Nucleotide Sequence of the p21 Transforming Protein of Harvey Murine Sarcoma Virus

Abstract

Harvey murine sarcoma virus is a retrovirus which transforms cells by means of a single virally encoded protein called p21 has. We have determined the nucleotide sequence of 1.0 kilobase in the 5' half of the viral genome which encompasses the has coding sequences and its associated regulatory signals. The nucleotide sequence has identified the amino acid sequence of two additional overlapping polypeptides which share their reading frames and the carboxyl termini with p21 but which contain additional NH2-terminal amino acids.

Expression of v-Ha-ras driven by the calcitonin/calcitonin gene-related peptide promoter: a novel transgenic murine model for medullary thyroid carcinoma

“…The rascal transgene, shown schematically in Figure 1, consists of three components; 2041 base pairs of the calcitonin/CGRP gene from 71934 to +107 bases around the transcriptional start site (at +1), 1013 bases of v-Ha-ras containing the coding sequence of p21, and 847 bases containing the early mRNA polyadenylation signals of the SV40 T antigen (Amara et al, 1984;Kimura et al, 1995;Berk and Sharp, 1978;Dhar et al, 1982). Five independent lineages have been derived.…”

“…Mutation of ras family members at speci®c residues activate them as oncogenes capable of transforming cells both in vivo and in vitro. v-Ha-ras, the viral homologue of c-Ha-ras, is mutated at residues 12 and 59 (Dhar et al, 1982). Transfection of v-Ha-ras into neural and neuroendocrine cell lines can lead to morphological and biochemical changes consistent with cell di erentiation.…”

Transcription of two classes of rat growth hormone gene-associated repetitive DNA: differences in activity and effects of tandem repeat structure

“…1). Another single TR is found 300-500 bp beyond the rGH gene polyadenylation signal ( The putative 'identifier" sequence is equivalent to the rGH TR sequences and therefore is a member of the TR family (3,(7)(8)(9)(10)(11)(12)(13)(14)(15).…”

An appraisal of the application of recombinant DNA techniques to chromosome defects

“…The ability of the viral oncogenes to transform may result from inappropriate expression of a normal gene product (Huebner & Todaro, 1969;Vande Woude et al, 1980), or from subtle differences between the viral oncogenes and their cellular counterparts (Schwartz et al, 1983;Takeya & Hanafusa, 1983;Ellis et al, 1982;Dhar et al, 1982;Capon et al, 1983). Regarding the idea of gene activation in carcinogenesis, translocation events represent one apparent means of activation and are the best studied chromosomal rearrangements involved in tumour development.…”