Analysis of the transforming potential of the human homolog of mos
The human homology, c- mos hu, of the mouse cellular mos proto-oncogene (c- mos mu) transforms NIH 3T3 cells at low efficiency. Furthermore, the c- mos hu-induced foci are less distinct, and transformed cells contain a high level of human mos protein. The transforming activity of hybrid mos genes de...
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| Veröffentlicht in: | Cell 1986-08, Vol.46 (5), p.785-794 |
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| container_issue | 5 |
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| container_title | Cell |
| container_volume | 46 |
| creator | Blair, D.G. Oskarsson, M.K. Seth, A. Dunn, K.J. Dean, M. Zweig, M. Tainsky, M.A. Vande Woude, G.F. |
| description | The human homology, c-
mos
hu, of the mouse cellular
mos proto-oncogene (c-
mos
mu) transforms NIH 3T3 cells at low efficiency. Furthermore, the c-
mos
hu-induced foci are less distinct, and transformed cells contain a high level of human
mos protein. The transforming activity of hybrid
mos genes derived from human and mouse sequences reveals three domains within the coding region, as well as a negative regulatory sequence upstream from the c-
mos
hu ORF that reduces its transforming efficiency. The
mos C-terminal region, however, which contains the
src-kinase homology domain, appears to have the greatest influence on transforming efficiency. The low transforming efficiency of c-
mos
hu may provide a selective advantage to the host, but it also may indicate a reduced or modified function of
mos in humans. |
| doi_str_mv | 10.1016/0092-8674(86)90354-5 |
| format | Article |
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mos
hu, of the mouse cellular
mos proto-oncogene (c-
mos
mu) transforms NIH 3T3 cells at low efficiency. Furthermore, the c-
mos
hu-induced foci are less distinct, and transformed cells contain a high level of human
mos protein. The transforming activity of hybrid
mos genes derived from human and mouse sequences reveals three domains within the coding region, as well as a negative regulatory sequence upstream from the c-
mos
hu ORF that reduces its transforming efficiency. The
mos C-terminal region, however, which contains the
src-kinase homology domain, appears to have the greatest influence on transforming efficiency. The low transforming efficiency of c-
mos
hu may provide a selective advantage to the host, but it also may indicate a reduced or modified function of
mos in humans.</description><identifier>ISSN: 0092-8674</identifier><identifier>EISSN: 1097-4172</identifier><identifier>DOI: 10.1016/0092-8674(86)90354-5</identifier><identifier>PMID: 2874888</identifier><identifier>CODEN: CELLB5</identifier><language>eng</language><publisher>Cambridge, MA: Elsevier Inc</publisher><subject>Animals ; Base Sequence ; Biological and medical sciences ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Cell Transformation, Neoplastic ; DNA, Recombinant - physiology ; Fundamental and applied biological sciences. Psychology ; Genes, Synthetic ; Humans ; Mice ; Molecular and cellular biology ; Oncogenes ; Poly A - biosynthesis ; Promoter Regions, Genetic ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - physiology ; Proto-Oncogenes ; Recombinant Proteins - biosynthesis ; RNA, Messenger - biosynthesis ; Transfection</subject><ispartof>Cell, 1986-08, Vol.46 (5), p.785-794</ispartof><rights>1986</rights><rights>1987 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c417t-35b72558018f1eedc4a9a0f18ff18e2545494b134ba15e7f0192ed53fa8338a73</citedby><cites>FETCH-LOGICAL-c417t-35b72558018f1eedc4a9a0f18ff18e2545494b134ba15e7f0192ed53fa8338a73</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(86)90354-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8252028$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2874888$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blair, D.G.</creatorcontrib><creatorcontrib>Oskarsson, M.K.</creatorcontrib><creatorcontrib>Seth, A.</creatorcontrib><creatorcontrib>Dunn, K.J.</creatorcontrib><creatorcontrib>Dean, M.</creatorcontrib><creatorcontrib>Zweig, M.</creatorcontrib><creatorcontrib>Tainsky, M.A.</creatorcontrib><creatorcontrib>Vande Woude, G.F.</creatorcontrib><title>Analysis of the transforming potential of the human homolog of mos</title><title>Cell</title><addtitle>Cell</addtitle><description>The human homology, c-
mos
hu, of the mouse cellular
mos proto-oncogene (c-
mos
mu) transforms NIH 3T3 cells at low efficiency. Furthermore, the c-
mos
hu-induced foci are less distinct, and transformed cells contain a high level of human
mos protein. The transforming activity of hybrid
mos genes derived from human and mouse sequences reveals three domains within the coding region, as well as a negative regulatory sequence upstream from the c-
mos
hu ORF that reduces its transforming efficiency. The
mos C-terminal region, however, which contains the
src-kinase homology domain, appears to have the greatest influence on transforming efficiency. The low transforming efficiency of c-
mos
hu may provide a selective advantage to the host, but it also may indicate a reduced or modified function of
mos in humans.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Cell Transformation, Neoplastic</subject><subject>DNA, Recombinant - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genes, Synthetic</subject><subject>Humans</subject><subject>Mice</subject><subject>Molecular and cellular biology</subject><subject>Oncogenes</subject><subject>Poly A - biosynthesis</subject><subject>Promoter Regions, Genetic</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogenes</subject><subject>Recombinant Proteins - biosynthesis</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Transfection</subject><issn>0092-8674</issn><issn>1097-4172</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1PxCAQhonR6PrxDzTpwRg9VIFCCxeT1fiVmHjRM2Hp4GLaskJrsv9e6q571AOQ4X1mMnkQOib4kmBSXmEsaS7Kip2L8kLigrOcb6EJwbLKGanoNppskD20H-MHxlhwznfRLhUVE0JM0M20080yuph5m_VzyPqgu2h9aF33ni18D13vdPObzodWd9nct77x7-Nn6-Mh2rG6iXC0fg_Q2_3d6-1j_vzy8HQ7fc5N2qbPCz6rKOcCE2EJQG2YlhrbVKUDlDPOJJuRgs004VBZTCSFmhdWi6IQuioO0Nlq7iL4zwFir1oXDTSN7sAPUVWllFSW7F-QMMFxgcsEshVogo8xgFWL4FodlopgNTpWo0A1CkyX-nGseGo7Wc8fZi3Um6a11JSfrnMdjW5sMmpc3GCCcorpiF2vMEjSvhwEFY2DzkDtAphe1d79vcc3o0OWmA</recordid><startdate>19860829</startdate><enddate>19860829</enddate><creator>Blair, D.G.</creator><creator>Oskarsson, M.K.</creator><creator>Seth, A.</creator><creator>Dunn, K.J.</creator><creator>Dean, M.</creator><creator>Zweig, M.</creator><creator>Tainsky, M.A.</creator><creator>Vande Woude, G.F.</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>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19860829</creationdate><title>Analysis of the transforming potential of the human homolog of mos</title><author>Blair, D.G. ; Oskarsson, M.K. ; Seth, A. ; Dunn, K.J. ; Dean, M. ; Zweig, M. ; Tainsky, M.A. ; Vande Woude, G.F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-35b72558018f1eedc4a9a0f18ff18e2545494b134ba15e7f0192ed53fa8338a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Cell Transformation, Neoplastic</topic><topic>DNA, Recombinant - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genes, Synthetic</topic><topic>Humans</topic><topic>Mice</topic><topic>Molecular and cellular biology</topic><topic>Oncogenes</topic><topic>Poly A - biosynthesis</topic><topic>Promoter Regions, Genetic</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogenes</topic><topic>Recombinant Proteins - biosynthesis</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Blair, D.G.</creatorcontrib><creatorcontrib>Oskarsson, M.K.</creatorcontrib><creatorcontrib>Seth, A.</creatorcontrib><creatorcontrib>Dunn, K.J.</creatorcontrib><creatorcontrib>Dean, M.</creatorcontrib><creatorcontrib>Zweig, M.</creatorcontrib><creatorcontrib>Tainsky, M.A.</creatorcontrib><creatorcontrib>Vande Woude, G.F.</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>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Blair, D.G.</au><au>Oskarsson, M.K.</au><au>Seth, A.</au><au>Dunn, K.J.</au><au>Dean, M.</au><au>Zweig, M.</au><au>Tainsky, M.A.</au><au>Vande Woude, G.F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of the transforming potential of the human homolog of mos</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>1986-08-29</date><risdate>1986</risdate><volume>46</volume><issue>5</issue><spage>785</spage><epage>794</epage><pages>785-794</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><coden>CELLB5</coden><abstract>The human homology, c-
mos
hu, of the mouse cellular
mos proto-oncogene (c-
mos
mu) transforms NIH 3T3 cells at low efficiency. Furthermore, the c-
mos
hu-induced foci are less distinct, and transformed cells contain a high level of human
mos protein. The transforming activity of hybrid
mos genes derived from human and mouse sequences reveals three domains within the coding region, as well as a negative regulatory sequence upstream from the c-
mos
hu ORF that reduces its transforming efficiency. The
mos C-terminal region, however, which contains the
src-kinase homology domain, appears to have the greatest influence on transforming efficiency. The low transforming efficiency of c-
mos
hu may provide a selective advantage to the host, but it also may indicate a reduced or modified function of
mos in humans.</abstract><cop>Cambridge, MA</cop><pub>Elsevier Inc</pub><pmid>2874888</pmid><doi>10.1016/0092-8674(86)90354-5</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Cell, 1986-08, Vol.46 (5), p.785-794 |
| issn | 0092-8674 1097-4172 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Animals Base Sequence Biological and medical sciences Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Cell Transformation, Neoplastic DNA, Recombinant - physiology Fundamental and applied biological sciences. Psychology Genes, Synthetic Humans Mice Molecular and cellular biology Oncogenes Poly A - biosynthesis Promoter Regions, Genetic Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - physiology Proto-Oncogenes Recombinant Proteins - biosynthesis RNA, Messenger - biosynthesis Transfection |
| title | Analysis of the transforming potential of the human homolog of mos |
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