Abelson murine leukemia virus

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Temperature-sensitive mutants of Abelson murine leukemia virus deficient in protein tyrosine kinase activity.

Temperature-sensitive mutants of Abelson murine leukemia virus deficient in protein tyrosine kinase activity.

4242-4251 0022-538X/90/094242-10$02.00/0 Copyright © 1990, American Society for Microbiology Temperature-Sensitive Mutants of Abelson Murine Leukemia Virus Deficient in Protein Tyrosine [r]

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Increased concentration of an apparently identical cellular protein in cells transformed by either Abelson murine leukemia virus or other transforming agents.

Increased concentration of an apparently identical cellular protein in cells transformed by either Abelson murine leukemia virus or other transforming agents.

336-346 0022-538X/81/040336-11$02.00/0 Increased Concentration of an Apparently Identical Cellular Protein in Cells Transformed by Either Abelson Murine Leukemia Virus or Other Transform[r]

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Transfection of Fibroblasts by Cloned Abelson Murine Leukemia Virus DNA and Recovery of Transmissible Virus by Recombination with Helper Virus

Transfection of Fibroblasts by Cloned Abelson Murine Leukemia Virus DNA and Recovery of Transmissible Virus by Recombination with Helper Virus

271-285 0022-538X/82/010271-15$02.00/0 Transfection of Fibroblasts by Cloned Abelson Murine Leukemia Virus DNA and Recovery of Transmissible Virus by Recombination with Helper Virus Mass[r]

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Absence of p53 Complements Defects in Abelson Murine Leukemia Virus Signaling

Absence of p53 Complements Defects in Abelson Murine Leukemia Virus Signaling

Abelson murine leukemia virus (Ab-MLV) transforms cells by expressing the v-Abl oncoprotein (21). Despite the presence of a strong viral oncogene, pre-B-cell transformation in vivo and in vitro is a multistep process (10, 18, 32, 33). When bone marrow populations are infected, pre-B cells undergo an initial proliferative phase called primary transformation, which is fol- lowed by a period of apoptosis and erratic growth called crisis. Some clones of primary transformants succumb to crisis, and others emerge as fully malignant cell lines (18, 26, 27). About half of the cell lines that survive acquire a mutation that ren- ders the p53 tumor suppressor nonfunctional (26), and most of the others down-modulate the p19Arf protein (18), a protein that leads to p53 activation through effects on Mdm2 (reviewed in reference 24). Consistent with the important role of the p53 pathway in the crisis phase of transformation, pre-B cells from animals lacking functional p53 or the Ink4a/Arf locus that en- codes p19Arf bypass crisis (18, 27).
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Site-directed deletions of Abelson murine leukemia virus define 3' sequences essential for transformation and lethality.

Site-directed deletions of Abelson murine leukemia virus define 3' sequences essential for transformation and lethality.

1028-1036 0022-538X/83/031028-09$02.00/0 Copyright X 1983, American Society for Microbiology Site-Directed Deletions of Abelson Murine Leukemia Virus Define 3' Sequences Essential for Tr[r]

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The nonstructural component of the Abelson murine leukemia virus polyprotein P120 is encoded by newly acquired genetic sequences.

The nonstructural component of the Abelson murine leukemia virus polyprotein P120 is encoded by newly acquired genetic sequences.

1041-1045 0022-538X/79/12-1041/05$02.00/0 The Nonstructural Component of the Abelson Murine Leukemia Virus Polyprotein P120 Is Encoded by Newly Acquired Genetic Sequences Received for pu[r]

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Cloning and analysis of reverse transcript P160 genomes of Abelson murine leukemia virus.

Cloning and analysis of reverse transcript P160 genomes of Abelson murine leukemia virus.

3 Cloning and Analysis of Reverse Transcript P160 Genomes of Abelson Murine Leukemia Virus Received 27 September 1982/Accepted 22 November 1982 Circular duplex reverse transcripts of the[r]

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Virus production by Abelson murine leukemia virus-transformed lymphoid cells.

Virus production by Abelson murine leukemia virus-transformed lymphoid cells.

2 Virus Production by Abelson Murine Leukemia Virus-Transformed Lymphoid Cells ANTHONY SHIELDS,' NAOMI ROSENBERG,2 AND DAVID BALTIMORE' * Department of Biology and Center for Cancer Rese[r]

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Gag Influences Transformation by Abelson Murine Leukemia Virus and Suppresses Nuclear Localization of the v-Abl Protein

Gag Influences Transformation by Abelson Murine Leukemia Virus and Suppresses Nuclear Localization of the v-Abl Protein

Mutations affecting MA or the majority of Gag sequences decrease transformation. In contrast to mutations affecting the p12 portion of the v-Abl protein, loss of MA sequences re- duced NIH 3T3 cell transformation by more than 200-fold (Table 1). Despite this marked reduction in transformation, both the ⌬ 35–81 mutant and the ⌬ 82–133 mutant gave rise to a small number of transformants; recovery of the viral se- quences from these cells and PCR analysis revealed that the original deletions were still present. These rare transformants could have arisen because of compensating mutations else- where in the virus or through the effects of complementary mutations present in a minority of NIH 3T3 cells. However, no changes that altered protein size, such as those observed by Prywes and coworkers (18, 19) that affected large portions of the carboxyl terminus, were detected (data not shown). No transformants were recovered from NIH 3T3 cells infected with the ⌬ 35–236 mutant, a mutant that encodes a v-Abl pro- FIG. 2. Ab-MLV mutants express v-Abl proteins that retain kinase
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Phosphorylation of the Abelson murine leukemia virus transforming protein.

Phosphorylation of the Abelson murine leukemia virus transforming protein.

The nucleic acid recombination in A-MuLV results in the production of a fused protein containing an amino-terminal region precisely homologous to Moloney murine leukemia virus gag gene s[r]

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Genome structure of Abelson murine leukemia virus variants: proviruses in fibroblasts and lymphoid cells.

Genome structure of Abelson murine leukemia virus variants: proviruses in fibroblasts and lymphoid cells.

To examine the genome structure of the A-MuLV variants in transformed lymphoid cells, DNA was isolated from a variety of cloned cell lines prepared by infection of bone marrow cells in v[r]

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Abelson murine leukemia virus mutants deficient in kinase activity and lymphoid cell transformation.

Abelson murine leukemia virus mutants deficient in kinase activity and lymphoid cell transformation.

The AMuLV strains encoding P160, P120, P100, and P90 all transform fibroblasts, and high-titer transforming virus stocks are obtained from using the agar transformation assay 11 and BALB[r]

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Protein stabilization explains the gag requirement for transformation of lymphoid cells by Abelson murine leukemia virus.

Protein stabilization explains the gag requirement for transformation of lymphoid cells by Abelson murine leukemia virus.

The results in these two cell lines show that in lymphoid cells there is a specific instability of the p15deleted Abelson protein, which presumably explains the inability of p15-deleted [r]

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Localization of the Abelson murine leukemia virus protein in a detergent-insoluble subcellular matrix: architecture of the protein.

Localization of the Abelson murine leukemia virus protein in a detergent-insoluble subcellular matrix: architecture of the protein.

Lanes 1, 4, and 5, labeled 2M3 cell extract, labeled 2M3 cell extract plus unlabeled ANN-I ceU extract, and labeled ANN-1 cell extract, respectively, all immunoprecipitated with normal g[r]

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Distinct helper virus requirements for Abelson murine leukemia virus-induced pre-B- and T-cell lymphomas.

Distinct helper virus requirements for Abelson murine leukemia virus-induced pre-B- and T-cell lymphomas.

Although we cannot exclude the possibility that some tumors contain recombinant proviruses having deleted or rearranged both their LTR and gp7O region, our data show that more than one-h[r]

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Abelson murine leukemia virus P120: identification and characterization of tyrosine phosphorylation sites.

Abelson murine leukemia virus P120: identification and characterization of tyrosine phosphorylation sites.

STEPHENSON"* Laboratory of Viral Carcinogenesis, National Cancer Institute-Frederick Cancer Research Facility,1 and Carcinogenesis Intramural Program, Frederick Cancer Research Facility,[r]

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Identification of a common helper provirus integration site in Abelson murine leukemia virus-induced lymphoma DNA.

Identification of a common helper provirus integration site in Abelson murine leukemia virus-induced lymphoma DNA.

To determine whether the rearrangements detected by the different Ahi-I probes were generated by the insertion of a provirus, to map the integration site of the proviruses more precisely[r]

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Abelson murine leukemia virus transformation-defective mutants with impaired P120-associated protein kinase activity.

Abelson murine leukemia virus transformation-defective mutants with impaired P120-associated protein kinase activity.

The demonstration of AbLV P120 expression in FRE Fisher rat and CCL64 mink cells nonproductively infected with td variants of AbLV suggested that if AbLV P120 is involved in transformati[r]

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Multiple steps are required for the induction of tumors by Abelson murine leukemia virus.

Multiple steps are required for the induction of tumors by Abelson murine leukemia virus.

Lanes: 1 to 3, DNAs from individual preleukemic colonies recovered from spleen cells of a BALB/cByJ mouse splenectomized 14 10 days after infection with helper virus-free A-MuLV; T, 2 ,u[r]

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Clonal dominance and progression in Abelson murine leukemia virus lymphomagenesis.

Clonal dominance and progression in Abelson murine leukemia virus lymphomagenesis.

To determine whether clonal dominance had been established in the transformed cells prior to overt tumor formation, mice were infected with A-MuLV, and at 10 to 14 days postinfection tot[r]

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