scholarly journals Vectors bicistronically linking a gene of interest to the SV40 large T antigen in combination with the SV40 origin of replication enhance transient protein expression and luciferase reporter activity

BioTechniques ◽  
2011 ◽  
Author(s):  
Matthew Mahon
Keyword(s):  
Protein Expression ◽  
T Antigen ◽  
Luciferase Reporter ◽  
Origin Of Replication ◽  
Large T Antigen ◽  
Sv40 Large T Antigen ◽  
Reporter Activity ◽  
Transient Protein Expression ◽  
Sv40 Origin

scholarly journals Protein expression of the RB-related gene family and SV40 large T antigen in mesothelioma and lung cancer

Oncogene ◽  
2000 ◽  
Vol 19 (40) ◽  
pp. 4632-4639 ◽  
Author(s):  
Sanjay Modi ◽  
Akihito Kubo ◽  
Herbert Oie ◽  
Amy B Coxon ◽  
Ahad Rehmatulla ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Gene Family ◽  
T Antigen ◽  
Large T Antigen ◽  
Related Gene ◽  
Sv40 Large T Antigen

scholarly journals SV40 Large T Antigen Is Not Responsible for the Loss of STING in 293T Cells but Can Inhibit cGAS-STING Interferon Induction

Viruses ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 137 ◽  
Author(s):  
Joshua B. Reus ◽  
Guillermo S. Trivino-Soto ◽  
Lily I. Wu ◽  
Kristiana Kokott ◽  
Efrem S. Lim
Keyword(s):  
T Antigen ◽  
Large T Antigen ◽  
Sv40 Large T Antigen ◽  
Dna Viruses ◽  
Antiviral Responses ◽  
Interferon Induction ◽  
Sv40 Origin ◽  
Immune Pathway ◽  
Sting Pathway ◽  
Lxcxe Motif

Several DNA viruses have evolved antagonists to inhibit the cyclic GMP–AMP synthase (cGAS)-stimulator of interferon genes (STING) DNA-sensing immune pathway. This includes DNA viral oncogenes that antagonize the cGAS-STING pathway by binding STING through the LxCxE motif. The 293T human cells are widely used in biology studies as they are highly transfectable. While parental 293 cells express high levels of STING, 293T cells lack STING and are unable to induce interferon antiviral responses to cytosolic DNA. Additionally, 293T cells express the SV40 polyomavirus large T antigen (LT) which enhances the replication of transfected DNA plasmids carrying the SV40 origin of replication. Since SV40 LT also encodes the LxCxE motif, the lack of STING expression in 293T cells is commonly assumed to be due to SV40 large T antigen. We find that SV40 LT does not alter exogenously expressed and endogenous levels of STING protein. We show that STING transcription is suppressed in 293T cells but is not driven by SV40. This study also revealed that SV40 LT does indeed inhibit cGAS-STING interferon induction, but through a mechanism distinct from other DNA virus oncogenes. Collectively, these results indicate that while SV40 LT can inhibit cGAS-STING interferon induction, it does so in an unanticipated manner.

scholarly journals Acitretin and Retinoic Acid Derivatives Inhibit BK Polyomavirus Replication in Primary Human Proximal Renal Tubular Epithelial and Urothelial Cells

2021 ◽  
Author(s):  
Zongsong Wu ◽  
Fabrice E Graf ◽  
Hans H. Hirsch
Keyword(s):  
Retinoic Acid ◽  
Protein Expression ◽  
Hemorrhagic Cystitis ◽  
Vero Cells ◽  
T Antigen ◽  
Large T Antigen ◽  
Urothelial Cells ◽  
Sv40 Large T Antigen ◽  
Treatment And Prevention ◽  
Bk Polyomavirus

Small-molecule drugs inhibiting BK polyomavirus (BKPyV) represent a significant unmet clinical need in view of polyomavirus-associated nephropathy or hemorrhagic cystitis which complicate 5% to 25% of kidney and hematopoietic cell transplantations. We characterized the inhibitory activity of acitretin on BKPyV-replication in primary human renal proximal tubular epithelial cells (RPTECs). Effective inhibitory concentration 50% (EC50) and 90% (EC90) were determined in dilution series measuring BKPyV loads, transcripts and protein expression, using cell proliferation, metabolic activity, and viability to estimate cytotoxic concentrations and selectivity indices (SI). Acitretin EC50 and EC90 in RPTECs were 0.64 (SI50 250) and 3.25 μM (SI90 49.2), respectively. Acitretin effectively inhibited BKPyV-replication until 72 h post-infection when added 24 h before until 12 h after infection, but decreased to <50% at later timepoints. Acitretin did not interfere with nuclear delivery of BKPyV genomes, but decreased large T-antigen transcription and protein expression. Acitretin did not inhibit the initial round of BKPyV-replication following transfection of full-length viral genomes, but affected subsequent rounds of re-infection. Acitretin also inhibited BKPyV-replication in human urothelial cells and in Vero cells, but not in COS-7 cells constitutively expressing SV40-large T-antigen. Retinoic acid-agonists (all-trans-retinoic acid, 9-cis-RA, 13-cis-RA, bexarotene, tamibarotene) and the RAR/RXR-antagonist RO41-5253 also inhibited BKPyV-replication, pointing to as yet undefined mechanism. Importance Acitretin selectively inhibits BKPyV-replication in primary human cell culture models of nephropathy and hemorrhagic cystitis. Since acitretin is an approved drug in clinical use reaching BKPyV-inhibiting concentrations in systemically treated patients, further studies are warranted to provide data for clinical repurposing of retinoids for treatment and prevention of replicative BKPyV-diseases.

Retroviral transduction of human periodontal cells with a temperature-sensitive SV40 large T antigen

1999 ◽  
Vol 44 (10) ◽  
pp. 823-834 ◽  
Author(s):  
M.H. Parkar ◽  
L. Kuru ◽  
M. O’Hare ◽  
H.N. Newman ◽  
F. Hughes ◽  
...  
Keyword(s):  
T Antigen ◽  
Temperature Sensitive ◽  
Large T Antigen ◽  
Sv40 Large T Antigen ◽  
Retroviral Transduction
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