ArticleGenome research2001
Genomewide trapping of genes that encode secreted and transmembrane proteins repressed by oncogenic signaling.
Article in Genome research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- High-throughput trapping of secretory pathway genes in mouse embryonic stem cells.Nucleic acids research · 2006Article
- Building a human kinase gene repository: bioinformatics, molecular cloning, and functional validation.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Genomewide production of multipurpose alleles for the functional analysis of the mouse genome.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- A large-scale, gene-driven mutagenesis approach for the functional analysis of the mouse genome.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A retroviral gene trap containing a human CD2 cell surface antigen/neomycin-phosphotransferase fusion gene in the U3 region of its LTR (U3Ceo) was used to screen the mammalian genome for genes encoding secreted and/or transmembrane proteins that are repressed by oncogenic transformation. From an integration library consisting of cells transformable by the insulin-like growth factor 1 (IGF-1), a collection of neomycin resistant (Neo(R)) clones was obtained; 86% also expressed the CD2 cell surface antigen. Molecular analysis of a random sample of Neo(R) clones revealed that the U3Ceo gene trap preferentially disrupted genes coding for secreted and transmembrane proteins. In each case, the signal sequence of the endogenous gene was fused in-frame to the CD2/neomycin-phosphotransferase reporter gene due to a cryptic splice acceptor site embedded in the coding region of the CD2 cDNA. When the library was transformed by IGF-1 and selected against CD2 expression, integrations were obtained in genes that are repressed by transformation. Molecular analysis of six randomly chosen integrations revealed that, in each case, U3Ceo captured a signal sequence from proteins involved in oncogenic transformation and metastatic spread.
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Registered trials
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