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523 results on '"Butel, Janet S."'

21. Cell Transformation by Viruses

Author

Melnick, Joseph L., Butel, Janet S., Tevethia, Satvir S., Biswal, Nilambar, and Benyesh-Melnick, Matilda

Published
1971

23. Lymphotropism of Merkel cell polyomavirus infection, Nova Scotia, Canada

Author

Toracchio, Sonia, Foyle, Annette, Sroller, Vojtech, Reed, Jon A., Wu, Jun, Kozinetz, Claudia A., and Butel, Janet S.

Subjects
Merkel cell carcinoma -- Diagnosis -- Development and progression, Lymph nodes -- Research -- Physiological aspects, Lymphocytes -- Research -- Physiological aspects, Disease susceptibility -- Research, Virus diseases -- Diagnosis -- Development and progression, Health
Abstract

Merkel cell polyomavirus (MCPyV) was first described in 2008 (1) as a new human virus associated with Merkel cell carcinoma (MCC), an uncommon but aggressive form of skin cancer. Subsequent [...]

Published
2010
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25. Bed rest and immunity

Author

Sonnenfeld, Gerald, Aviles, Hernan, Butel, Janet S., Shearer, William T., Niesel, David, Pandya, Utpal, Allen, Christopher, Ochs, Hans D., Blancher, Antoine, and Abbal, Michel

Published
2007
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37. Loss of T-antigen sequences allows SV40-transformed human cells in crisis to acquire a senescent-like phenotype

Author

Rubelj, Ivica, Venable, Susan F., Lednicky, John, Butel, Janet S., Bilyeu, Timothy, Darlington, Gretchen, Surmacz, Ewa, Campisi, Judith, and Pereira-Smith, Olivia M.

Subjects
Cells -- Aging, Promoters (Genetics) -- Research, Cell death -- Research, Health, Seniors
Abstract

Normal human cells transfected with SV40 DNA exhibit an extended proliferative potential compared with controls, but they eventually enter a phase known as 'crisis.' During crisis, extensive cell death occurs and the cells exhibit some gene expression changes similar to senescent cells. This article presents results which indicate that crisis most likely depends on expression of the viral gene T-antigen. We have obtained a unique subpopulation of cells that have deleted the T-antigen gene and, rather than dying as cells do in crisis, remain viable and exhibit some senescent-like characteristics. We also found that the SV40 promoter is poorly expressed in senescent versus young cells. We hypothesize that decreased activity of the viral promoter may result in decreased expression of T-antigen, which is challenged by over-expression of the cell cycle inhibitors such as [p21.sup.Sdi1]. Conflicting signals to proceed/halt cell cycle progression result in the cell death associated with crisis.

Published
1997

38. Apolipoprotein B gene regulatory factor-2 (BRF-2) is structurally and immunologically highly related to hepatitis B virus X associated protein-1 (XAP-1)

Author

Krishnamoorthy, Raghu R., Lee, Teh-Hsiu, Butel, Janet S., and Das, Hriday K.

Subjects
Immunology -- Methods, Hepatitis B virus -- Research, Apolipoproteins -- Research, Biological sciences, Chemistry
Abstract

The apoB gene regulatory factor-2 (BRF-2) was documented by high-performance liquid chromatography to exist in two isoforms, of which the amino acid sequence of the homo-oligomer (BRF-2D) form was found homologous to the hepatitis B virus X associated protein-1 (XAP-1) sequence. The monomoeric form (BRF-FM), however, did not exhibit any sequence specificity. BRF-2 was also found structurally and immunologically related to XAP-1, based on the results of Western Blotting. Thus, the two are considered highly related trans-activators of the apoB gene.

Published
1997

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