inc</general><general>Cell Press</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>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19910906</creationdate><title>The trk proto-oncogene rescues NGF responsiveness in mutant NGF-nonresponsive PC12 cell lines</title><author>Loeb, David M. ; Maragos, Johnna ; Martin-Zanca, Dionisio ; Chao, Moses V. ; Parada, Luis F. ; Greene, Lloyd A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-2f27c3e4fd7fccf7d7fab2e28e976b0d3b6b2bc1c44623c4e992ce6c4911e1d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Adrenal Gland Neoplasms - genetics</topic><topic>Adrenal Gland Neoplasms - pathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Northern</topic><topic>Carbazoles - pharmacology</topic><topic>Cell Differentiation</topic><topic>Cell Division</topic><topic>Cell physiology</topic><topic>Cell Survival</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression</topic><topic>In Vitro Techniques</topic><topic>Indole Alkaloids</topic><topic>Molecular and cellular biology</topic><topic>Nerve Growth Factors - physiology</topic><topic>Pheochromocytoma - physiopathology</topic><topic>Protein Kinase Inhibitors</topic><topic>Protein-Tyrosine Kinases - physiology</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Rats</topic><topic>Receptor, trkA</topic><topic>Receptors, Cell Surface - physiology</topic><topic>Receptors, Nerve Growth Factor</topic><topic>RNA, Messenger - genetics</topic><topic>Signal Transduction</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Loeb, David M.</creatorcontrib><creatorcontrib>Maragos, Johnna</creatorcontrib><creatorcontrib>Martin-Zanca, Dionisio</creatorcontrib><creatorcontrib>Chao, Moses V.</creatorcontrib><creatorcontrib>Parada, Luis F.</creatorcontrib><creatorcontrib>Greene, Lloyd A.</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>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Loeb, David M.</au><au>Maragos, Johnna</au><au>Martin-Zanca, Dionisio</au><au>Chao, Moses V.</au><au>Parada, Luis F.</au><au>Greene, Lloyd A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The trk proto-oncogene rescues NGF responsiveness in mutant NGF-nonresponsive PC12 cell lines</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>1991-09-06</date><risdate>1991</risdate><volume>66</volume><issue>5</issue><spage>961</spage><epage>966</epage><pages>961-966</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><coden>CELLB5</coden><abstract>The
trk tyrosine kinase proto-oncogene product gp140
prototrk binds nerve growth factor (NGF) and is rapidly and selectively activated by this neurotrophic factor. To determine whether gp140
prototrk is involved in transducing a functional NGF signal, PC12 cell mutants (PC12nnr) deficient in high affinity NGF binding and unresponsive to NGF were used. Northern analysis revealed that these mutant cells have greatly reduced levels of
trk expression. PC12nnr cultures were transiently transfected with expression vectors encoding the full-length rat
trk cDNA and assessed for responsiveness to NGF. Expression of exogenous
trk rescued the capacity for NGF-promoted neurite outgrowth, cellular hypertrophy, and serum-free survival by these cells. These results indicate that gp140
prototrk is necessary for functional NGF signal transduction.</abstract><cop>Cambridge, MA</cop><pub>Elsevier Inc</pub><pmid>1653650</pmid><doi>10.1016/0092-8674(91)90441-Z</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Cell, 1991-09, Vol.66 (5), p.961-966 |
| issn | 0092-8674 1097-4172 |
| language | eng |
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| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Adrenal Gland Neoplasms - genetics Adrenal Gland Neoplasms - pathology Animals Biological and medical sciences Blotting, Northern Carbazoles - pharmacology Cell Differentiation Cell Division Cell physiology Cell Survival Fundamental and applied biological sciences. Psychology Gene Expression In Vitro Techniques Indole Alkaloids Molecular and cellular biology Nerve Growth Factors - physiology Pheochromocytoma - physiopathology Protein Kinase Inhibitors Protein-Tyrosine Kinases - physiology Proto-Oncogene Proteins - genetics Rats Receptor, trkA Receptors, Cell Surface - physiology Receptors, Nerve Growth Factor RNA, Messenger - genetics Signal Transduction Transfection Tumor Cells, Cultured |
| title | The trk proto-oncogene rescues NGF responsiveness in mutant NGF-nonresponsive PC12 cell lines |
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