Productive Replication of Human Adenoviruses in Mouse Epidermal Cells

Ganly, Ian; Mautner, Vivien; Balmain, Allan

doi:10.1128/jvi.74.6.2895-2899.2000

Cited by 52 publications

(39 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In all cases, infection of primary keratinocytes was performed for 1 h in low-calcium medium; keratinocytes were then incubated in low-calcium medium and analyzed 36 h postinfection; switch to high-calcium medium (2 mM) was for 12 h. Given the high susceptibility to adenoviral infection exhibited by keratinocytes p120 Catenin, RhoA, and Epithelial Morphogenesis Vol. 14, May 2003 (Ganly et al, 2000), an m.o.i. of 15-30 was sufficient for a 100% infection of keratinocytes.…”

Section: Adenoviral Infectionmentioning

confidence: 99%

p120 Catenin Is Required for Growth Factor–dependent Cell Motility and Scattering in Epithelial Cells

Cozzolino

Stagni

Spinardi

et al. 2003

MBoC

View full text Add to dashboard Cite

Cadherin-mediated cell-cell adhesion is dynamically modulated during epithelial-mesenchymal transition triggered by activation of receptor tyrosine kinases (RTK) in epithelial cells. Several cadherin-binding proteins have been identified that control cell-cell adhesion. However, the mechanisms by which intercellular adhesion and cell motility are coregulated are still unknown. Here, we delineate a hitherto uncharted cooperation between RTKs, RhoA GTPase, and p120 catenin in instructing a motile behavior to epithelial cells. We found that expression of an N-terminus-deleted p120 catenin in a variety of epithelial cell types, including primary keratinocytes, effectively competes for endogenous p120 at cadherin binding sites and abrogates EGFstimulated cell motility as well as HGF-induced cell scattering. The deleted mutant also inhibits the PI3K-dependent RhoA activation ensuing receptor activation. Conversely, we also show that the ectopic expression of full-length p120 in epithelial cells promotes cytoskeletal changes, stimulates cell motility, and activates RhoA. Both motogenic response to p120 and RhoA activation require coactivation of signaling downstream of RTKs as they are suppressed by ablation of the Ras/PI3K pathway. These studies demonstrate that p120 catenin is a necessary target of RTKs in regulating cell motility and help define a novel pathway leading to RhoA activation, which may contribute to the early steps of metastatic invasion.

show abstract

Section: Adenoviral Infectionmentioning

confidence: 99%

p120 Catenin Is Required for Growth Factor–dependent Cell Motility and Scattering in Epithelial Cells

Cozzolino

Stagni

Spinardi

et al. 2003

MBoC

View full text Add to dashboard Cite

show abstract

“…One approach employs certain permissive murine tumor cell lines grown in immunocompetent animals to study human adenovirus replication. [7][8][9] However, the inefficient replication of human adenovirus in these cell lines, as well as the artificial establishment of these tumors as subcutaneous syngeneic grafts, raises concerns as to how well this model supports human adenovirus replication and how accurately the tumor grafts represent their natural human counterparts. An alternative approach that we have pursued is to use syngeneic Ad vectors in their natural host system.…”

Section: Introductionmentioning

confidence: 99%

Infectivity enhancement for adenoviral transduction of canine osteosarcoma cells

Rivera

Glasgow

et al. 2005

Gene Ther

View full text Add to dashboard Cite

The full realization of conditionally replicative adenoviruses (CRAds) for cancer therapy has been hampered by the limited knowledge of CRAd function in vivo and particularly in an immunocompetent host. To address this issue, we previously proposed a canine adenovirus type 2 (CAV2)-based CRAd for clinical evaluation in canine patients with osteosarcoma (OS). In this study, we evaluated infectivityenhancement strategies to establish the foundation for designing a potent CAV2 CRAd with effective transduction capacity in dog osteosarcoma cells. The results indicate that the native CAV2 fiber-knob can mediate increased binding, and consequently gene transfer, in both canine osteosarcoma immortalized and primary cell lines relative to previously reported Ad5 infectivity-enhancement strategies. Gene delivery was further enhanced by incorporating a polylysine polypeptide onto the carboxy terminus of the CAV2 knob. This vector demonstrated improved gene delivery in osteosarcoma xenograft tumors. These data provide the rationale for generation of infectivity-enhanced syngeneic CAV2 CRAds for clinical evaluation in a dog osteosarcoma model.

show abstract

“…HAdVs can enter but do not replicate in mouse cells. 36,37 Since shRNA-mediated Mdm2 or Mdm4 knockdown improved viral gene expression in permissive human cells (Fig. 1), we wished to assess whether complete knockout of the Mdm2 or Mdm4 gene in mouse cells could also enhance HAdV gene expression.…”

Section: -35mentioning

confidence: 99%

Downregulation of Mdm2 and Mdm4 enhances viral gene expression during adenovirus infection

Yang

Zheng²,

Zhao³

et al. 2012

Cell Cycle

View full text Add to dashboard Cite

Productive Replication of Human Adenoviruses in Mouse Epidermal Cells

Cited by 52 publications

References 19 publications

p120 Catenin Is Required for Growth Factor–dependent Cell Motility and Scattering in Epithelial Cells

p120 Catenin Is Required for Growth Factor–dependent Cell Motility and Scattering in Epithelial Cells

Infectivity enhancement for adenoviral transduction of canine osteosarcoma cells

Downregulation of Mdm2 and Mdm4 enhances viral gene expression during adenovirus infection

Contact Info

Product

Resources

About