DNA-mediated transfer of the adenine phosphoribosyltransferase locus into mammalian cells.

Wigler, Michael; Pellicer, Ángel Antonio Blasco; Silverstein, Saul; Axel, Richard; Urlaub, Gail; Chasin, Lawrence A.

doi:10.1073/pnas.76.3.1373

Cited by 1,195 publications

(519 citation statements)

References 13 publications

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“…The representative transfected cell lines retain the ability to grow in the presence of Geneticin even after passaging through the animals. They are therefore likely to contain an integrated form of the neo gene which is expressed and functional (Wigler et al, 1979). The integration of multiple copies of the plasmid pSV2neo and human S100A4 gene into S5-R37 and S3-R37 cells has been con®rmed by slot hybridization with a S100A4 probe.…”

Section: Discussionmentioning

confidence: 99%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

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The rodent S100-related calcium-binding protein, S100A4 induces metastasis in non-metastatic rat and mouse benign mammary cells and co-operates with benign-tumour-inducing changes in two transgenic mouse models, to yield metastatic mammary tumours. Cotransfection of the human gene for S100A4 with pSV2neo into the benign rat mammary cell line, Rama 37, yielded cells which expressed a low level of the endogenous S100A4 mRNA, and either high or undetectable levels of human S100A4 mRNA. The cells which expressed a high level of human S100A4 mRNA induced metastasis in the benign rat mammary cell line Rama 37 in an in vivo assay, whereas the cells which expressed an undetectable level of human S100A4 did not induce any detectable metastases. The primary tumours arising from the S100A4-expressing cells contained high levels of immunocytochemically-detected S100A4 and this high level of S100A4 and the metastatic potential were maintained when cells from a metastasis were re-injected into syngeneic rats. The results show that the human S100A4 possesses metastasis-inducing capabilities.

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Section: Discussionmentioning

confidence: 99%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

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“…[23][24][25][26][27][28][29][30][31] These studies indicated that transfection of genomic DNA from one cell type to another resulted in integration of the exogenous DNA and stable expression of the trans-ferred genes. This was the case for genes specifying missing enzymes, as well as for genes specifying membraneassociated determinants.…”

Section: Fibroblasts Survived Significantly Longer Than Mice In Variomentioning

confidence: 99%

“…LM-IL-2, LM-IL-2K b and BLK-IL-2 cells were transfected with DNA from the melanoma cells, using the method described by Wigler et al, as described previously. 23 In brief, high molecular weight DNA from the melanoma cells was sheared by three passages through a 25-gauge needle. Afterwards, 100 g of the sheared DNA was mixed with 10 g pHyg (from L Lau, University of Illinois at Chicago), a plasmid that encoded the E. coli enzyme hygromycin B phosphotransferase gene, conferring resistance to hygromycin B, used for selection.…”

Section: Transfection Of the Modified Fibroblast Cell Lines With Genomentioning

confidence: 99%

An optimum anti-melanoma response in mice immunized with fibroblasts transfected with DNA from mouse melanoma cells requires the expression of both syngeneic and allogeneic MHC-determinants

2002

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“…Retrovirus production 293T cells were transiently transfected by either CaPO 4 coprecipitation (Wigler et al, 1979) or TransIT-293 transfection reagent (Mirus corporation) using 1-2 mg pEco and the appropriate MSCV-neo constructs (1-10 mg). For CaPO 4 coprecipitation, cells were transfected for 16 h at 371C, where the media was then aspirated, changed, and cells were grown for an additional 30 h at 371C prior to harvest of the viral supernatant.…”

Section: Plasmid Constructionmentioning

confidence: 99%

GRB2-mediated recruitment of GAB2, but not GAB1, to SF-STK supports the expansion of Friend virus-infected erythroid progenitor cells

et al. 2005

Oncogene

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Friend virus induces the development of erythroleukemia in mice through the interaction of a viral glycoprotein, gp55, with a truncated form of the Stk receptor tyrosine kinase, short form-Stk (Sf-Stk), and the EpoR. We have shown previously that the ability of Sf-Stk to participate in the transformation of Friend virus-infected cells requires the kinase activity and Grb2-binding site of Sf-Stk. Here we show that Grb2 heterozygous mice exhibit decreased susceptibility to Friend erythroleukemia and that expansion of erythroid progenitors in response to infection requires the C-terminal SH3 domain of Grb2. A fusion protein in which the Grb2-binding site in Sf-Stk is replaced by Gab2, supports the growth of progenitors from mice lacking Sf-Stk, whereas a Sf-Stk/Gab1 fusion protein does not. Gab2 is expressed in spleens from Friend virus-infected mice, co-immunoprecipitates with Sf-Stk and is tyrosine phosphorylated in the presence of Sf-Stk. Mice with a targeted deletion in Gab2 are less susceptible to Friend erythroleukemia and the expansion of erythroid progenitor cells in response to infection can be rescued by expression of Gab2, but not Gab1. Taken together, these data indicate that a Sf-Stk/Grb2/Gab2 complex mediates the growth of primary erythroid progenitor cells in response to Friend virus.

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DNA-mediated transfer of the adenine phosphoribosyltransferase locus into mammalian cells.

Cited by 1,195 publications

References 13 publications

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

An optimum anti-melanoma response in mice immunized with fibroblasts transfected with DNA from mouse melanoma cells requires the expression of both syngeneic and allogeneic MHC-determinants

GRB2-mediated recruitment of GAB2, but not GAB1, to SF-STK supports the expansion of Friend virus-infected erythroid progenitor cells

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