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Gene Review

Nyx  -  nyctalopin

Mus musculus

Synonyms: CLNP, CSNB1, CSNB4, Nyctalopin, nob
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Disease relevance of Nyx

  • Nyx expression was found during all stages of postnatal retinal development and was confined to cells of the inner nuclear layer and the ganglion cell layer in adult mouse and rat retinas [1].
  • PURPOSE: The available evidence indicates that the naturally occurring mouse mutant nob (no b-wave) provides an animal model for the complete form of human X-linked congenital stationary night blindness (CSNB1) [2].

High impact information on Nyx

  • Transgenic rescue of the mutated protein (nyctalopin) within nob retinal interneurons, without rescuing expression in either retinal projection neurons or their postsynaptic targets in the dLGN, restores spontaneous retinal activity patterns and prevents desegregation [3].
  • Failure to Maintain Eye-Specific Segregation in nob, a Mutant with Abnormally Patterned Retinal Activity [3].
  • METHODS: Nyx was isolated by conventional DNA library screening and polymerase chain reaction (PCR)-based approaches [1].
  • Deletion of the ER signal sequence in Nyx delocalized the intracellular V5-Nyx protein and caused its dispersion in the cytosol [4].
  • This model will be useful in defining the role of nyctalopin in signal transmission between photoreceptors and retinal bipolar cells [2].

Biological context of Nyx


Anatomical context of Nyx

  • PURPOSE: To describe a naturally occurring X-linked recessive mutation, no b-wave (nob), that compromises visual transmission between photoreceptors and second-order neurons in mice [5].

Associations of Nyx with chemical compounds

  • The nyctalopin protein contains 11 leucine-rich repeats and is flanked by cysteine rich regions, which identifies it as a member of the small leucine rich proteoglycan family [2].

Other interactions of Nyx


Analytical, diagnostic and therapeutic context of Nyx


  1. Isolation of the mouse nyctalopin gene nyx and expression studies in mouse and rat retina. Pesch, K., Zeitz, C., Fries, J.E., Münscher, S., Pusch, C.M., Kohler, K., Berger, W., Wissinger, B. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
  2. Identification of the gene and the mutation responsible for the mouse nob phenotype. Gregg, R.G., Mukhopadhyay, S., Candille, S.I., Ball, S.L., Pardue, M.T., McCall, M.A., Peachey, N.S. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
  3. Failure to Maintain Eye-Specific Segregation in nob, a Mutant with Abnormally Patterned Retinal Activity. Demas, J., Sagdullaev, B.T., Green, E., Jaubert-Miazza, L., McCall, M.A., Gregg, R.G., Wong, R.O., Guido, W. Neuron (2006) [Pubmed]
  4. NYX (nyctalopin on chromosome X), the gene mutated in congenital stationary night blindness, encodes a cell surface protein. Zeitz, C., Scherthan, H., Freier, S., Feil, S., Suckow, V., Schweiger, S., Berger, W. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
  5. A naturally occurring mouse model of X-linked congenital stationary night blindness. Pardue, M.T., McCall, M.A., LaVail, M.M., Gregg, R.G., Peachey, N.S. Invest. Ophthalmol. Vis. Sci. (1998) [Pubmed]
  6. Localization of nyctalopin in the mammalian retina. Morgans, C.W., Ren, G., Akileswaran, L. Eur. J. Neurosci. (2006) [Pubmed]
  7. Localization of the mouse nob (no b-wave) gene to the centromeric region of the X chromosome. Candille, S.I., Pardue, M.T., McCall, M.A., Peachey, N.S., Gregg, R.G. Invest. Ophthalmol. Vis. Sci. (1999) [Pubmed]
  8. Contribution of Kir4.1 to the mouse electroretinogram. Wu, J., Marmorstein, A.D., Kofuji, P., Peachey, N.S. Mol. Vis. (2004) [Pubmed]
  9. The nob mutation does not protect against light-induced retinal degeneration. Pardue, M.T., Grimm, C., Wenzel, A., Remé, C.E. Adv. Exp. Med. Biol. (2003) [Pubmed]
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