Rescue in Vivo in Adult Mice of Murine Sarcoma Virus (MSV) from a Nonproducer Rat Neoplasm

1969 ◽  
Vol 131 (3) ◽  
pp. 960-963 ◽  
Author(s):  
L. W. Law ◽  
R. C. Ting
1980 ◽  
Vol 33 (2) ◽  
pp. 573-582 ◽  
Author(s):  
W Ostertag ◽  
K Vehmeyer ◽  
B Fagg ◽  
I B Pragnell ◽  
W Paetz ◽  
...  

1986 ◽  
Vol 6 (1) ◽  
pp. 116-122
Author(s):  
J E Buss ◽  
B M Sefton

p21v-H-ras, the transforming protein of Harvey murine sarcoma virus, contains a covalently attached lipid. Using thin-layer chromatography, we identified the acyl group as the 16-carbon saturated fatty acid palmitic acid. No myristic acid was detected in fatty acids released from in vivo-labeled p21v-H-ras. The p21v-K-ras protein encoded by Kirsten sarcoma virus was also palmitylated. The processing and acylation of p21v-K-ras however differed from that of p21v-H-ras. Three forms of [3H]palmitic acid-labeled p21ras proteins were detected in Kirsten sarcoma virus-transformed cells. This contrasted with Harvey sarcoma virus, in which two forms of p21v-H-ras contained palmitic acid. Analysis by partial proteolysis of p21v-H-ras labeled with [3H]palmitic acid suggested that all of the lipid found in intact p21v-H-ras was located in the C-terminal region. On sodium dodecyl sulfate-polyacrylamide gels, p21v-H-ras labeled with [3H]palmitic acid migrated slightly ahead of the majority of p21v-H-ras. Of the mature forms of p21v-H-ras, apparently only a subpopulation contains palmitic acid.


1978 ◽  
Vol 60 (4) ◽  
pp. 875-880 ◽  
Author(s):  
James A. Otten ◽  
Fred E. Myer ◽  
Raymond W. Tennant ◽  
Arthur Brown

1973 ◽  
Vol 51 (5) ◽  
pp. 1541-1549 ◽  
Author(s):  
W. R. Thomas ◽  
E. J. Aw ◽  
J. M. Papadimitriou ◽  
P. J. Simons

1997 ◽  
Vol 323 (3) ◽  
pp. 685-692 ◽  
Author(s):  
Ann-Muriel STEFF ◽  
Serge CARILLO ◽  
Magali PARIAT ◽  
Marc PIECHACZYK

The c-Fos and c-Jun transcription factors are rapidly turned over in vivo. One of the multiple pathways responsible for their breakdown is probably initiated by calpains, which are cytoplasmic calcium-dependent cysteine proteases. The c-fos gene has been transduced by two murine oncogenic retroviruses called Finkel-Biskis-Jenkins murine sarcoma virus (FBJ-MSV) and Finkel-Biskis-Reilly murine sarcoma virus (FBR-MSV); c-jun has been transduced by the chicken avian sarcoma virus 17 (ASV17) retrovirus. Using an in vitro degradation assay, we show that the mutated v-FosFBR, but not v-FosFBJ or v-JunASV17, is resistant to calpains. This property raises the interesting possibility that decreased sensitivity to calpains might contribute to the tumorigenic potential of FBR-MSV by allowing greater accumulation of the protein that it encodes in infected cells. It has also been demonstrated that resistance to cleavage by calpains does not result from mutations that have accumulated in the Fos moiety of the viral protein but rather from the addition of atypical peptide motifs at its both ends. This observation raises the interesting possibility that homologous regions in viral and cellular Fos either display slightly different conformations or are differentially accessible to interacting proteins.


1971 ◽  
Vol 137 (1) ◽  
pp. 310-314 ◽  
Author(s):  
A. F. Gazdar ◽  
E. Russell ◽  
R. H. Bassin

2002 ◽  
Vol 46 (7) ◽  
pp. 2185-2193 ◽  
Author(s):  
J. Balzarini ◽  
C. Pannecouque ◽  
E. De Clercq ◽  
S. Aquaro ◽  
C.-F. Perno ◽  
...  

ABSTRACT A novel class of acyclic nucleoside phosphonates has been discovered in which the base consists of a pyrimidine preferably containing an amino group at C-2 and C-4 and a 2-(phosphonomethoxy)ethoxy (PMEO) or a 2-(phosphonomethoxy)propoxy (PMPO) group at C-6. The 6-PMEO 2,4-diaminopyrimidine (compound 1) and 6-PMPO 2,4-diaminopyrimidine (compound 11) derivatives showed potent activity against human immunodeficiency virus (HIV) in the laboratory (i.e., CEM and MT-4 cells) and in primary (i.e., peripheral blood lymphocyte and monocyte/macrophage) cell cultures and pronounced activity against Moloney murine sarcoma virus in newborn NMRI mice. Their in vitro and in vivo antiretroviral activity was comparable to that of reference compounds 9-[(2-phosphonomethoxy)ethyl]adenine (adefovir) and (R)-9-[(2-phosphonomethoxy)-propyl]adenine (tenofovir), and the enantiospecificity of (R)- and (S)-PMPO pyrimidine derivatives as regards their antiretroviral activity was identical to that of the classical (R)- and (S)-9-(2-phosphonomethoxy)propyl purine derivatives. The prototype PMEO and PMPO pyrimidine analogues were relatively nontoxic in cell culture and did not markedly interfere with host cell macromolecular (i.e., DNA, RNA, or protein) synthesis. Compounds 1 and 11 should be considered attractive novel pyrimidine nucleotide phosphonate analogues to be further pursued for their potential as antiretroviral agents in the clinical setting.


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