@article {709,
	title = {MHC class I molecules are enriched in caveolae but do not enter with simian virus 40.},
	journal = {J Gen Virol},
	volume = {79 ( Pt 6)},
	year = {1998},
	month = {1998 Jun},
	pages = {1469-77},
	abstract = {Simian virus 40 (SV40) binds to MHC class I molecules anywhere on the cell surface and then enters through caveolae. The fate of class I molecules after SV40 binding is not known. Sensitivity of 125I-surface-labelled class I molecules to papain cleavage was used to distinguish internalized class I molecules from class I molecules remaining at the cell surface. Whereas the caveolae-enriched membrane microdomain was found to also be enriched for class I molecules, no internalized papain-resistant 125I-surface-labelled class I molecules could be detected at any time in either control cells or in cells preadsorbed with saturating amounts of SV40. Instead, 125I-surface-labelled class I molecules, as well as preadsorbed 125I-labelled anti-class I antibodies, accumulated in the medium, coincident with the turnover of class I molecules at the cell surface. The class I heavy chains that accumulated in the medium were truncated and their release was specifically prevented by the metalloprotease inhibitor 1,10-phenanthroline. Thus, whereas class I molecules mediate SV40 binding, they do not appear to mediate SV40 entry.},
	keywords = {Animals, Caveolin 1, Caveolins, Cell Line, Cell Membrane, Cercopithecus aethiops, Histocompatibility Antigens Class I, Humans, Membrane Proteins, Simian virus 40},
	issn = {0022-1317},
	author = {Anderson, H A and Chen, Y and Norkin, L C}
}
@article {708,
	title = {Bound simian virus 40 translocates to caveolin-enriched membrane domains, and its entry is inhibited by drugs that selectively disrupt caveolae.},
	journal = {Mol Biol Cell},
	volume = {7},
	year = {1996},
	month = {1996 Nov},
	pages = {1825-34},
	abstract = {Simian virus 40 (SV40) entry leading to infection occurred only after the virus was at the cell surface for 1.5 to 2 h. SV40 infectious entry was not sensitive to cytosol acidification, a treatment that blocks endocytosis via clathrin-coated vesicles. Instead, SV40 infectious entry was blocked by treating cells with the phorbol ester PMA or nystatin, which selectively disrupts caveolae. In control experiments, transferrin internalization was sensitive to cytosol acidification but was not sensitive to PMA or nystatin. Also, absorbed transferrin entered cells within minutes. Finally, bound SV40 translocated to caveolin-enriched membrane complexes isolated by a Triton X-100 insolubility protocol. Treatment with nystatin did not impair SV40 binding but did block the partitioning of virus into the caveolin-enriched complexes.},
	keywords = {Animals, Antigens, Polyomavirus Transforming, Caveolin 1, Caveolins, Cell Line, Cell Membrane, Coated Vesicles, Endocytosis, Membrane Proteins, Nystatin, Organelles, Simian virus 40, Tetradecanoylphorbol Acetate},
	issn = {1059-1524},
	author = {Anderson, H A and Chen, Y and Norkin, L C}
}
@article {707,
	title = {Extracellular simian virus 40 induces an ERK/MAP kinase-independent signalling pathway that activates primary response genes and promotes virus entry.},
	journal = {J Gen Virol},
	volume = {77 ( Pt 9)},
	year = {1996},
	month = {1996 Sep},
	pages = {2173-82},
	abstract = {Simian virus 40 (SV40) binding to growth-arrested cells activated an intracellular signalling pathway that induced the up-regulation of the primary response genes c-myc, c-jun and c-sis within 30 min and of JE within 90 min. The up-regulation of the primary response genes occurred in the presence of cycloheximide and when UV-inactivated SV40 was adsorbed to cells. SV40 binding did not activate Raf or mitogen-activated protein kinase (MAP/ERK1), or mobilize intracellular Ca2+. The SV40-induced up-regulation of c-myc and c-jun was blocked by the tyrosine kinase inhibitor, genistein, and by the protein kinase C (PKC) inhibitor, calphostin C, but not by expression of the MAP kinase-specific phosphatase, MKP-1. These results suggest that the SV40-induced signalling pathway includes the activities of a tyrosine kinase and a Ca(2+)-independent isoform of PKC, but not of Raf or MAP kinase. Finally, SV40 infectious entry into cells was specifically and reversibly blocked by genistein.},
	keywords = {Animals, Calcium, Calcium-Calmodulin-Dependent Protein Kinases, Cell Cycle Proteins, Cell Line, Cercopithecus aethiops, Dual Specificity Phosphatase 1, Enzyme Inhibitors, Gene Expression Regulation, Viral, Genistein, Humans, Immediate-Early Proteins, Isoflavones, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinases, Naphthalenes, Phosphoprotein Phosphatases, Platelet-Derived Growth Factor, Protein Kinase C, Protein Phosphatase 1, Protein Tyrosine Phosphatases, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-jun, Proto-Oncogene Proteins c-myc, Proto-Oncogene Proteins c-raf, Proto-Oncogene Proteins c-sis, Signal Transduction, Simian virus 40, Up-Regulation},
	issn = {0022-1317},
	author = {Dangoria, N S and Breau, W C and Anderson, H A and Cishek, D M and Norkin, L C}
}
@article {706,
	title = {Multiple stages of virus-receptor interactions as shown by simian virus 40.},
	journal = {Adv Exp Med Biol},
	volume = {408},
	year = {1996},
	month = {1996},
	pages = {159-67},
	keywords = {Animals, Cell Membrane, Histocompatibility Antigens Class I, Humans, Receptors, Virus, Signal Transduction, Simian virus 40},
	issn = {0065-2598},
	author = {Norkin, L C and Anderson, H A}
}
