Lindsay J. Georgopoulos
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Lindsay J. Georgopoulos has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Bo Nilsson
Department of Immunology, Genetics, and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden
1 shared publication - George Eric Blair
School of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, UK
1 shared publication Graciela Elgue
Institute of Oncology, Radiology and Clinical Immunology, Rudbeck Laboratory, 751 85 Uppsala, Sweden
1 shared publication- Janet Strath
Institute of Molecular and Cellular Biology, University of Leeds, Leeds, LS2 9JT, UK
1 shared publication Javier Sanchez
Institute of Oncology, Radiology and Clinical Immunology, Rudbeck Laboratory, 751 85 Uppsala, Sweden
1 shared publication- John D. Lambris
University of Pennsylvania
1 shared publication
Latest Publications
- 8 August 2009
- Published by Elsevier in Molecular Immunology
- Vol. 46 (15) , 2911-2917
Preclinical evaluation of innate immunity to baculovirus gene therapy vectors in whole human blood
- 8 August 2009
- Published by Elsevier in Molecular Immunology
- Vol. 46 (15) , 2911-2917
Preclinical evaluation of innate immunity to baculovirus gene therapy vectors in whole human blood
- Open Access
- 6 February 2009
- Published by Springer Nature in BMC Genomics
- Vol. 10 (1) , 67
Identification of genes differentially expressed as result of adenovirus type 5- and adenovirus type 12-transformation
Background: Cells transformed by human adenoviruses (Ad) exhibit differential capacities to induce tumours in immunocompetent rodents; for example, Ad12-transformed rodent cells are oncogenic whereas Ad5-transformed cells are not. The E1A gene determines oncogenic phenotype, is a transcriptional regulator and dysregulates host cell gene expression, a key factor in both cellular transformation and oncogenesis. To reveal differences in gene expression between cells transformed with oncogenic and non-oncogenic adenoviruses we have performed comparative analysis of transcript profiles with the aim of identifying candidate genes involved in the process of neoplastic transformation.Results: Analysis of microarray data revealed that a total of 232 genes were differentially expressed in Ad12 E1- or Ad5 E1-transformed BRK cells compared to untransformed baby rat kidney (BRK) cells. Gene information was available for 193 transcripts and using gene ontology (GO) classifications and literature searches it was possible to assign known or suggested functions to 166 of these identified genes. A subset of differentially-expressed genes from the microarray was further examined by real-time PCR and Western blotting using BRK cells immortalised by Ad12 E1A or Ad5 E1A in addition to Ad12 E1- or Ad5 E1-transformed BRK cells. Up-regulation of RelA and significant dysregulation of collagen type I mRNA transcripts and proteins were found in Ad-transformed cells.Conclusion: These results suggest that a complex web of cellular pathways become altered in Ad-transformed cells and that Ad E1A is sufficient for the observed dysregulation. Further work will focus on investigating which splice variant of Ad E1A is responsible for the observed dysregulation at the pathway level, and the mechanisms of E1A-mediated transcriptional regulation.
- 6 February 2009
- Published by Springer Nature in BMC Genomics
- Vol. 10 (1) , 67
Open AccessIdentification of genes differentially expressed as result of adenovirus type 5- and adenovirus type 12-transformation
Background: Cells transformed by human adenoviruses (Ad) exhibit differential capacities to induce tumours in immunocompetent rodents; for example, Ad12-transformed rodent cells are oncogenic whereas Ad5-transformed cells are not. The E1A gene determines oncogenic phenotype, is a transcriptional regulator and dysregulates host cell gene expression, a key factor in both cellular transformation and oncogenesis. To reveal differences in gene expression between cells transformed with oncogenic and non-oncogenic adenoviruses we have performed comparative analysis of transcript profiles with the aim of identifying candidate genes involved in the process of neoplastic transformation.Results: Analysis of microarray data revealed that a total of 232 genes were differentially expressed in Ad12 E1- or Ad5 E1-transformed BRK cells compared to untransformed baby rat kidney (BRK) cells. Gene information was available for 193 transcripts and using gene ontology (GO) classifications and literature searches it was possible to assign known or suggested functions to 166 of these identified genes. A subset of differentially-expressed genes from the microarray was further examined by real-time PCR and Western blotting using BRK cells immortalised by Ad12 E1A or Ad5 E1A in addition to Ad12 E1- or Ad5 E1-transformed BRK cells. Up-regulation of RelA and significant dysregulation of collagen type I mRNA transcripts and proteins were found in Ad-transformed cells.Conclusion: These results suggest that a complex web of cellular pathways become altered in Ad-transformed cells and that Ad E1A is sufficient for the observed dysregulation. Further work will focus on investigating which splice variant of Ad E1A is responsible for the observed dysregulation at the pathway level, and the mechanisms of E1A-mediated transcriptional regulation.