Abstract
In this report we demonstrate that lowered expression of the H-2 antigens on RadLV-induced tumour cells is a result of depressed levels of stable mRNA in these cells. Whether this observation is a result of lowered transcription or of mRNA instability is under investigation. In an effort to determine which viral sequences are essential for mediating both the H-2 regulatory function and the transforming function of RadLV, we have begun to assemble newly integrated proviral genomes from tumours. The restriction enzyme cleavage sites of four isolates are presented; these isolates differ substantially from RadLV genomes previously presented. One of these molecular clones is shown to encode a non-defective B-tropic, ecotropic virus which when reinjected into resistant mouse strains can mediate the up-regulation of H-2Dd antigen expression. Finally, possible mechanisms of H-2 regulation are discussed.
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