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Gene Review

Pcgf2  -  polycomb group ring finger 2

Mus musculus

Synonyms: DNA-binding protein Mel-18, Mel-18, Mel18, Melanoma nuclear protein 18, Polycomb group RING finger protein 2, ...
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Disease relevance of Pcgf2


High impact information on Pcgf2

  • The bmi-1 and mel-18 gene products define a new family of DNA-binding proteins involved in cell proliferation and tumorigenesis [4].
  • These alterations are enhanced by Zfp144 mutation but repressed by Mll mutation (a trithorax-group gene) [5].
  • We therefore propose that mel-18 negatively regulates the cell cycle through a c-myc/cdc25 cascade [6].
  • Strikingly, the axial skeleton and lymphoid phenotypes are identical in both mel-18 and bmi-1 mutants, indicating that the Mel-18 and Bmi-1 gene products might act in the same genetic cascade [7].
  • In this study, the severe combined immunodeficiency observed in mel-18 mutant mice is correlated with the impaired mitotic response of lymphocyte precursors upon interleukin-7 stimulation [7].

Biological context of Pcgf2


Anatomical context of Pcgf2

  • Our results provide genetic evidence that Cited2 controls the expression of INK4a/ARF and fibroblast proliferation, at least in part via the polycomb-group genes Bmi1 and Mel18 [1].
  • In this report we demonstrate that the loss of the PcG gene mel-18 impairs the expansion of the most immature T progenitor cells at a stage before the rearrangement of the TCR beta-chain gene in vivo and in vitro [12].
  • Here, we demonstrate that mel-18 negatively regulates the self-renewal activity of hematopoietic stem cells (HSCs) [11].
  • Mice lacking the gene mel-18, a member of the mammalian Polycomb group genes, displayed impaired thymic T cell development [13].
  • Here, we show in vitro by pull-down assays and in vivo in transiently transfected COS-7 cells that Mel-18 forms homodimers [14].

Regulatory relationships of Pcgf2

  • RESULTS: The Hoxb4 gene was highly expressed in HSCs derived from mel-18(-/-) mice [11].

Other interactions of Pcgf2

  • Collectively, these data indicate that mel-18 contributes to the maintenance of the active state of the Hes-1 gene as a cellular memory system, thereby supporting the expansion of early T progenitors [12].
  • However, expression of the other PcG members Mel-18 and Hpc-2 correlated with the cell cycle regulators [2].
  • CONCLUSION: Loss or knockdown of mel-18 leads to the expression of Hoxb4, an increase in the proportion of HSCs in G0 phase, and the subsequent promotion of HSC self-renewal [11].
  • Chemokine-mediated thymopoiesis is regulated by a mammalian Polycomb group gene, mel-18 [13].

Analytical, diagnostic and therapeutic context of Pcgf2


  1. Transcriptional coactivator Cited2 induces Bmi1 and Mel18 and controls fibroblast proliferation via Ink4a/ARF. Kranc, K.R., Bamforth, S.D., Bragança, J., Norbury, C., van Lohuizen, M., Bhattacharya, S. Mol. Cell. Biol. (2003) [Pubmed]
  2. Implication of Polycomb Members Bmi-1, Mel-18, and Hpc-2 in the Regulation of p16INK4a, p14ARF, h-TERT, and c-Myc Expression in Primary Breast Carcinomas. Silva, J., Garc??a, J.M., Pe??a, C., Garc??a, V., Dom??nguez, G., Su??rez, D., Camacho, F.I., Espinosa, R., Provencio, M., Espa??a, P., Bonilla, F. Clin. Cancer Res. (2006) [Pubmed]
  3. Mutation analysis of the mel-18 gene that shows decreased expression in human breast cancer cell lines. Matsuo, F., Yano, K., Saito, H., Morotomi, K., Kato, M., Yoshimoto, M., Kasumi, F., Akiyama, F., Sakamoto, G., Miki, Y. Breast Cancer (2002) [Pubmed]
  4. The bmi-1 and mel-18 gene products define a new family of DNA-binding proteins involved in cell proliferation and tumorigenesis. Goebl, M.G. Cell (1991) [Pubmed]
  5. Mammalian polycomb-mediated repression of Hox genes requires the essential spliceosomal protein Sf3b1. Isono, K., Mizutani-Koseki, Y., Komori, T., Schmidt-Zachmann, M.S., Koseki, H. Genes Dev. (2005) [Pubmed]
  6. mel-18 negatively regulates cell cycle progression upon B cell antigen receptor stimulation through a cascade leading to c-myc/cdc25. Tetsu, O., Ishihara, H., Kanno, R., Kamiyasu, M., Inoue, H., Tokuhisa, T., Taniguchi, M., Kanno, M. Immunity (1998) [Pubmed]
  7. The role of mel-18, a mammalian Polycomb group gene, during IL-7-dependent proliferation of lymphocyte precursors. Akasaka, T., Tsuji, K., Kawahira, H., Kanno, M., Harigaya, K., Hu, L., Ebihara, Y., Nakahata, T., Tetsu, O., Taniguchi, M., Koseki, H. Immunity (1997) [Pubmed]
  8. mel-18, a Polycomb group-related mammalian gene, encodes a transcriptional negative regulator with tumor suppressive activity. Kanno, M., Hasegawa, M., Ishida, A., Isono, K., Taniguchi, M. EMBO J. (1995) [Pubmed]
  9. A role for mel-18, a Polycomb group-related vertebrate gene, during theanteroposterior specification of the axial skeleton. Akasaka, T., Kanno, M., Balling, R., Mieza, M.A., Taniguchi, M., Koseki, H. Development (1996) [Pubmed]
  10. Mice doubly deficient for the Polycomb Group genes Mel18 and Bmi1 reveal synergy and requirement for maintenance but not initiation of Hox gene expression. Akasaka, T., van Lohuizen, M., van der Lugt, N., Mizutani-Koseki, Y., Kanno, M., Taniguchi, M., Vidal, M., Alkema, M., Berns, A., Koseki, H. Development (2001) [Pubmed]
  11. Polycomb group gene mel-18 modulates the self-renewal activity and cell cycle status of hematopoietic stem cells. Kajiume, T., Ninomiya, Y., Ishihara, H., Kanno, R., Kanno, M. Exp. Hematol. (2004) [Pubmed]
  12. Polycomb group gene mel-18 regulates early T progenitor expansion by maintaining the expression of Hes-1, a target of the Notch pathway. Miyazaki, M., Kawamoto, H., Kato, Y., Itoi, M., Miyazaki, K., Masuda, K., Tashiro, S., Ishihara, H., Igarashi, K., Amagai, T., Kanno, R., Kanno, M. J. Immunol. (2005) [Pubmed]
  13. Chemokine-mediated thymopoiesis is regulated by a mammalian Polycomb group gene, mel-18. Miyazaki, K., Inoue, H., Onai, N., Ishihara, H., Kanno, M. Immunol. Lett. (2002) [Pubmed]
  14. Dimerization of the Polycomb-group protein Mel-18 is regulated by PKC phosphorylation. Fujisaki, S., Ninomiya, Y., Ishihara, H., Miyazaki, M., Kanno, R., Asahara, T., Kanno, M. Biochem. Biophys. Res. Commun. (2003) [Pubmed]
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