Rotter, Varda and Boss, Michael A. and Baltimore, David (1981) Increased concentration of an apparently identical cellular protein in cells transformed by either Abelson murine leukemia virus or other transforming agents. Journal of Virology, 38 (1). pp. 336-346. ISSN 0022-538X. http://resolver.caltech.edu/CaltechAUTHORS:ROTjvir81
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Abelson murine leukemia virus (A-MuLV)-transformed cells, simian virus 40 (SV40)-transformed cells, and chemically transformed cells all have increased levels of a 50,000-molecular-weight host cell protein. The protein was detected with sera raised to the A-MuLV-transformed and chemically transformed cells and was tightly bound to T-antigen in extracts of SV40-transformed cells. Partial protease digests showed that the proteins from all three sources were indistinguishable. The three proteins were phosphorylated in cells, and the linkage of phosphate to the A-MuLV-associated P50 was to a serine residue. By immunofluorescence methods, P50-related protein was found on the surface of both normal lymphoid cells and A-MuLV-transformed lymphoid cells, but cell fractionation showed that the majority of P50 was free in the cytoplasm of the transformed cells. Immunofluorescence also showed that P50 was found in granules in the cytoplasm of both untransformed and SV40-transformed fibroblasts. Other cells gave indistinct patterns. Cocapping experiments showed that the A-MuLV-specified P120 protein is weakly associated with the surface P50-related protein of lymphoid cells, but no association of P120 and P50 could be demonstrated by immunoprecipitation methods. Although a monoclonal antiserum to P50 was used in many of these studies, the identity of the bulk P50 protein with the molecules that are reactive at the cell surface requires further study.
|Additional Information:||Copyright © 1981 by the American Society for Microbiology. Received 13 November 1980/Accepted 7 January 1981 We thank A. Levine and A. DeLeo for providing some of the cell lines and antisera used in this work. This research was supported by American Cancer Society grant #MV-34L and by Public Health Service grant CA-14051 from the National Cancer Institute (to S. E. Luria). V.R. was supported by Public Health Service International Research Fellowship 02765. M.B. was supported by a Science Research Council/NATO postdoctoral fellowship.|
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|Deposited On:||14 Apr 2006|
|Last Modified:||26 Dec 2012 08:50|
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