Nucleotide sequence of avian retroviral oncogene v-mil: homologue of murine retroviral oncogene v-raf

  title={Nucleotide sequence of avian retroviral oncogene v-mil: homologue of murine retroviral oncogene v-raf},
  author={Pramod Sutrave and Tom I. Bonner and Ulf R{\"u}diger Rapp and Hans Willi Dr. Jansen and Tilo Patschinsky and Klaus Bister},
Eukaryotic cells contain genes termed proto-oncogenes (c-onc) which have the potential to transform cells in culture and induce tumours in vivo. Most of these genes have been identified by their occasional incorporation into retroviral genomes which can act as natural transducing vectors for these and perhaps other cellular genes1,2. Cell-derived oncogenes of retroviruses (v-onc) are associated mostly with the induction of mesenchymal tumours whereas carcinoma induction is rare3. One of these… 
The v-myc oncogene
In v-myc-transformed myelomonocytic cells, secondary events occur, such as the expression of colony stimulating factor-1 (CSF-1) which play a critical role in immortalization and subsequent tumor progression.
Fusion proteins in retroviral transformation.
Oncogene requirements for tumorigenicity: cooperative effects between retroviral oncogenes.
  • S. Palmieri
  • Biology
    Current topics in microbiology and immunology
  • 1989
A unique group of avian retroviruses exists in which each virus encodes pairs of cooperating oncogenes, which implies that oncogene complementation represents one process of rapid tumor formation in nature and is not merely a novel laboratory phenomenon.
The raf Oncogene
v-raf is the oncogene of 3611 MSV and was isolated from mouse cells by transduction with murine leukemia virus (MuLV). v-raf is a new member of the src family of oncogenes and has associated ser/thr
Structure and transforming function of transduced mutant alleles of the chicken c-myc gene
It is concluded that neither major structural changes, such as in-frame fusion with virion genes or internal deletions, nor specific, if any, missense mutations of the c-myc coding region are necessary for activation of the basic oncogenic function of transduced myc alleles.
Homology among oncogenes.
All acutely transforming retroviruses identified to date are unable to support their replication, because transforming sequences are acquired at the expense of viral genes whose products are essential for propagation.
Abrogation of IL-3 and IL-2 dependence by recombinant murine retroviruses expressing v-myc oncogenes
The effects of recombinant murine retroviruses capable of expressing the avian v-myc on haematopoietic/lymphoid cell differentiation, immortalization and factor dependence for growth are examined.
Genes and gene products involved in growth regulation of tumor cells.
It was recently demonstrated that combinations of “complementary” oncogenes may act synergistically to transform a particular cell type.


Homologous cell-derived oncogenes in avian carcinoma virus MH2 and murine sarcoma virus 3611
It is reported here that the two independently transduced oncogenes v-mil and v-raf are closely related and that they were apparently derived from homologous cellular genes of avian and mammalian species.
Structure and biological activity of v-raf, a unique oncogene transduced by a retrovirus.
Comparison of the transforming gene from 3611-MSV, designated v-raf, with previously isolated retrovirus oncogenes either by direct hybridization or by comparison of restriction fragments of their cellular homologs shows it to be unique.
New mammalian transforming retrovirus: demonstration of a polyprotein gene product
A new acute transforming type C retrovirus was isolated from mice inoculated with a virus stock obtained by iododeoxyuridine induction of methylcholanthrene-transformed C3H/10T1/2 mouse cells, and the 3611-MSV transforming gene was found to be distinct from previously described mammalian cellular oncogenic sequences.
Two unrelated cell‐derived sequences in the genome of avian leukemia and carcinoma inducing retrovirus MH2.
The presence in the MH2 genome of two unrelated cell‐derived sequences and their independent expression may be significant for the oncogenic specificities of this virus.
A common onc gene sequence transduced by avian carcinoma virus MH2 and by murine sarcoma virus 3611.
The data indicate that the number of cellular proto- onc genes is limited because, like other viruses of different taxonomic groups, MH2 and MSV 3611 have transduced the same onc gene-specific sequences from different cell species and that specific deletion and linkage of the same proto-onc sequences to different viral vector elements affect the oncogenic potential of the resulting viruses.
Avian oncovirus MH2: molecular cloning of proviral DNA and structural analysis of viral RNA and protein
The data on viral RNA, proviral DNA, and protein of MH2 reveal a unique genetic structure for this virus of the MC29 subgroup and suggest that its v-myc gene is not expressed as a gag-related protein.
Nucleotide sequence of Abelson murine leukemia virus genome: structural similarity of its transforming gene product to other onc gene products with tyrosine-specific kinase activity.
The amino acid sequence of the putative abl gene, when compared with the sequences of other tyrosine-specific protein kinases, revealed significant homologies, indicating that all these functionally related transforming genes are derived from divergent members of the same protooncogene family.
Tripartite structure of the avian erythroblastosis virus E26 transforming gene
In vitro translation shows that the p135 gene of E26 is a genetic hybrid of three distinct elements, ∼1.2kb derived from the 5′ region of the retroviral gag gene, mybE and the ets sequence, linked in the order 5′-Δgag–mybE–ets-3′.