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Gene Review

MAGEC2  -  melanoma antigen family C, 2

Homo sapiens

Synonyms: CT10, Cancer/testis antigen 10, HCA587, Hepatocellular carcinoma-associated antigen 587, MAGE-C2, ...
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Disease relevance of MAGEC2


High impact information on MAGEC2

  • An antitumor cytotoxic T lymphocyte (CTL) recognizing a MAGE-C2 antigen showed a much higher enrichment with a frequency of approximately 10%, 1,000 times higher than its blood frequency [5].
  • CTLp's recognizing MAGE-C2 and gp100 antigens were already present before vaccination, but new clonotypes appeared afterwards [6].
  • These antibodies detected several of the same tyrosine phosphoproteins in chicken embryo fibroblasts transformed by avian retroviruses Y73 and CT10, encoding the yes and crk oncogenes, respectively [7].
  • IC50imatinib was determined in pretherapy blood samples by measuring the in vitro imatinib-induced reduction of the phosphorylated form of the adaptor protein Crkl (CT10 regulator of kinase like) [8].
  • The transforming gene of the avian sarcoma virus CT10 encodes a fusion protein (p47gag-crk or v-Crk) containing viral Gag sequences fused to cellular sequences consisting primarily of Src homology regions 2 and 3 (SH2 and SH3 sequences) [9].

Biological context of MAGEC2

  • Chromosome mapping localized CT10 to Xq27, in close proximity to CT7/MAGE-C1 and MAGE-A genes [10].
  • The genome of avian sarcoma virus CT10 encodes a fusion protein in which viral Gag sequences are fused to cellular Crk sequences containing primarily Src homology 2 (SH2) and Src homology 3 (SH3) domains [11].
  • Melatonin (0.9 to 30 microg/mouse, s.c.) administration during 3 days at the end of the subjective day (CT 10) to C3H/HeN mice kept in constant dark phase advanced circadian rhythms of wheel running activity in a dose-dependent manner [EC50=0.72 microg/mouse; 0.98+/-0.08 h (n=15) maximal advance at 9 microg/mouse] [12].
  • We therefore suggest that the competitive binding of overexpressed v-Crk affects an efficient interaction of Csk with tyrosine-phosphorylated paxillin in CT10-transformed CEF [13].
  • We have constructed a series of mutants with deletion, linker insertion, and point mutations in the v-crk oncogene of avian sarcoma virus CT10 [14].

Anatomical context of MAGEC2

  • Two such proteins, HCA587 and HCA661, were predominantly detected in testis, but not in other normal tissues, except for a weak expression in normal pancreas [15].
  • Two new tumor-specific antigenic peptides encoded by gene MAGE-C2 and presented to cytolytic T lymphocytes by HLA-A2 [1].
  • CT10 mRNA is expressed in testis and in 20 to 30% of various human cancers [10].
  • The CTL clones recognizing these 2 peptides also recognized allogeneic tumor cell lines expressing MAGE-C2 and HLA-A2 [1].
  • No HCA587 protein was shown in normal tissues except germ cells in testis and Purkinji cells in cerebellum [2].

Associations of MAGEC2 with chemical compounds

  • Neither the selective MT2 melatonin receptor antagonists 4P-ADOT and 4P-PDOT (90 microg/mouse, s.c.) nor luzindole (300 microg/mouse, s.c.), which shows 25-fold higher affinity for the MT2 than the mt1 subtype, affected the phase of circadian activity rhythms when given alone at CT 10 [12].
  • To extend these findings to p130, the major phosphotyrosine-containing protein in CT10-transformed cells, we utilized a nitrocellulose filter binding assay [16].
  • Infection with CT10 causes a dramatic increase in the level of tyrosine phosphorylation of several cellular proteins [14].
  • In contrast, injection of shifters at CT 10 was associated with a pronounced rise in serum cortisol levels.(ABSTRACT TRUNCATED AT 400 WORDS)[17]
  • Pre-treatment of hamsters at CT 6 with the serotonergic antagonist ritanserin (1-5 mg/kg, which acts at both 5-HT2 and the putative 5-HT7 receptor, impaired the phase-advancing response to arousal at CT 10 but the drug was without effect on phase advances induced by exposure to light [18].

Other interactions of MAGEC2


Analytical, diagnostic and therapeutic context of MAGEC2

  • Additionally, patients with CT10-positive tumors had an improved disease-free survival (P=0.008) and overall survival (P=0.037) compared with patients with CT10-negative tumors [22].
  • Our data suggest that identification of this new HCA587/HLA-A*0201 peptide FLAKLNNTV may facilitate the design of peptide-based immunotherapies for the treatment of HCA587-bearing HCC patients [19].
  • An intraperitoneal injection of 1-100 microg/kg melatonin 2-h before the activity onset time (CT 10) induced phase advances of free-running activity rhythms in a dose-dependent manner (ED50=1.3 microg/kg) [23].
  • Western blot results proved the recombinant protein HCA587 had the similar antigenicity with its native counterpart [20].


  1. Two new tumor-specific antigenic peptides encoded by gene MAGE-C2 and presented to cytolytic T lymphocytes by HLA-A2. Ma, W., Germeau, C., Vigneron, N., Maernoudt, A.S., Morel, S., Boon, T., Coulie, P.G., Van den Eynde, B.J. Int. J. Cancer (2004) [Pubmed]
  2. HCA587 antigen expression in normal tissues and cancers: correlation with tumor differentiation in hepatocellular carcinoma. Li, B., Qian, X.P., Pang, X.W., Zou, W.Z., Wang, Y.P., Wu, H.Y., Chen, W.F. Lab. Invest. (2003) [Pubmed]
  3. Sequence similarity of phospholipase C with the non-catalytic region of src. Stahl, M.L., Ferenz, C.R., Kelleher, K.L., Kriz, R.W., Knopf, J.L. Nature (1988) [Pubmed]
  4. Epstein-Barr virus latent membrane protein 2A (LMP2A) employs the SLP-65 signaling module. Engels, N., Merchant, M., Pappu, R., Chan, A.C., Longnecker, R., Wienands, J. J. Exp. Med. (2001) [Pubmed]
  5. Contrasting frequencies of antitumor and anti-vaccine T cells in metastases of a melanoma patient vaccinated with a MAGE tumor antigen. Lurquin, C., Lethé, B., De Plaen, E., Corbière, V., Théate, I., van Baren, N., Coulie, P.G., Boon, T. J. Exp. Med. (2005) [Pubmed]
  6. High frequency of antitumor T cells in the blood of melanoma patients before and after vaccination with tumor antigens. Germeau, C., Ma, W., Schiavetti, F., Lurquin, C., Henry, E., Vigneron, N., Brasseur, F., Lethé, B., De Plaen, E., Velu, T., Boon, T., Coulie, P.G. J. Exp. Med. (2005) [Pubmed]
  7. Monoclonal antibodies to individual tyrosine-phosphorylated protein substrates of oncogene-encoded tyrosine kinases. Kanner, S.B., Reynolds, A.B., Vines, R.R., Parsons, J.T. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  8. In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de novo CML. White, D., Saunders, V., Lyons, A.B., Branford, S., Grigg, A., To, L.B., Hughes, T. Blood (2005) [Pubmed]
  9. Expression of the v-crk oncogene product in PC12 cells results in rapid differentiation by both nerve growth factor- and epidermal growth factor-dependent pathways. Hempstead, B.L., Birge, R.B., Fajardo, J.E., Glassman, R., Mahadeo, D., Kraemer, R., Hanafusa, H. Mol. Cell. Biol. (1994) [Pubmed]
  10. CT10: a new cancer-testis (CT) antigen homologous to CT7 and the MAGE family, identified by representational-difference analysis. Güre, A.O., Stockert, E., Arden, K.C., Boyer, A.D., Viars, C.S., Scanlan, M.J., Old, L.J., Chen, Y.T. Int. J. Cancer (2000) [Pubmed]
  11. Identification and characterization of a high-affinity interaction between v-Crk and tyrosine-phosphorylated paxillin in CT10-transformed fibroblasts. Birge, R.B., Fajardo, J.E., Reichman, C., Shoelson, S.E., Songyang, Z., Cantley, L.C., Hanafusa, H. Mol. Cell. Biol. (1993) [Pubmed]
  12. Selective MT2 melatonin receptor antagonists block melatonin-mediated phase advances of circadian rhythms. Dubocovich, M.L., Yun, K., Al-Ghoul, W.M., Benloucif, S., Masana, M.I. FASEB J. (1998) [Pubmed]
  13. Possible v-Crk-induced transformation through activation of Src kinases. Sabe, H., Shoelson, S.E., Hanafusa, H. J. Biol. Chem. (1995) [Pubmed]
  14. Mutagenic analysis of the v-crk oncogene: requirement for SH2 and SH3 domains and correlation between increased cellular phosphotyrosine and transformation. Mayer, B.J., Hanafusa, H. J. Virol. (1990) [Pubmed]
  15. Large scale identification of human hepatocellular carcinoma-associated antigens by autoantibodies. Wang, Y., Han, K.J., Pang, X.W., Vaughan, H.A., Qu, W., Dong, X.Y., Peng, J.R., Zhao, H.T., Rui, J.A., Leng, X.S., Cebon, J., Burgess, A.W., Chen, W.F. J. Immunol. (2002) [Pubmed]
  16. Tyrosine-phosphorylated epidermal growth factor receptor and cellular p130 provide high affinity binding substrates to analyze Crk-phosphotyrosine-dependent interactions in vitro. Birge, R.B., Fajardo, J.E., Mayer, B.J., Hanafusa, H. J. Biol. Chem. (1992) [Pubmed]
  17. Non-photic circadian entrainment in the Syrian hamster is not associated with phosphorylation of the transcriptional regulator CREB within the suprachiasmatic nucleus, but is associated with adrenocortical activation. Sumova, A., Ebling, F.J., Maywood, E.S., Herbert, J., Hastings, M.H. Neuroendocrinology (1994) [Pubmed]
  18. Serotonergic antagonists impair arousal-induced phase shifts of the circadian system of the syrian hamster. Sumova, A., Maywood, E.S., Selvage, D., Ebling, F.J., Hastings, M.H. Brain Res. (1996) [Pubmed]
  19. Identification of a new HLA-A*0201-restricted CD8+ T cell epitope from hepatocellular carcinoma-associated antigen HCA587. Li, B., Wang, Y., Chen, J., Wu, H., Chen, W. Clin. Exp. Immunol. (2005) [Pubmed]
  20. Expression, purification and serological analysis of hepatocellular carcinoma associated antigen HCA587 in insect cells. Li, B., Wu, H.Y., Qian, X.P., Li, Y., Chen, W.F. World J. Gastroenterol. (2003) [Pubmed]
  21. Elicitation of both CD4 and CD8 T-cell-mediated specific immune responses to HCA587 protein by autologous dendritic cells. Li, B., He, X., Pang, X., Zhang, H., Chen, J., Chen, W. Scand. J. Immunol. (2004) [Pubmed]
  22. Cancer-testis antigens: expression and correlation with survival in human urothelial carcinoma. Sharma, P., Shen, Y., Wen, S., Bajorin, D.F., Reuter, V.E., Old, L.J., Jungbluth, A.A. Clin. Cancer Res. (2006) [Pubmed]
  23. Methylcobalamin amplifies melatonin-induced circadian phase shifts by facilitation of melatonin synthesis in the rat pineal gland. Ikeda, M., Asai, M., Moriya, T., Sagara, M., Inoué, S., Shibata, S. Brain Res. (1998) [Pubmed]
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