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From The Cell Biology Section, Viral Biology Branch, National Cancer Institute, Bethesda, Maryland 20014
Abstract
G (Gross) leukemia virus-associated surface antigens (G antigens) on AKR virus-induced Fischer rat lymphoma cells were measured with radioiodine-labeled syngeneic antiserum. Treatment of the lymphoma cells with trypsin resulted in a 3-fold increase in the number of surface antigen sites as compared to EDTA-treated cells. An increase in sites was seen after treatment with as low as 0.025 mg/ml trypsin. Prolonged treatment with trypsin did not decrease the number of G surface antigens, although all of the sites could be removed from the cells by treatment with papain. No increase in the number of antigen sites was observed after neuraminidase treatment of the cells. Blocking experiments with C57BL/6 anti-K36 (G-typing) mouse serum confirmed that the majority of the sites remaining on the cells after trypsin treatment were G cell surface antigens (GCSA). G antigens were also released from the cells by treatment with either trypsin or papain. Released G antigens were sensitive to degradation by trypsin.
Footnotes
1 This work was taken from a dissertation submitted by the first author to the Graduate School, Temple University, Philadelphia, Pennsylvania, in partial fulfillment of the requirements for the Ph.D. degree.
2 Present address: Immunology Section, Viral Leukemia and Lymphoma Branch, National Cancer Institute, Bethesda, Maryland 20014.
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