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Gene Review

Ndn  -  necdin

Mus musculus

Synonyms: AI528698, Necdin, Peg6
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Disease relevance of Ndn

  • Essential role for the Prader-Willi syndrome protein necdin in axonal outgrowth [1].
  • Morphological abnormalities in axonal outgrowth and fasciculation manifest in several regions of the nervous system in necdin null mouse embryos, including axons of sympathetic, retinal ganglion cell, serotonergic and catecholaminergic neurons [1].
  • A ternary complex of necdin, MAGE-D1, and Msx2 was formed in vitro, and an endogenous complex containing these three proteins was detected in differentiating embryonal carcinoma cells [2].
  • Moreover, necdin bound to adenovirus E1A, another viral oncoprotein that forms a specific complex with Rb [3].
  • In addition, necdin suppressed the colony formation of Rb-deficient SAOS-2 osteosarcoma cells [3].
  • These data suggest that inhibition of muscle wasting using necdin is a feasible approach to treat cachexia in neoplastic patients [4].

Psychiatry related information on Ndn

  • RESULTS: We have now identified the NDNL2 (also known as MAGE-G) gene within the 15q autistic disorder susceptibility region and have mapped its murine homolog to the region of conserved synteny near necdin (Ndn) on mouse Chr 7 [5].

High impact information on Ndn


Chemical compound and disease context of Ndn


Biological context of Ndn

  • We have localized the mouse locus Ndn encoding necdin to chromosome 7 in a region of conserved synteny with human chromosome 15q11-q13, by genetic mapping in an interspecific backcross panel [12].
  • After activity deprivation, CGNs underwent apoptosis, which was augmented in those prepared from mice defective in the paternal Ndn allele (Ndn(+m/-p)) [13].
  • Necdin is postulated to govern the permanent arrest of cell growth of post-mitotic neurons during murine nervous system development [12].
  • The normal imprinted expression and methylation patterns of necdin, a gene outside the deletion region, indicate that the deletion is not an imprinting mutation [14].
  • We then examined the ability of necdin to bind to the transcription factor E2F1, a cellular Rb-binding factor involved in cell-cycle progression [3].

Anatomical context of Ndn

  • These data demonstrate that necdin mediates intracellular processes essential for neurite outgrowth and that loss of necdin impinges on axonal outgrowth [1].
  • Necdin is a potent growth suppressor that is expressed predominantly in postmitotic cells such as neurons and skeletal muscle cells [2].
  • The subcellular fractionation analysis revealed that necdin was concentrated in the cytosol fraction of brain cells [15].
  • Finally we also exclude an anti-proliferative role of Necdin in developing sensory neurons [16].
  • Viable NECDIN: mutants show a reduction in both oxytocin-producing and luteinizing hormone-releasing hormone (LHRH)-producing neurons in hypothalamus [17].

Associations of Ndn with chemical compounds


Physical interactions of Ndn

  • Recently, Necdin and other MAGE proteins were found to interact in vitro with the intracellular domain of the p75NTR neurotrophin receptor, but this interaction has not been validated in vivo [21].

Regulatory relationships of Ndn


Other interactions of Ndn

  • Necdin and Magel2 are related proteins inactivated in Prader-Willi syndrome (PWS), a sporadic chromosomal deletion disorder [1].
  • In vitro binding and co-immunoprecipitation analyses revealed that MAGE-D1 directly interacted with necdin via the homology domain and Msx1 (or Msx2) via the repeat domain [2].
  • These results suggest that necdin and MAGE-D1 cooperate to modulate the function of Dlx/Msx homeodomain proteins in cellular differentiation [2].
  • Necdin shows a significant homology to MAGE (melanoma antigen) family proteins, all of which contain a large homology domain [2].
  • We report here that the spatial and temporal expression of p75NTR is included in Necdin expression domain [21].

Analytical, diagnostic and therapeutic context of Ndn


  1. Essential role for the Prader-Willi syndrome protein necdin in axonal outgrowth. Lee, S., Walker, C.L., Karten, B., Kuny, S.L., Tennese, A.A., O'Neill, M.A., Wevrick, R. Hum. Mol. Genet. (2005) [Pubmed]
  2. Necdin interacts with the Msx2 homeodomain protein via MAGE-D1 to promote myogenic differentiation of C2C12 cells. Kuwajima, T., Taniura, H., Nishimura, I., Yoshikawa, K. J. Biol. Chem. (2004) [Pubmed]
  3. Necdin, a postmitotic neuron-specific growth suppressor, interacts with viral transforming proteins and cellular transcription factor E2F1. Taniura, H., Taniguchi, N., Hara, M., Yoshikawa, K. J. Biol. Chem. (1998) [Pubmed]
  4. Necdin is expressed in cachectic skeletal muscle to protect fibers from tumor-induced wasting. Sciorati, C., Touvier, T., Buono, R., Pessina, P., François, S., Perrotta, C., Meneveri, R., Clementi, E., Brunelli, S. J. Cell. Sci. (2009) [Pubmed]
  5. A necdin/MAGE-like gene in the chromosome 15 autism susceptibility region: expression, imprinting, and mapping of the human and mouse orthologues. Chibuk, T.K., Bischof, J.M., Wevrick, R. BMC Genet. (2001) [Pubmed]
  6. Disruption of the mouse necdin gene results in early post-natal lethality. Gérard, M., Hernandez, L., Wevrick, R., Stewart, C.L. Nat. Genet. (1999) [Pubmed]
  7. Necdin-deficient mice do not show lethality or the obesity and infertility of Prader-Willi syndrome. Tsai, T.F., Armstrong, D., Beaudet, A.L. Nat. Genet. (1999) [Pubmed]
  8. Prediction of preadipocyte differentiation by gene expression reveals role of insulin receptor substrates and necdin. Tseng, Y.H., Butte, A.J., Kokkotou, E., Yechoor, V.K., Taniguchi, C.M., Kriauciunas, K.M., Cypess, A.M., Niinobe, M., Yoshikawa, K., Patti, M.E., Kahn, C.R. Nat. Cell Biol. (2005) [Pubmed]
  9. Neuronally-expressed necdin gene: an imprinted candidate gene in Prader-Willi syndrome. Sutcliffe, J.S., Han, M., Christian, S.L., Ledbetter, D.H. Lancet (1997) [Pubmed]
  10. NSCL-1 and NSCL-2 synergistically determine the fate of GnRH-1 neurons and control necdin gene expression. Krüger, M., Ruschke, K., Braun, T. EMBO J. (2004) [Pubmed]
  11. Structure and expression of the mouse necdin gene. Identification of a postmitotic neuron-restrictive core promoter. Uetsuki, T., Takagi, K., Sugiura, H., Yoshikawa, K. J. Biol. Chem. (1996) [Pubmed]
  12. The necdin gene is deleted in Prader-Willi syndrome and is imprinted in human and mouse. MacDonald, H.R., Wevrick, R. Hum. Mol. Genet. (1997) [Pubmed]
  13. Necdin downregulates CDC2 expression to attenuate neuronal apoptosis. Kurita, M., Kuwajima, T., Nishimura, I., Yoshikawa, K. J. Neurosci. (2006) [Pubmed]
  14. Paternal deletion from Snrpn to Ube3a in the mouse causes hypotonia, growth retardation and partial lethality and provides evidence for a gene contributing to Prader-Willi syndrome. Tsai, T.F., Jiang, Y.H., Bressler, J., Armstrong, D., Beaudet, A.L. Hum. Mol. Genet. (1999) [Pubmed]
  15. Cellular and subcellular localization of necdin in fetal and adult mouse brain. Niinobe, M., Koyama, K., Yoshikawa, K. Dev. Neurosci. (2000) [Pubmed]
  16. Sensory defects in Necdin deficient mice result from a loss of sensory neurons correlated within an increase of developmental programmed cell death. Andrieu, D., Meziane, H., Marly, F., Angelats, C., Fernandez, P.A., Muscatelli, F. BMC Dev. Biol. (2006) [Pubmed]
  17. Disruption of the mouse Necdin gene results in hypothalamic and behavioral alterations reminiscent of the human Prader-Willi syndrome. Muscatelli, F., Abrous, D.N., Massacrier, A., Boccaccio, I., Le Moal, M., Cau, P., Cremer, H. Hum. Mol. Genet. (2000) [Pubmed]
  18. Biochemical characterization of mouse brain necdin. Maruyama, E. Biochem. J. (1996) [Pubmed]
  19. Disruption of the paternal necdin gene diminishes TrkA signaling for sensory neuron survival. Kuwako, K., Hosokawa, A., Nishimura, I., Uetsuki, T., Yamada, M., Nada, S., Okada, M., Yoshikawa, K. J. Neurosci. (2005) [Pubmed]
  20. Necdin-related MAGE proteins differentially interact with the E2F1 transcription factor and the p75 neurotrophin receptor. Kuwako, K., Taniura, H., Yoshikawa, K. J. Biol. Chem. (2004) [Pubmed]
  21. Expression of the Prader-Willi gene Necdin during mouse nervous system development correlates with neuronal differentiation and p75NTR expression. Andrieu, D., Watrin, F., Niinobe, M., Yoshikawa, K., Muscatelli, F., Fernandez, P.A. Gene Expr. Patterns (2003) [Pubmed]
  22. Necdin is required for terminal differentiation and survival of primary dorsal root ganglion neurons. Takazaki, R., Nishimura, I., Yoshikawa, K. Exp. Cell Res. (2002) [Pubmed]
  23. Necdin acts as a transcriptional repressor that interacts with multiple guanosine clusters. Matsumoto, K., Taniura, H., Uetsuki, T., Yoshikawa, K. Gene (2001) [Pubmed]
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