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Gene Review

Emv11  -  endogenous ecotropic MuLV 11

Mus musculus

Synonyms: Akv-1, Emv-11
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Disease relevance of Emv11

  • Akv-1 and Akv-2 (Emv-12), an ecotropic provirus carried by AKR/N but not AKR/J, have previously been mapped to chromosome 7 and 16, respectively [1].
  • MCF lymphomagenicity was strain specific, however, in that AKR MCF viruses did not induce lymphomas in many murine strains; they were moderately lymphomagenic in C3H/Bi mice and in National Institutes of Health Swiss partially congenic for Akv-1 or Akv-2 [2].
  • Heterogenous nonacute transforming retroviruses are associated with the etiology of the disease: the endogenous ecotropic viruses (inherited in AKR mice at two non-linked chromosomal loci, Akv-1 and Akv-2), the xenotropic virus and recombinant viruses [3].
  • Whereas Akv-3 is known to encode a defective virus, Akv-4 has been shown to code for an infectious virus thought to be very similar or identical to that of Akv-1 [4].
  • Akv-1 and -2 share 55--75% of their large T1-resistant oligonucleotides with four MCF viruses isolated from AKR mice or from NIH Swiss mice that inherit either the Akv-1 or Akv-2 virus-inducing locus of AKR [5].

High impact information on Emv11

  • (AKR x NZB)F1 mice possess the dominant genes, Akv-1, Akv-2, Nzv-1a and Nzv-2a, which determine the expression of ecotropic and xenotropic viruses [6].
  • T1 RNA fingerprints of the genomes of Akv-1 and Akv-2 C-type viruses are indistinguishable and oligonucleotide maps of these viruses are probably the same [5].
  • Definitive evidence that the murine C-type virus inducing locus Akv-1 is viral genetic material [7].
  • Finally, comparison of the new sequences of Emv-3 with those of the Akv virus (also designated AKR-623 and Emv-11) and Emv-1 shows that this endogenous virus locus is very closely related to the other Emv loci at the nucleotide sequence level [8].
  • Strains which transmit Emv-11 or Emv-14 or both were found to produce virus spontaneously, whereas strains that transmit Emv-13 alone were negative for virus expression [9].

Chemical compound and disease context of Emv11

  • Treatment with monoclonal antibody Hy-72 reacting only with Akv1 type ecotropic viruses, or with mAb 18-5 with specificity for both ecotropic and MCF recombinant virus envelope glycoprotein (administered from birth for 10 days) inhibited similarly T cell lymphoma development [3].

Biological context of Emv11

  • We used two-dimensional gel electrophoresis to obtain fingerprints of RNase T1-resistant oligonucleotides derived from the genomes of Akv-1 and Akv-2 type C viruses of AKR mice [10].
  • Sequence analysis reveals that pSR3 is closely related to p623, a plasmid derived from Emv-11 (also referred to as AKV-1) [11].
  • Based on these data, the present experiments were performed with various AKXL RI mouse strains of the responder H-2b haplotype which had inherited different combinations of the Akv-1, -3, and -4 proviruses, to determine whether these strains were able to mount specific antiviral CTL responses [12].
  • In this paper, we describe for the first time the sequencing of the entire BM5eco viral genome as well as analysis of homology with two other previously sequenced and well-characterized MuLVs, Emv-11 and Emv-2, the latter constituting the parental virus for BM5eco [13].

Other interactions of Emv11


  1. Chromosomal assignment of two endogenous ecotropic murine leukemia virus proviruses of the AKR/J mouse strain. Taylor, B.A., Rowe, L., Jenkins, N.A., Copeland, N.G. J. Virol. (1985) [Pubmed]
  2. Lymphomagenicity of recombinant mink cell focus-inducing murine leukemia viruses. Cloyd, M.W., Hartley, J.W., Rowe, W.P. J. Exp. Med. (1980) [Pubmed]
  3. The effects of passive antiviral immunotherapy in AKR mice: I. The susceptibility of AKR mice to spontaneous and induced T cell lymphomagenesis. Haran-Ghera, N., Peled, A., Wu, L., Shortman, K., Brightman, B.K., Fan, H. Leukemia (1995) [Pubmed]
  4. Cytolytic T lymphocyte-defined retroviral antigens on normal cells: encoding by the Akv-1 proviral locus. Green, W.R., Graziano, R.F. Immunogenetics (1986) [Pubmed]
  5. Characterization and mapping of RNase T1-resistant oligonucleotides derived from the genomes of Akv and MCF murine leukemia viruses. Rommelaere, J., Faller, D.V., Hopkins, N. Proc. Natl. Acad. Sci. U.S.A. (1978) [Pubmed]
  6. Phenotypic alteration in retroviral gene expression by leukemia-resistant thymocytes differentiating in leukemia-susceptible recipients. Datta, S.K., Waksal, S.D., Schwartz, R.S. Cell (1980) [Pubmed]
  7. Definitive evidence that the murine C-type virus inducing locus Akv-1 is viral genetic material. Chattopadhyay, S.K., Rowe, W.P., Teich, N.M., Lowy, D.R. Proc. Natl. Acad. Sci. U.S.A. (1975) [Pubmed]
  8. A replication-competent, endogenous retrovirus from an aged DBA/2 mouse contains the complete env from Emv-3 and a novel gag partially related to AKT-8. Bartman, T., Murasko, D.M., Blank, K.J. J. Virol. (1995) [Pubmed]
  9. Emv-13 (Akv-3): a noninducible endogenous ecotropic provirus of AKR/J mice. Bedigian, H.G., Copeland, N.G., Jenkins, N.A., Salvatore, K., Rodick, S. J. Virol. (1983) [Pubmed]
  10. RNase T1-resistant oligonucleotides of Akv-1 and Akv-2 type C viruses of AKR mice. Rommelaere, J., Faller, D.V., Hopkins, N. J. Virol. (1977) [Pubmed]
  11. Analysis of variability among endogenous ecotropic MuLV loci in laboratory mice. Nouvel, P., Philippe, H., Condamine, H., Panthier, J.J. Virology (1993) [Pubmed]
  12. Genetic control of CTL responses to AKR/Gross virus: effect of inheritance of Akv proviruses. Green, W.R., Rich, R.F. Immunogenetics (1988) [Pubmed]
  13. Analysis of the helper virus in murine retrovirus-induced immunodeficiency syndrome: evidence for immunoselection of the dominant and subdominant CTL epitopes of the BM5 ecotropic virus. Gaur, A., Green, W.R. Viral Immunol. (2003) [Pubmed]
  14. Identification of DNA fragments carrying ecotropic proviruses of AKR mice. Steffen, D., Bird, S., Rowe, W.P., Weinberg, R.A. Proc. Natl. Acad. Sci. U.S.A. (1979) [Pubmed]
  15. The origin of SL family mice. Abujiang, P., Yamada, Y., Haller, O., Kobayashi, H., Kamoto, T., Lu, L.M., Ogawa, M., Ishimoto, A., Katoh, H., Kanehira, K., Ikegami, S., Fukumoto, M., Hiai, H. Lab. Anim. Sci. (1996) [Pubmed]
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