SV40 Virus Transformation of Genetic Mutant Cell Cultures1

2015 ◽  
pp. 248-252
Author(s):  
Arthur E. Greene ◽  
Marion Manduka ◽  
Lewis L. Coriell
Keyword(s):  
Mutant Cell ◽  
Sv40 Virus ◽  
Virus Transformation

Fixation of cellular aging processes by SV40 virus transformation

1980 ◽  
Vol 12 (2) ◽  
pp. 197-209 ◽  
Author(s):  
Hideko Kaji ◽  
Hiroto Hara ◽  
Kim D. Lamon
Keyword(s):  
Cellular Aging ◽  
Sv40 Virus ◽  
Virus Transformation

An embryo protein induced by SV40 virus transformation of mouse cells

Nature ◽  
1980 ◽  
Vol 288 (5792) ◽  
pp. 722-724 ◽  
Author(s):  
Peter T. Mora ◽  
K. Chandrasekaran ◽  
Vivian W. McFarland
Keyword(s):  
Sv40 Virus ◽  
Mouse Cells ◽  
Virus Transformation

scholarly journals SV40 virus transformation down-regulates endothelin receptor

1999 ◽  
Vol 1450 (1) ◽  
pp. 35-44 ◽  
Author(s):  
William J. Chiou ◽  
Jiahong Wang ◽  
Cathleen E. Berg ◽  
Jinshyun R. Wu-Wong
Keyword(s):  
Endothelin Receptor ◽  
Sv40 Virus ◽  
Virus Transformation

scholarly journals Fibrils attached to the nuclear pore prevent egress of SV40 particles from the infected nucleus.

1976 ◽  
Vol 70 (3) ◽  
pp. 714-719 ◽  
Author(s):  
G G Maul
Keyword(s):  
Nuclear Pore Complex ◽  
Nuclear Pore ◽  
High Concentration ◽  
Sv40 Virus ◽  
Productive Phase

SV40 particles can apparently enter the nucleus intact. However, they do not leave the nucleus despite the high concentration present during the productive phase. We found structural evidence that SV40 virus is prevented from approaching the most likely site of exit, the nuclear pore complex. From these images, it is concluded that the fibrils attached to the nuclear pore complex prevent egress of SV40 particles from the infected nucleus.

scholarly journals Akt kinase LANCL2 functions as a key driver in EGFR-mutant lung adenocarcinoma tumorigenesis

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Yuqing Lou ◽  
Jianlin Xu ◽  
Yanwei Zhang ◽  
Wei Zhang ◽  
Xueyan Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Line ◽  
Quantitative Polymerase Chain Reaction ◽  
Mutant Cell ◽  
A549 Cells ◽  
The Cancer Genome Atlas ◽  
Akt Kinase ◽  
Egfr Expression

AbstractEpidermal growth factor receptor (EGFR) is a key oncogene in lung adenocarcinoma (LUAD). Resistance to EGFR tyrosine kinase inhibitors is a major obstacle for EGFR-mutant LUAD patients. Our gene chip array, quantitative polymerase chain reaction validation, and shRNA-based high-content screening identified the Akt kinase lanthionine synthetase C-like protein 2 (LANCL2) as a pro-proliferative gene in the EGFR-mutant LUAD cell line PC9. Therefore, we investigated whether LANCL2 plays a role in promoting cell proliferation and drug resistance in EGFR-mutant LUAD. In silico clinical correlation analysis using the Cancer Genome Atlas Lung Adenocarcinoma dataset revealed a positive correlation between LANCL2 and EGFR expression and an inverse relationship between LANCL2 gain-of-function and survival in LUAD patients. The EGFR-mutant LUAD cell lines PC9 and HCC827 displayed higher LANCL2 expression than the non-EGFR-mutant cell line A549. In addition, LANCL2 was downregulated following gefitinib+pemetrexed combination therapy in PC9 cells. LANCL2 knockdown reduced proliferation and enhanced apoptosis in PC9, HCC827, and A549 cells in vitro and suppressed murine PC9 xenograft tumor growth in vivo. Notably, LANCL2 overexpression rescued these effects and promoted gefitinib + pemetrexed resistance in PC9 and HCC827 cells. Pathway analysis and co-immunoprecipitation followed by mass spectrometry of differentially-expressed genes in LANCL2 knockdown cells revealed enrichment of several cancer signaling pathways. In addition, Filamin A and glutathione S-transferase Mu 3 were identified as two novel protein interactors of LANCL2. In conclusion, LANCL2 promotes tumorigenic proliferation, suppresses apoptosis, and promotes gefitinib+pemetrexed resistance in EGFR-mutant LUAD cells. Based on the positive association between LANCL2, EGFR, and downstream Akt signaling, LANCL2 may be a promising new therapeutic target for EGFR-mutant LUAD.

scholarly journals A mammalian mutant cell lacking detectable lanosterol 14 alpha-methyl demethylase activity.

1988 ◽  
Vol 263 (3) ◽  
pp. 1248-1254
Author(s):  
H W Chen ◽  
D A Leonard ◽  
R T Fischer ◽  
J M Trzaskos
Keyword(s):  
Mutant Cell ◽  
Demethylase Activity
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