The EV-O-Derived Cell Line DF-1 Supports the Efficient Replication of Avian Leukosis-Sarcoma Viruses and Vectors

Schaefer-Klein, Janet; Givol, I; Barsov, Eugene V.; Whitcomb, Jeannette M.; VanBrocklin, Matthew W.; Foster, Douglas N.; Federspiel, Mark J.; Hughes, Stephen H.

doi:10.1006/viro.1998.9291

Cited by 178 publications

(152 citation statements)

References 11 publications

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“…HA-tagged b-cateninS37A cDNA was excised from pMHS37Ab-catenin (Zorn et al, 1999) with Asp718 and Apa1, treated with T4 polymerase to form blunt ends, and cloned into the Pme1 site of the ALV retroviral vector RCAS-Y (Dunn et al, 2000). To produce recombinant retroviruses, the retroviral constructs were transfected into DF-1 chicken fibroblasts as described previously (Himly et al, 1998;Schaefer-Klein et al, 1998). To transduce b-cateninS37A and GFP cDNAs into 293Top cells, supernatants from virus producing DF-1 cells were filtered and diluted 1:1 with fresh growth media before infecting cells plated at 10% confluency.…”

Section: Viral Constructs and Infectionsmentioning

confidence: 99%

FGF-20 and DKK1 are transcriptional targets of β-catenin and FGF-20 is implicated in cancer and development

Chamorro

Schwartz

Vonica

et al. 2004

EMBO J

288

219

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b-catenin is the major effector of the canonical Wnt signaling pathway. Mutations in components of the pathway that stabilize b-catenin result in augmented gene transcription and play a major role in many human cancers. We employed microarrays to identify transcriptional targets of deregulated b-catenin in a human epithelial cell line (293) engineered to produce mutant b-catenin and in ovarian endometrioid adenocarcinomas characterized with respect to mutations affecting the Wnt/b-catenin pathway. Two genes strongly induced in both systems-FGF20 and DKK1-were studied in detail. Elevated levels of FGF20 RNA were also observed in adenomas from mice carrying the Apc Min allele. Both XFGF20 and Xdkk-1 are expressed early in Xenopus embryogenesis under the control of the Wnt signaling pathway. Furthermore, FGF20 and DKK1 appear to be direct targets for b-catenin/TCF transcriptional regulation via LEF/TCF-binding sites. Finally, by using small inhibitory RNAs specific for FGF20, we show that continued expression of FGF20 is necessary for maintenance of the anchorage-independent growth state in RK3E cells transformed by b-catenin, implying that FGF-20 may be a critical element in oncogenesis induced by the Wnt signaling pathway.

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Section: Viral Constructs and Infectionsmentioning

confidence: 99%

FGF-20 and DKK1 are transcriptional targets of β-catenin and FGF-20 is implicated in cancer and development

Chamorro

Schwartz

Vonica

et al. 2004

EMBO J

288

219

View full text Add to dashboard Cite

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“…Large debris was allowed to settle, and single cells were plated and grown in DMEM with 10% FCS (GIBCO BRL). DF-1 cells (gift from D. Foster; Schaefer-Klein et al 1998) were grown in DMEM with 5% FCS, 5% calf serum, 1% chicken serum, and 10% tryptose phosphate broth (GIBCO BRL).…”

Section: Transgenes and Viral Vectorsmentioning

confidence: 99%

Modeling mutations in the G₁ arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a–ARF induces hyperploidy in cultured mouse astrocytes

et al. 1998

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Nearly all human gliomas exhibit alterations in one of three genetic loci governing G 1 arrest: INK4a-ARF, CDK4, or RB. To discern the roles of CDK4 amplification and INK4a-ARF loss in gliomagenesis, we compared the behavior of astrocytes lacking a functional INK4a-ARF locus with astrocytes overexpressing CDK4. Either a deficiency of p16 INK4a and p19 ARF or an increase in Cdk4 allows cultured astrocytes to grow without senescence. Astrocytes overexpressing CDK4 grow more slowly than INK4a-ARF-deficient astrocytes and convert to a tetraploid state at high efficiency; in contrast, INK4a-ARF-deficient cells remain pseudodiploid, consistent with properties observed in human gliomas with corresponding lesions in these genes. Received July 20, 1998; revised version accepted October 14, 1998. Over half of high-grade human gliomas lack a functional INK4a-ARF locus (Jen et al. 1994;Schmidt et al. 1994) and hence can produce neither p16 INK4a nor p19 ARF , the two proteins encoded by this locus (Quelle et al. 1995). Most of the remaining gliomas either lack the RB gene or demonstrate a 10-to 100-fold amplification of the CDK4 locus (He et al. 1994(He et al. , 1995Ichimura et al. 1996). We are developing animal models for gliomagenesis in hopes of understanding these patterns and discerning the contributions made to tumor formation by each abnormality . We have taken advantage of two genetic alterations in mice: disruption of the INK4a-ARF locus by targeted mutation (Serrano et al. 1996) and astrocyte-specific expression of a transgene encoding TVA, the receptor for subgroup A avian leukosis viruses (ALV) (Holland and Varmus 1998). Production of TVA molecules by these cells makes them susceptible to infection by RCAS vectors carrying coding domains for CDK4 and other genes .We have used this gene transfer system to investigate the effects of INK4a-ARF loss and CDK4 overexpression in astrocyte cell culture and to determine whether similarities exist between the cultured cells and human gliomas with similar abnormalities. Results and Discussion Loss of INK4a-ARF and overexpression of CDK4 both immortalize astrocyte culturesTo compare the growth properties of INK4a-ARF-deficient and CDK4-overexpressing astrocytes, we subjected appropriately selected cultures to repeated passage at standard density and counted the number of cells at each passage. Astrocytes overexpressing CDK4 were prepared by infecting primary brain cultures from Gtv-a mice [carrying a tv-a transgene under the control of the astrocytespecific glial fibrillary acidic protein (GFAP) promoter] with an RCAS vector carrying the human CDK4 cDNA (RCAS-cdk4). Cultures of INK4a-ARF-deficient astrocytes were prepared by infecting primary brain cell cultures from Gtv-a transgenic; INK4a-ARF −/− mice with an RCAS vector bearing the puro-R gene (RCAS-puro) ) and selecting for resistance to puromycin. Parallel cultures were prepared by infecting brain cells from Gtv-a transgenic mice with RCAS vectors carrying the alkaline phosphatase (AP) or the basic fibroblast grow...

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“…15,23 Briefly, virus propagation was initiated by transfection of retroviral plasmid constructs into the DF-1 chick fibroblast cell line. 16,17 After several passages of DF-1 cells, the supernatants were collected and concentrated by centrifugation at 22 000 rpm for 3 h in a Beckman SW 28 rotor and stored in aliquots at À801C. Typical virus titers were 1-5 Â 10 8 cfu/ml.…”

Section: Constructs and Virus Generationmentioning

confidence: 99%

“…16,17 A few DF-1 cells appeared to undergo PCD 24 h after the conventional transfection procedure of viral constructs expressing human Bax (hBax). Following several passages, however, DF-1 cells expressing hBax or its fusion protein with enhanced green fluorescent protein (EGFP) could be cultured normally in growth medium although hBax or EGFP-Bax were abundantly expressed in DF-1 cells (Figure 1b).…”

Section: Introductionmentioning

confidence: 99%

Distinct susceptibility of developing neurons to death following Bax overexpression in the chicken embryo

et al. 2005

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Bax is a proapoptotic protein that is required for programmed cell death (PCD) of many neuronal populations. Here we show that, during an early period of retinal PCD and in naturally occurring sensory and motor neuron (MN) death in the spinal cord, Bax delivery results in enhanced death of these neural populations. In contrast, Bax overexpression fails to enhance an early phase of MN death that occurs in the cervical spinal cord, although overexpressed Bax appears to be activated in dying MNs. Bax overexpression does not also affect the survival of immature neurons prior to the PCD period. Taken together, these data provide the first in vivo evidence suggesting that Bax appears to act selectively as an executioner only in neurons undergoing PCD. Furthermore, although Bax appears to mediate the execution pathway for PCD, the effect of Bax overexpression on susceptibility to death differs between different neuronal populations.

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The EV-O-Derived Cell Line DF-1 Supports the Efficient Replication of Avian Leukosis-Sarcoma Viruses and Vectors

Cited by 178 publications

References 11 publications

FGF-20 and DKK1 are transcriptional targets of β-catenin and FGF-20 is implicated in cancer and development

FGF-20 and DKK1 are transcriptional targets of β-catenin and FGF-20 is implicated in cancer and development

Modeling mutations in the G₁ arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a–ARF induces hyperploidy in cultured mouse astrocytes

Distinct susceptibility of developing neurons to death following Bax overexpression in the chicken embryo

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The EV-O-Derived Cell Line DF-1 Supports the Efficient Replication of Avian Leukosis-Sarcoma Viruses and Vectors

Cited by 178 publications

References 11 publications

FGF-20 and DKK1 are transcriptional targets of β-catenin and FGF-20 is implicated in cancer and development

FGF-20 and DKK1 are transcriptional targets of β-catenin and FGF-20 is implicated in cancer and development

Modeling mutations in the G1 arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a–ARF induces hyperploidy in cultured mouse astrocytes

Distinct susceptibility of developing neurons to death following Bax overexpression in the chicken embryo

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Modeling mutations in the G₁ arrest pathway in human gliomas: overexpression of CDK4 but not loss of INK4a–ARF induces hyperploidy in cultured mouse astrocytes