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  • 1
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    Complete nucleotide sequence and organization of the Moloney murine sarcoma virus genome (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-10-23
    Description: The complete nucleotide sequence of a mammalian transforming retrovirus. Moloney murine sarcoma virus, has been determined. MSV, recombinant virus derived of helper viral and cellular sequences, possesses termini resembling prokaryotic transposable elements. The viral genome has the coding capacity for the Moloney murine leukemia virus gag gene product and contains large deletions in pol and env genes. A large open reading frame encompassing its cell-derived sequences codes for its putative transforming protein. The nature of some of the important domains in the viral genome has been established, and their structure is discussed in relation to their function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, E P -- Smith, M J -- Aaronson, S A -- New York, N.Y. -- Science. 1981 Oct 23;214(4519):445-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6170110" target="_blank"〉PubMed〈/a〉
    Keywords: Antigens, Viral/genetics ; Base Sequence ; Binding Sites ; Cell Transformation, Viral ; DNA, Viral/*genetics ; Defective Viruses/genetics ; Gene Products, gag ; *Genes, Viral ; Moloney murine leukemia virus/*genetics ; RNA, Transfer/genetics ; RNA-Directed DNA Polymerase/genetics ; Repetitive Sequences, Nucleic Acid ; Sarcoma Viruses, Murine/*genetics ; Transcription, Genetic ; Viral Proteins/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Nucleotide sequence of the transforming gene of avian myeloblastosis virus (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-06-25
    Description: Avian myeloblastosis virus is defective in reproductive capacity, requiring a helper virus to provide the viral proteins essential for synthesis of new infectious virus. This virus arose by recombination of the nondefective helper virus and host cellular sequences present within the normal avian genome. These latter sequences are essential for leukemogenic activity. The complete nucleotide sequence of this region is reported. Within the acquired cellular sequences there is an open reading frame of 795 nucleotides starting with the initiation codon ATG (adenine, thymine, guanine) and terminating with the triplet TAG. This open reading frame could code for the putative transforming protein of 265 amino acids with a molecular weight of approximately 30,000.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rushlow, K E -- Lautenberger, J A -- Papas, T S -- Baluda, M A -- Perbal, B -- Chirikjian, J G -- Reddy, E P -- New York, N.Y. -- Science. 1982 Jun 25;216(4553):1421-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6283631" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Avian Leukosis Virus/*genetics ; Avian Myeloblastosis Virus/*genetics ; Avian Sarcoma Viruses/genetics ; Base Sequence ; Cell Transformation, Viral ; Chickens/genetics ; DNA Restriction Enzymes ; Gene Expression Regulation ; *Genes, Viral ; RNA, Viral/analysis ; Viral Proteins/biosynthesis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    In vivo identification of the transforming gene product of simian sarcoma virus (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-12-10
    Description: Simian sarcoma virus (SSV) deletion mutants were constructed from a molecular clone containing the entire infectious provirus. Transfection analysis of these mutants localized the SSV transforming gene to a small region of the viral genome encompassing its cell-derived sequence (v-sis). Antiserum to a peptide synthesized on the basis of the predicted amino acid sequence of the SSV transforming gene detected a 28,000-dalton protein that was specifically expressed in SSV transformed cells and that corresponded in size to that predicted from the v-sis coding sequence. The v-sis gene product designated p28sis was not a phosphoprotein, nor did it possess detectable protein kinase activity. These findings distinguish p28sis from a number of other retroviral onc proteins.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robbins, K C -- Devare, S G -- Reddy, E P -- Aaronson, S A -- New York, N.Y. -- Science. 1982 Dec 10;218(4577):1131-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6293053" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Viral ; Base Sequence ; *Cell Transformation, Viral ; *Genes, Viral ; Mice ; Molecular Weight ; *Oncogenes ; Phosphoproteins/genetics ; Protein Kinases/genetics ; Retroviridae/*genetics ; Sarcoma Virus, Woolly Monkey/*genetics ; Viral Proteins/*genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Gene product of v-fgr onc: hybrid protein containing a portion of actin and a tyrosine-specific protein kinase (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-06
    Description: The nucleotide sequence of the region of Gardner-Rasheed feline sarcoma virus (GR-FeSV) encoding its primary translation product, p70gag-fgr, has been determined. From the nucleotide sequence, the amino acid sequence of this transforming protein was deduced. Computer analysis indicates that a portion of P70gag-fgr has extensive amino acid sequence homology with actin, a eukaryotic cytoskeletal protein. A second region of P70gag-fgr is closely related to the tyrosine-specific kinase gene family. Thus, the v-fgr oncogene appears to have arisen as a result of recombinational events involving two distinct cellular genes, one coding for a structural protein and the other for a protein kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naharro, G -- Robbins, K C -- Reddy, E P -- New York, N.Y. -- Science. 1984 Jan 6;223(4631):63-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6318314" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/analysis ; Amino Acid Sequence ; Base Sequence ; Computers ; Gene Products, gag ; *Genes, Viral ; *Oncogenes ; Protein Kinases/analysis ; Protein-Tyrosine Kinases ; Recombination, Genetic ; Retroviridae/*genetics ; Sarcoma Viruses, Feline/*genetics ; Viral Proteins/analysis/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    DNA rearrangement and altered RNA expression of the c-myb oncogene in mouse plasmacytoid lymphosarcomas (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-05-20
    Description: Three types of tumors termed plasmacytomas (ABPC's), lymphosarcomas (ABLS's), and plasmacytoid lymphosarcomas (ABPL's) arise in BALB/c mice treated with pristane and Abelson murine leukemia virus (A-MuLV). While most ABPC's and BLS's contain integrated A-MuLV proviral genome and synthesize the v-abl RNA, most ABPL's do not. The ABPL tumors were examined for the expression of other oncogenes that may be associated with their transformed state, in the absence of transforming virus. These tumors expressed abundant c-myb RNA of unusually large size and showed DNA rearrangements of the c-myb locus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mushinski, J F -- Potter, M -- Bauer, S R -- Reddy, E P -- New York, N.Y. -- Science. 1983 May 20;220(4599):795-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6687762" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/genetics ; Animals ; Cell Transformation, Neoplastic/metabolism ; Cloning, Molecular ; DNA, Neoplasm/*genetics ; *Gene Expression Regulation ; Humans ; Lymphoma, Non-Hodgkin/*genetics ; Mice ; Mice, Inbred BALB C ; *Oncogenes ; Plasmacytoma/genetics ; RNA, Neoplasm/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Nitrite inhibition of Clostridium botulinum: electron spin resonance detection of iron-nitric oxide complexes (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-19
    Description: Vegetative cells of Clostridium botulinum were shown to contain iron-sulfur proteins that react with added nitrite to form iron-nitric oxide complexes, with resultant destruction of the iron-sulfur cluster. Inactivation of iron-sulfur enzymes (especially ferredoxin) by binding of nitric oxide would almost certainly inhibit growth, and thus is probably the mechanism of botulinal inhibition by nitrite in foods.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, D -- Lancaster, J R Jr -- Cornforth, D P -- New York, N.Y. -- Science. 1983 Aug 19;221(4612):769-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6308761" target="_blank"〉PubMed〈/a〉
    Keywords: Clostridium botulinum/*drug effects ; Electron Spin Resonance Spectroscopy ; Iron ; Iron-Sulfur Proteins/*antagonists & inhibitors ; Metalloproteins/*antagonists & inhibitors ; Nitric Oxide ; Nitrites/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Nucleotide sequence analysis of the T24 human bladder carcinoma oncogene (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-03
    Description: The nucleotide sequence of the T24 human bladder carcinoma oncogene was determined, and the coding and noncoding sequences of the genome were identified. The amino acid sequence of p21, the translational product of the T24 oncogene, was predicted from the nucleotide sequence of the oncogene. Comparison of this sequence with that of the normal cellular homolog showed that a single point mutation in the coding sequences of the T24 oncogene resulted in the acquisition of transforming properties. Other differences between the T24 oncogene and its normal cellular homolog were found in the 5' noncoding and 3' noncoding sequences, but these differences appear to be due to polymorphism and do not play a significant role in the transformation process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reddy, E P -- New York, N.Y. -- Science. 1983 Jun 3;220(4601):1061-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6844927" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Carcinoma/*genetics ; Cell Transformation, Neoplastic/metabolism ; Humans ; Mice ; Neoplasm Proteins/genetics ; *Oncogenes ; Oncogenic Viruses/genetics ; Rats ; Urinary Bladder Neoplasms/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Activation of the c-myb locus by viral insertional mutagenesis in plasmacytoid lymphosarcomas (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-30
    Description: Rearrangement in the c-myb locus of each of four independently derived BALB/c plasmacytoid lymphosarcoma (ABPL's) is due to the insertion of a defective Moloney murine leukemia virus (M-MuLV) into a 1.5-kilobase-pair stretch of cellular DNA at the 5' end of the v-myb-related sequences. This retroviral insertion is associated with abnormal transcription of myb sequences and probably represents a step in the neoplastic transformation of ABPL cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shen-Ong, G L -- Potter, M -- Mushinski, J F -- Lavu, S -- Reddy, E P -- New York, N.Y. -- Science. 1984 Nov 30;226(4678):1077-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6093260" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Chromosome Deletion ; Cloning, Molecular ; DNA Restriction Enzymes ; DNA Transposable Elements ; *Genes, Viral ; Lymphoma, Non-Hodgkin/genetics/*microbiology ; Mice ; Mice, Inbred BALB C ; Moloney murine leukemia virus/*genetics ; *Mutation ; Nucleic Acid Hybridization ; *Oncogenes
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Molecular dissection of transcriptional control elements within the long terminal repeat of the retrovirus (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-01-20
    Description: The retroviral long terminal repeat (LTR) contains transcriptional control elements that affect viral gene expression. By deletion mutagenesis of the genome of the cloned Abelson murine leukemia virus, regulatory signals could be mapped to at least three domains within the LTR. A defective 5' LTR that did not sustain transforming gene function was complemented by an intact LTR positioned at the 3' end of the genome. This versatility of the retroviral genome with respect to its transcriptional control elements appears to provide a strong selective advantage for viral gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Srinivasan, A -- Reddy, E P -- Dunn, C Y -- Aaronson, S A -- New York, N.Y. -- Science. 1984 Jan 20;223(4633):286-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6322296" target="_blank"〉PubMed〈/a〉
    Keywords: Abelson murine leukemia virus/*genetics ; Animals ; Cell Line ; Cell Transformation, Viral ; Cloning, Molecular ; *Gene Expression Regulation ; *Genes, Viral ; Leukemia Virus, Murine/*genetics ; Mice ; Mutation ; *Repetitive Sequences, Nucleic Acid ; *Transcription, Genetic ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Malignant activation of a K-ras oncogene in lung carcinoma but not in normal tissue of the same patient (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-02-17
    Description: A single genetic alteration, a guanine-to-cytosine transversion, is responsible for the acquisition of malignant properties by K-ras genes of two human tumor cell lines established from carcinomas of the bladder (A1698) and lung (A2182). As a consequence, arginine instead of the normal glycine is incorporated into the K-ras-coded p21 proteins at amino acid position 12. This mutation creates a restriction enzyme polymorphism that can be used to screen human cells for transforming K-ras genes. This approach was used to identify the mutational event responsible for the malignant activation of a K-ras oncogene in a squamous cell lung carcinoma of a 66-year-old man; this point mutation was not present in either the normal bronchial or parenchymal tissue or in the blood lymphocytes. Hence, malignant activation of a ras oncogene appears to be specifically associated with the development of a human neoplasm.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santos, E -- Martin-Zanca, D -- Reddy, E P -- Pierotti, M A -- Della Porta, G -- Barbacid, M -- New York, N.Y. -- Science. 1984 Feb 17;223(4637):661-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6695174" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; *Cell Transformation, Neoplastic ; DNA, Neoplasm/genetics ; Genes, Dominant ; Humans ; Lung Neoplasms/*genetics ; Mutation ; *Oncogenes ; Organ Specificity ; Polymorphism, Genetic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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