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Gene Review

MYC  -  v-myc avian myelocytomatosis viral...

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Disease relevance of MYC

  • These results establish a novel pathway of promoter insertion oncogenesis that stands in contrast to the pathways used in the activation of c-myc in B lymphomas [1].
  • The pattern of c-myc transcription observed by others in a vast majority of avian leukosis virus-induced neoplasms is not observed in any of the five cell lines examined [2].
  • The latter finding is in contrast to the frequent deletions observed within the c-myc-linked proviruses in B-cell lymphomas [3].
  • Myelocytomatosis virus MC29 is a defective avian retrovirus with a hybrid transforming gene (delta gag-myc) consisting of a 1,358-base pair (bp) sequence from the retroviral gag gene and a 1,568-bp sequence (v-myc) shared with a cellular locus, termed c-myc [4].
  • Using the insertional activation model of c-myc by avian leukosis virus in the induction of bursal lymphoma in chickens, we have now characterized the c-myc locus in feline tissues and investigated the possibility that FeLV may also insert within feline c-myc [5].

High impact information on MYC

  • Bursal lymphocytes expressing either a retroviral v-myc or a c-myc gene deregulated by adjacent retroviral integration retain the ability of embryonic bursal lymphocytes to diversify their immunoglobulin light chain genes [6].
  • In lymphoid leukosis, a cellular oncogene, c-myc, is activated by the insertion of ALV LTR [7].
  • We have analyzed a recovered MC29 virus, HBI, which has a myc gene containing c-myc sequences, acquired by recombination with the cellular gene, and some v-myc sequences [8].
  • However, MC29 has never been reported to cause lymphoid tumors, the disease associated with activation of the c-myc gene by the insertion of a lymphoid leukosis virus genome [8].
  • A cellular homologue, c-myc, has been implicated in B-cell malignancies in mice and humans but is also expressed in many normal cell types and may be important in the control of normal cell proliferation. c-myc is highly conserved in vertebrates [9].

Chemical compound and disease context of MYC


Biological context of MYC

  • Nucleotide sequence analysis of the chicken c-myc gene reveals homologous and unique coding regions by comparison with the transforming gene of avian myelocytomatosis virus MC29, delta gag-myc [4].
  • The chicken c-myc gene, as defined by its homology to the v-myc gene of MC29 virus, is comprised of two exons [2].
  • The myc mRNA in four of these lines also contains increased levels of the first noncoding exon, and evidence is presented that the long terminal repeat (LTR) in the vicinity of c-myc is functioning as an enhancer of c-myc transcription rather than as a promoter in several of these cell lines [2].
  • Using RNA blot analysis, we have localized a noncoding exon to a region that is separated from the c-myc coding sequences by an intron of 700-800 base pairs [11].
  • We have subjected to sequence analysis 2,735 bp of the cloned c-myc gene, which includes the v-myc-related region of 1,568 bp, an intervening sequence of 971 bp, and unique flanking sequences of 45 bp and 195 bp at the 5' and 3' ends, respectively [4].

Anatomical context of MYC

  • In addition, and in a manner consistent with the behavior of its messenger RNA, the immunoprecipitable c-myc protein is sharply induced by the action of mitogens on resting human T cells [12].
  • The deregulation of c-myc expression induced by nearby proviral integration appears to initiate preneoplastic change in a specific window of development, i.e., the bursal stem cell [13].
  • Rapid regulation of c-myc protooncogene expression by progesterone in the avian oviduct [14].
  • Several mutations, deletions and frameshifts, were introduced into the c-myc gene, and these mutant genes were tested for their ability to collaborate with the EJ-ras oncogene to transform rat embryo fibroblasts [15].
  • This analog decreased clonal growth and expression of c-myc oncogene in HL-60 cells by 50% within ten hours of exposure [16].

Associations of MYC with chemical compounds

  • We find that the level of c-myc messenger RNA shows a rapid biphasic change in MEL cells induced to differentiate by dimethyl sulphoxide or hypoxanthine [9].
  • Further, the results demonstrate that the increase in intracellular concentration of c-myc RNA induced by cycloheximide treatment of normal cells is the result of stabilization of this message [17].
  • We performed Northern blot analysis to study the expression of c-jun, c-fos, and c-myc mRNAs during MI using 1 mM NaCN and 20 mM 2-deoxy-d-glucose, and also during the recovery from MI of 30 min [18].
  • Early regulated genes such as c-myc may represent the initial site of action of steroid receptors in the genome [14].
  • Levels of c-myc mRNA began to decrease in response to progesterone by 10 min after injection [14].

Physical interactions of MYC

  • In addition, we showed that completely preventing phosphorylation by substituting all serines within this site resulted in markedly enhanced repression of the CTS-bearing vertebrate c-myc promoters, but did not alter CTCF nuclear localization or in vitro DNA-binding characteristics assayed with c-myc CTSs [19].

Other interactions of MYC

  • Using the techniques of runoff transcription, primer extension, and S1 nuclease protection, we demonstrate that there is a third c-myc exon of approximately equal to 345 base pairs (bp) located 0.7 kbp upstream of the 5' end of the v-myc homology [2].
  • A novel sequence-specific DNA-binding protein, CTCF, which interacts with the chicken c-myc gene promoter, has been identified and partially characterized (V. V. Lobanenkov, R. H. Nicolas, V. V. Adler, H. Paterson, E. M. Klenova, A. V. Polotskaja, and G. H. Goodwin, Oncogene 5:1743-1753, 1990) [20].
  • In the dedifferentiation process, expression of the c-myc gene was enhanced and the transcription of PEC-specific genes (MMP115, pP344) was completely repressed [21].
  • Other genes whose transcription was monitored, c-myc and delta-crystallin, showed distinct patterns of transcriptional regulation, indicating that the changes in HSP70 transcription are specific [22].
  • In this paper we report a comparative study on the parameters affecting turnover of nuclear oncoproteins c-myc, c-myb, and the rapidly metabolized cytoplasmic enzyme ornithine decarboxylase [23].

Analytical, diagnostic and therapeutic context of MYC

  • We used the 1.5 kilobase (kb) PstI fragment of MC29 v-myc in Southern blot analysis to characterize the structure of the c-myc locus in the DNA of 31 naturally occurring feline lymphomas [5].
  • The present study uses the polymerase chain reaction and in situ hybridization to examine c-myc and N-myc mRNA in the embryonic chicken lens at 6, 10, 14 and 19 days of development and compares the pattern of expression obtained with the developmental pattern of cell proliferation and differentiation [24].
  • Enhanced c-myc transcript abundance has been observed in a variety of human malignancies, in normal liver tissue induced to proliferate in vivo by partial hepatectomy and in cells in culture induced to proliferate with the addition of protein hormones and growth factors [25].
  • This paper describes the use of Southwestern blot and DNA gel shift analyses with RBF protein to identify a minimal 54-base pair RBF-binding element in the matrix-associated region (MAR) of the Pg-regulated c-myc gene promoter [26].
  • A nested PCR assay was developed to analyse the appearance of proviral c-myc integrations after ALV infection of lymphoma-susceptible birds, and to determine whether these integrations arise in lymphoma-resistant birds [27].


  1. c-erbB activation in ALV-induced erythroblastosis: novel RNA processing and promoter insertion result in expression of an amino-truncated EGF receptor. Nilsen, T.W., Maroney, P.A., Goodwin, R.G., Rottman, F.M., Crittenden, L.B., Raines, M.A., Kung, H.J. Cell (1985) [Pubmed]
  2. Transcription of three c-myc exons is enhanced in chicken bursal lymphoma cell lines. Linial, M., Groudine, M. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  3. c-erbB activation in avian leukosis virus-induced erythroblastosis: clustered integration sites and the arrangement of provirus in the c-erbB alleles. Raines, M.A., Lewis, W.G., Crittenden, L.B., Kung, H.J. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  4. Nucleotide sequence analysis of the chicken c-myc gene reveals homologous and unique coding regions by comparison with the transforming gene of avian myelocytomatosis virus MC29, delta gag-myc. Watson, D.K., Reddy, E.P., Duesberg, P.H., Papas, T.S. Proc. Natl. Acad. Sci. U.S.A. (1983) [Pubmed]
  5. Isolation of a feline leukaemia provirus containing the oncogene myc from a feline lymphosarcoma. Levy, L.S., Gardner, M.B., Casey, J.W. Nature (1984) [Pubmed]
  6. The effect of alterations in myc gene expression on B cell development in the bursa of Fabricius. Thompson, C.B., Humphries, E.H., Carlson, L.M., Chen, C.L., Neiman, P.E. Cell (1987) [Pubmed]
  7. Activation of the cellular oncogene c-erbB by LTR insertion: molecular basis for induction of erythroblastosis by avian leukosis virus. Fung, Y.K., Lewis, W.G., Crittenden, L.B., Kung, H.J. Cell (1983) [Pubmed]
  8. A recovered avian myelocytomatosis virus that induces lymphomas in chickens: pathogenic properties and their molecular basis. Enrietto, P.J., Payne, L.N., Hayman, M.J. Cell (1983) [Pubmed]
  9. Expression of c-myc changes during differentiation of mouse erythroleukaemia cells. Lachman, H.M., Skoultchi, A.I. Nature (1984) [Pubmed]
  10. The control of chondrocyte differentiation during endochondral bone growth in vivo: changes in TGF-beta and the proto-oncogene c-myc. Loveridge, N., Farquharson, C., Hesketh, J.E., Jakowlew, S.B., Whitehead, C.C., Thorp, B.H. J. Cell. Sci. (1993) [Pubmed]
  11. Nucleotide sequence 5' of the chicken c-myc coding region: localization of a noncoding exon that is absent from myc transcripts in most avian leukosis virus-induced lymphomas. Shih, C.K., Linial, M., Goodenow, M.M., Hayward, W.S. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  12. Antibodies to human c-myc oncogene product: evidence of an evolutionarily conserved protein induced during cell proliferation. Persson, H., Hennighausen, L., Taub, R., DeGrado, W., Leder, P. Science (1984) [Pubmed]
  13. Retrovirus-induced B cell neoplasia in the bursa of Fabricius. Neiman, P.E. Adv. Immunol. (1994) [Pubmed]
  14. Rapid regulation of c-myc protooncogene expression by progesterone in the avian oviduct. Fink, K.L., Wieben, E.D., Woloschak, G.E., Spelsberg, T.C. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  15. Evolutionarily conserved regions of the human c-myc protein can be uncoupled from transforming activity. Sarid, J., Halazonetis, T.D., Murphy, W., Leder, P. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  16. Novel vitamin D analogs that modulate leukemic cell growth and differentiation with little effect on either intestinal calcium absorption or bone mobilization. Zhou, J.Y., Norman, A.W., Lübbert, M., Collins, E.D., Uskokovic, M.R., Koeffler, H.P. Blood (1989) [Pubmed]
  17. Enhanced transcription of c-myc in bursal lymphoma cells requires continuous protein synthesis. Linial, M., Gunderson, N., Groudine, M. Science (1985) [Pubmed]
  18. Immediate-early gene induction and MAP kinase activation during recovery from metabolic inhibition in cultured cardiac myocytes. Yao, A., Takahashi, T., Aoyagi, T., Kinugawa, K., Kohmoto, O., Sugiura, S., Serizawa, T. J. Clin. Invest. (1995) [Pubmed]
  19. Functional phosphorylation sites in the C-terminal region of the multivalent multifunctional transcriptional factor CTCF. Klenova, E.M., Chernukhin, I.V., El-Kady, A., Lee, R.E., Pugacheva, E.M., Loukinov, D.I., Goodwin, G.H., Delgado, D., Filippova, G.N., León, J., Morse, H.C., Neiman, P.E., Lobanenkov, V.V. Mol. Cell. Biol. (2001) [Pubmed]
  20. CTCF, a conserved nuclear factor required for optimal transcriptional activity of the chicken c-myc gene, is an 11-Zn-finger protein differentially expressed in multiple forms. Klenova, E.M., Nicolas, R.H., Paterson, H.F., Carne, A.F., Heath, C.M., Goodwin, G.H., Neiman, P.E., Lobanenkov, V.V. Mol. Cell. Biol. (1993) [Pubmed]
  21. Genetic characterization of the multipotent dedifferentiated state of pigmented epithelial cells in vitro. Agata, K., Kobayashi, H., Itoh, Y., Mochii, M., Sawada, K., Eguchi, G. Development (1993) [Pubmed]
  22. Expression of HSP70 mRNA in the embryonic chicken lens: association with differentiation. Dash, A., Chung, S., Zelenka, P.S. Exp. Eye Res. (1994) [Pubmed]
  23. c-myc and c-myb protein degradation: effect of metabolic inhibitors and heat shock. Lüscher, B., Eisenman, R.N. Mol. Cell. Biol. (1988) [Pubmed]
  24. Contrasting patterns of c-myc and N-myc expression in proliferating, quiescent, and differentiating cells of the embryonic chicken lens. Harris, L.L., Talian, J.C., Zelenka, P.S. Development (1992) [Pubmed]
  25. Steroid-induced cell proliferation in vivo is associated with increased c-myc proto-oncogene transcript abundance. Rempel, S.A., Johnston, R.N. Development (1988) [Pubmed]
  26. A DNA-binding element for a steroid receptor-binding factor is flanked by dual nuclear matrix DNA attachment sites in the c-myc gene promoter. Lauber, A.H., Barrett, T.J., Subramaniam, M., Schuchard, M., Spelsberg, T.C. J. Biol. Chem. (1997) [Pubmed]
  27. Resistance to avian leukosis virus lymphomagenesis occurs subsequent to proviral c-myc integration. Bird, K.J., Semus, H.L., Ruddell, A. Oncogene (1999) [Pubmed]
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