scholarly journals Nucleotide sequence and biochemical activities of the Moloney murine sarcoma virus strain HT-1 mos gene.

1985 ◽  
Vol 56 (1) ◽  
pp. 144-152 ◽  
Author(s):  
A Seth ◽  
G F Vande Woude
1992 ◽  
Vol 66 (9) ◽  
pp. 5329-5337 ◽  
Author(s):  
L Huai ◽  
S M Chiocca ◽  
M A Gilbreth ◽  
J R Ainsworth ◽  
L A Bishop ◽  
...  

1985 ◽  
Vol 53 (3) ◽  
pp. 984-987 ◽  
Author(s):  
E P Reddy ◽  
D Lipman ◽  
P R Andersen ◽  
S R Tronick ◽  
S A Aaronson

1985 ◽  
Vol 5 (8) ◽  
pp. 1959-1968 ◽  
Author(s):  
B J Graves ◽  
S P Eisenberg ◽  
D M Coen ◽  
S L McKnight

The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.


1986 ◽  
Vol 6 (5) ◽  
pp. 1706-1710 ◽  
Author(s):  
M Ruta ◽  
R Wolford ◽  
R Dhar ◽  
D Defeo-Jones ◽  
R W Ellis ◽  
...  

We present the nucleotide sequence of the coding region of the rat c-rasH-1 gene and a partial sequence analysis of the rat c-rasH-2 gene. By comparing these sequences with the Harvey murine sarcoma virus ras gene, we predict that the p21 protein encoded by the Harvey virus differs from the cellular c-rasH-1-encoded p21 at only two amino acids; those at positions 12 and 59. Alterations at each of these positions may play a role in activating the viral p21 protein. The c-rasH-2 gene is likely to be a nonfunctional pseudogene because it lacks introns, cannot be activated to transform NIH 3T3 cells, and differs in sequence from both c-rasH-1 and v-rasH at several base pair positions.


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