Showing papers by "David Baltimore published in 1980"
TL;DR: It was shown that the 3′ ends of the two μ mRNAs do not cross-hybridize, and apparently two separate 3′ terminal sequences for μ mRNA are encoded in the genome, one that specifies an amino acid sequence appropriate for membrane-binding and a second that is involved in secretion.
494 citations
TL;DR: The Abelson murine leukaemia virus protein (P120) can become phosphorylated in vitro by [γ-32P]ATP and is linked to P120 at tyrosine, a linkage not previously reported for a phosphorylation reaction.
Abstract: The Abelson murine leukaemia virus protein (P120) can become phosphorylated in vitro by [γ-32P]ATP. The protein has been purified from cell membranes to the point that in specific conditions virtually all of the incorporated 32P is in P120. The reaction is stimulated by Mn2+ and Mg2+ but not Ca2+ and is very rapid even at 0 °C. The phosphate is linked to P120 at tyrosine, a linkage not previously reported for a phosphorylation reaction. Phosphorylation may be involved in the transforming activity of viruses that cause leukaemia as well as sarcomas.
474 citations
TL;DR: Circular double-stranded DNA produced after infection of mouse cells with Abelson murine leukemia virus was isolated and cloned in the phage vector Charon 21A and showed homology to the ends of Moloney MuLV and to a 3.5 kb central region containing sequences unique to Abelson virus.
426 citations
TL;DR: Closed circular Moloney murine leukemia virus (M-MuLV) DNA was prepared from recently infected cells and cloned in a lambda vector, providing explicit information concerning the mechanism by which retrovirus DNA integrates into host cell DNA.
Abstract: Closed circular Moloney murine leukemia virus (M-MuLV) DNA was prepared from recently infected cells and cloned in a lambda vector. Four classes of cloned M-MuLV inserts were found: Class I, full length 8.8-kilobase (kb) inserts with two tandem long terminal repeats (LTRs) of 600 base pairs; class 2, 8.2-kb inserts with a single copy of a LTR; class 3, M-MuLV DNA inserts with various portions deleted; and class 4, an 8.8-kb insert with an internal sequence inversion. Determination of nucleotide sequence at the junction between the two LTRs from a class 1 insert suggested that circularization occurred by blunt-end ligation of an 8.8-kb linear DNA. The class 4 molecule had an inversion that was flanked by inverted LTRs, each of which had lost two terminal base pairs at the inversion end points. Also, four base pairs that were present only once in standard M-MuLV DNA were duplicated at either end of the inversion. This molecule was interpreted as resulting from an integrative inversion in which M-MuLV DNA has integrated into itself. Its analysis thus provided explicit information concerning the mechanism by which retrovirus DNA integrates into host cell DNA. Models of retrovirus integration based on bacterial DNA transposition mechanisms are proposed.
265 citations
TL;DR: Two cloned lambda 1-producing myelomas (HopC-1, MOPC-104E) contain rearranged kappa genes and levels of mature-sized kappa RNA comparable to those found in kappa- producing myeloma cells, and at least two lines contain kappa protein fragments.
206 citations
TL;DR: The selective accentuation of this protein in A-MuLV transformants and its strong antigenicity in syngeneic animals suggest that it is a unique and functionally important protein.
Abstract: When BALB/c mice were injected with a syngeneic cell line transformed by Abelson murine leukemia virus (A-MuLV), the tumor was usually lethal. In sera from tumor-bearing mice, and at highest levels in sera from mice that reject their tumors, was an antibody that immunoprecipitates a specific protein from [35S]-methionine-labeled A-MuLV-transformed BALB/c cells. This protein was not the previously characterized A-MuLV-specific protein (P120) but a 50,000-molecular-weight protein (P50). Such sera may also immunoprecipitate P120, but no other protein was reproducibly precipitated by them. A monoclonal antibody (RA3-2C2) that has been shown to stain normal B-lymphocytes also selectively immunoprecipitated P50. P50 was present in A-MuLV-transformed lymphoid and fibroblastic cells of a variety of mouse strains. One A-MuLV-transformed cell line had a very low P50 level, the L1-2 tumor of C57L origin. This tumor was previously shown to be rejected by C57L mice and is used to produce anti-P120 (anti-AbT) sera. P50 was not a Moloney MuLV protein and was found at low levels in normal cells of cells transformed by agents other than A-MuLV; thus, it was probably a host cell protein whose concentration was selectively accentuated by A-MuLV transformation. P50 was phosphorylated and, by using indirect immunofluorescence, anti-P50 serum stained live A-MuLV-transformed cells. The protein was not glycosylated and did not label by lactoperoxidase-catalyzed iodination. Thus, P50 was very like P120 in its cellular localization and properties, but it did not exhibit proptein kinase activity in vitro. The selective accentuation of this protein in A-MuLV transformants and its strong antigenicity in syngeneic animals suggest that it is a unique and functionally important protein.
176 citations
TL;DR: Three of the viral systems may well have shared genes but the double-stranded RNA viruses appear to represent a very different evolutionary line.
Abstract: These arguments lead to the suggestion that four independent evolutionary lines exist within the general group of RNA viruses. These are positive strand viruses, negative strand viruses, double stranded viruses, and retroviruses. Three of the viral systems may well have shared genes but the double-stranded RNA viruses appear to represent a very different evolutionary line.
147 citations
TL;DR: It appears that poliovirus inhibits cellular protein synthesis by inactivation of some crucial property of the cap-binding protein, and the restoring factor could be crosslinked to the 5'-terminal cap on mRNA.
Abstract: It was previously shown that the poliovirus-induced inhibition of translation of capped mRNAs can be reversed by a protein found in preparations of the eukaryotic initiation factor eIF-4B [Rose, J. K., Trachsel, H., Leong, K. & Baltimore, D. (1978) Proc. Natl. Acad. Sci. USA 75, 2732--2736]. This "restoring factor" has now been purified from a high-salt wash of rabbit reticulocyte ribosomes by taking advantage of its tight association with factor eIF-3 at low salt concentrations. It did not copurify with the major Mr 80,000 polypeptide of eIF-4B preparations but did copurify with a Mr 24,000 polypeptide previously shown to bind to the cap structures of mRNAs [Sonenberg, N., Rupprecht, K. M., Hecht, S. M. & Shatkin, A. J. (1979) Proc. Natl. Acad. Sci. USA 76, 4345--4349]. Both the electrophoretic mobility and the tryptic peptide pattern of the restoring factor were indistinguishable from those of the cap-binding protein, and the restoring factor could be crosslinked to the 5'-terminal cap on mRNA. Thus, is appears that poliovirus inhibits cellular protein synthesis by inactivation of some crucial property of the cap-binding protein.
147 citations
TL;DR: A transformation-defective mutant of Abelson murine leukemia virus (A-MuLV) called AMuLV-P92td has been isolated as mentioned in this paper, which lacks the ability to transform either fibroblasts or bone marrow lymphoid cells.
Abstract: A transformation-defective mutant of Abelson murine leukemia virus (A-MuLV), called A-MuLV-P92td, has been isolated. The mutant encodes a serologically identifiable A-MuLV protein of molecular weight 92,000 (P92) but it lacks the ability to transform either fibroblasts or bone marrow lymphoid cells. In contrast to the protein made by transforming strains of A-MuLV, the protein made by A-MuLV-P92td does not becme phosphorylated during in vitro incubation with [gamma-32P]ATP. If the protein is mixed with proteins from cells transformed by a functional A-MuLV strain, phosphorylation of P92 occurs, showing that its ability to accept phosphate is not altered by the mutation. These parallel changes provide genetic evidence that the A-MuLV protein is a transforming protein and that its associated protein kinase activity (EC 2.7.1.37) is a crucial part of its transforming ability.
121 citations
TL;DR: With the purified replicase-host factor combination, only poly(A)-containing RNAs were copied, and a preference for poliovirus RNA was shown, suggesting that the factor acts at the initiation step of RNA replication.
118 citations
TL;DR: Using a rapid phenol extraction assay, an enzyme was purified from uninfected HeLa cells that can cleave the 5'-terminal protein (VPg) from poliovirus RNA with minimal degradation of the RNA or of VPg.
TL;DR: It is demonstrated that terminal transferase is synthesized in both the murine thymus and the bone marrow at a rate proportional to its biochemically measured steady state level.
TL;DR: The hypothesis is advanced that integration into the recipient cell of the DNA copy of the large cellular insert, carried by the Abelson virus, may perform a function similar to the effects of gene duplication by trisomy in the more slowly developing murine leukemias.
Abstract: The karyotype of Abelson-virus-induced murine leukemias was studied by G-banding In contrast to the regular trisomy of chromosome 15 in most murine T-cell leukemias, Abelson leukemias were purely diploid, and remained diploid for up to seven consecutive passages in vivo The hypothesis is advanced that integration into the recipient cell of the DNA copy of the large cellular insert, carried by the Abelson virus, may perform a function similar to the effects of gene duplication by trisomy in the more slowly developing murine leukemias
TL;DR: The results show that murine leukemia virus DNA sequences are distributed among many mouse chromosomes in this strain of A/HeJ mice.
Abstract: We used mouse-Chinese hamster somatic cell hybrids which lose mouse chromosomes to examine the distribution of murine leukemia virus DNA sequences in the genome of A/HeJ mice. We analyzed total cellular DNA from various hybrid clones for the presence of viral sequences by molecular hybridization and used the Southern blot hybridization procedure to identify viral DNA in cellular restriction endonuclease fragments. Our results show that murine leukemia virus DNA sequences are distributed among many mouse chromosomes in this strain. Chromosome 4 was shown to contain murine leukemia virus DNA sequences.
01 Jan 1980