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Gene Review

T(16C3-4;17A2)65Dn  -  reciprocal translocation, Chr 16,...

Mus musculus

Synonyms: T(16;17)65Dn, T65Dn, Ts65Dn
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Disease relevance of T(16C3-4;17A2)65Dn


Psychiatry related information on T(16C3-4;17A2)65Dn


High impact information on T(16C3-4;17A2)65Dn


Chemical compound and disease context of T(16C3-4;17A2)65Dn


Biological context of T(16C3-4;17A2)65Dn


Anatomical context of T(16C3-4;17A2)65Dn


Associations of T(16C3-4;17A2)65Dn with chemical compounds


Physical interactions of T(16C3-4;17A2)65Dn


Regulatory relationships of T(16C3-4;17A2)65Dn


Other interactions of T(16C3-4;17A2)65Dn


Analytical, diagnostic and therapeutic context of T(16C3-4;17A2)65Dn

  • RNA gel blot analysis and in situ hybridization showed a marked increase in amyloid precursor protein mRNA in the trisomy 16 mouse head and brain when compared with euploid littermates or with trisomy 19 mice [23].
  • Western blot analysis showed that MT-I/II was upregulated and the protein carbonyl content was higher in trisomy 16 compared with euploid cultures [27].
  • Here we show that restoration of the physiological level of the TrkB.T1 receptor by gene targeting rescues Ts16 cortical cell and hippocampal neuronal death [34].
  • Cholinergic function of normal neurons was significantly down-regulated by coculture with Ts16 glia [35].
  • Denervation of the hippocampus produced a significant increase in the size of Ts 16 cholinergic neurons [36].


  1. Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: An animal model of down syndrome. Opazo, P., Saud, K., de Saint Pierre, M., C??rdenas, A.M., Allen, D.D., Segura-Aguilar, J., Caviedes, R., Caviedes, P. J. Neurosci. Res. (2006) [Pubmed]
  2. Choline acetyltransferase activity at different ages in brain of Ts65Dn mice, an animal model for Down's syndrome and related neurodegenerative diseases. Contestabile, A., Fila, T., Bartesaghi, R., Contestabile, A., Ciani, E. J. Neurochem. (2006) [Pubmed]
  3. Nerve growth factor reverses neuronal atrophy in a Down syndrome model of age-related neurodegeneration. Holtzman, D.M., Li, Y., Chen, K., Gage, F.H., Epstein, C.J., Mobley, W.C. Neurology (1993) [Pubmed]
  4. Abnormal lymphatic development in trisomy 16 mouse embryos precedes nuchal edema. Gittenberger-De Groot, A.C., Van Den Akker, N.M., Bartelings, M.M., Webb, S., Van Vugt, J.M., Haak, M.C. Dev. Dyn. (2004) [Pubmed]
  5. Muscularizing tissues in the endocardial cushions of the avian heart are characterized by the expression of h1-calponin. Moralez, I., Phelps, A., Riley, B., Raines, M., Wirrig, E., Snarr, B., Jin, J.P., Van Den Hoff, M., Hoffman, S., Wessels, A. Dev. Dyn. (2006) [Pubmed]
  6. Transplants of mouse trisomy 16 hippocampus provide a model of Alzheimer's disease neuropathology. Richards, S.J., Waters, J.J., Beyreuther, K., Masters, C.L., Wischik, C.M., Sparkman, D.R., White, C.L., Abraham, C.R., Dunnett, S.B. EMBO J. (1991) [Pubmed]
  7. Regional alterations in amyloid precursor protein and nerve growth factor across age in a mouse model of Down's syndrome. Hunter, C.L., Isacson, O., Nelson, M., Bimonte-Nelson, H., Seo, H., Lin, L., Ford, K., Kindy, M.S., Granholm, A.C. Neurosci. Res. (2003) [Pubmed]
  8. Developmental abnormalities and age-related neurodegeneration in a mouse model of Down syndrome. Holtzman, D.M., Santucci, D., Kilbridge, J., Chua-Couzens, J., Fontana, D.J., Daniels, S.E., Johnson, R.M., Chen, K., Sun, Y., Carlson, E., Alleva, E., Epstein, C.J., Mobley, W.C. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  9. Ts65Dn mice, a model for Down syndrome, have deficits in context discrimination learning suggesting impaired hippocampal function. Hyde, L.A., Frisone, D.F., Crnic, L.S. Behav. Brain Res. (2001) [Pubmed]
  10. A mouse model for Down syndrome exhibits learning and behaviour deficits. Reeves, R.H., Irving, N.G., Moran, T.H., Wohn, A., Kitt, C., Sisodia, S.S., Schmidt, C., Bronson, R.T., Davisson, M.T. Nat. Genet. (1995) [Pubmed]
  11. Down's syndrome-like skeletal abnormalities in Ets2 transgenic mice. Sumarsono, S.H., Wilson, T.J., Tymms, M.J., Venter, D.J., Corrick, C.M., Kola, R., Lahoud, M.H., Papas, T.S., Seth, A., Kola, I. Nature (1996) [Pubmed]
  12. Down syndrome, Alzheimer's disease and the trisomy 16 mouse. Coyle, J.T., Oster-Granite, M.L., Reeves, R.H., Gearhart, J.D. Trends Neurosci. (1988) [Pubmed]
  13. Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome. Fernandez, F., Morishita, W., Zuniga, E., Nguyen, J., Blank, M., Malenka, R.C., Garner, C.C. Nat. Neurosci. (2007) [Pubmed]
  14. Stem cell deficiencies and thymic abnormalities in fetal mouse trisomy 16. Epstein, C.J., Hofmeister, B.G., Yee, D., Smith, S.A., Philip, R., Cox, D.R., Epstein, L.B. J. Exp. Med. (1985) [Pubmed]
  15. Altered Ca2+ signaling and mitochondrial deficiencies in hippocampal neurons of trisomy 16 mice: a model of Down's syndrome. Schuchmann, S., Müller, W., Heinemann, U. J. Neurosci. (1998) [Pubmed]
  16. Brain accumulation of myo-inositol in the trisomy 16 mouse, an animal model of Down's syndrome. Shetty, H.U., Holloway, H.W., Acevedo, L.D., Galdzicki, Z. Biochem. J. (1996) [Pubmed]
  17. Behavioral and neurobiological markers of Alzheimer's disease in Ts65Dn mice: effects of estrogen. Hunter, C.L., Bimonte-Nelson, H.A., Nelson, M., Eckman, C.B., Granholm, A.C. Neurobiol. Aging (2004) [Pubmed]
  18. Diminished glutathione levels cause spontaneous and mitochondria-mediated cell death in neurons from trisomy 16 mice: a model of Down's syndrome. Schuchmann, S., Heinemann, U. J. Neurochem. (2000) [Pubmed]
  19. Fluoxetine rescues deficient neurogenesis in hippocampus of the Ts65Dn mouse model for Down syndrome. Clark, S., Schwalbe, J., Stasko, M.R., Yarowsky, P.J., Costa, A.C. Exp. Neurol. (2006) [Pubmed]
  20. Genetic linkage in the mouse of genes involved in Down syndrome and Alzheimer's disease in man. Reeves, R.H., Robakis, N.K., Oster-Granite, M.L., Wisniewski, H.M., Coyle, J.T., Gearhart, J.D. Brain Res. (1987) [Pubmed]
  21. Ts65Dn -- localization of the translocation breakpoint and trisomic gene content in a mouse model for Down syndrome. Akeson, E.C., Lambert, J.P., Narayanswami, S., Gardiner, K., Bechtel, L.J., Davisson, M.T. Cytogenet. Cell Genet. (2001) [Pubmed]
  22. App gene dosage modulates endosomal abnormalities of Alzheimer's disease in a segmental trisomy 16 mouse model of down syndrome. Cataldo, A.M., Petanceska, S., Peterhoff, C.M., Terio, N.B., Epstein, C.J., Villar, A., Carlson, E.J., Staufenbiel, M., Nixon, R.A. J. Neurosci. (2003) [Pubmed]
  23. Neuroanatomical localization and quantification of amyloid precursor protein mRNA by in situ hybridization in the brains of normal, aneuploid, and lesioned mice. Bendotti, C., Forloni, G.L., Morgan, R.A., O'Hara, B.F., Oster-Granite, M.L., Reeves, R.H., Gearhart, J.D., Coyle, J.T. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  24. Ts1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities. Sago, H., Carlson, E.J., Smith, D.J., Kilbridge, J., Rubin, E.M., Mobley, W.C., Epstein, C.J., Huang, T.T. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  25. Long-term basal forebrain cholinergic-rich grafts derived from trisomy 16 mice do not develop beta-amyloid pathology and neurodegeneration but demonstrate neuroinflammatory responses. Stahl, T., Goldammer, A., Luschekina, E., Beck, M., Schliebs, R., Bigl, V. Int. J. Dev. Neurosci. (1998) [Pubmed]
  26. Estrogen alters amyloid precursor protein as well as dendritic and cholinergic markers in a mouse model of Down syndrome. Granholm, A.C., Sanders, L., Seo, H., Lin, L., Ford, K., Isacson, O. Hippocampus. (2003) [Pubmed]
  27. In cortical cultures of trisomy 16 mouse brain the upregulated metallothionein-I/II fails to respond to H2O2 exposure or glutamate receptor stimulation. Scortegagna, M., Galdzicki, Z., Rapoport, S.I., Hanbauer, I. Brain Res. (1998) [Pubmed]
  28. Activator protein-1 DNA binding activation by hydrogen peroxide in neuronal and astrocytic primary cultures of trisomy-16 and diploid mice. Scortegagna, M., Galdzicki, Z., Rapoport, S.I., Hanbauer, I. Brain Res. Mol. Brain Res. (1999) [Pubmed]
  29. Abnormal expression of the G-protein-activated inwardly rectifying potassium channel 2 (GIRK2) in hippocampus, frontal cortex, and substantia nigra of Ts65Dn mouse: a model of Down syndrome. Harashima, C., Jacobowitz, D.M., Witta, J., Borke, R.C., Best, T.K., Siarey, R.J., Galdzicki, Z. J. Comp. Neurol. (2006) [Pubmed]
  30. Genetic dissection of region associated with behavioral abnormalities in mouse models for Down syndrome. Sago, H., Carlson, E.J., Smith, D.J., Rubin, E.M., Crnic, L.S., Huang, T.T., Epstein, C.J. Pediatr. Res. (2000) [Pubmed]
  31. Dysregulation of gene expression in mouse trisomy 16, an animal model of Down syndrome. Holtzman, D.M., Bayney, R.M., Li, Y.W., Khosrovi, H., Berger, C.N., Epstein, C.J., Mobley, W.C. EMBO J. (1992) [Pubmed]
  32. Altered signaling pathways underlying abnormal hippocampal synaptic plasticity in the Ts65Dn mouse model of Down syndrome. Siarey, R.J., Kline-Burgess, A., Cho, M., Balbo, A., Best, T.K., Harashima, C., Klann, E., Galdzicki, Z. J. Neurochem. (2006) [Pubmed]
  33. Ts65Dn, a Mouse Model of Down Syndrome, Exhibits Increased GABAB-Induced Potassium Current. Best, T.K., Siarey, R.J., Galdzicki, Z. J. Neurophysiol. (2007) [Pubmed]
  34. In vivo restoration of physiological levels of truncated TrkB.T1 receptor rescues neuronal cell death in a trisomic mouse model. Dorsey, S.G., Renn, C.L., Carim-Todd, L., Barrick, C.A., Bambrick, L., Krueger, B.K., Ward, C.W., Tessarollo, L. Neuron (2006) [Pubmed]
  35. Cerebral cortical astroglia from the trisomy 16 mouse, a model for down syndrome, produce neuronal cholinergic deficits in cell culture. Nelson, P.G., Fitzgerald, S., Rapoport, S.I., Neale, E.A., Galdzicki, Z., Dunlap, V., Bowers, L., v Agoston, D. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  36. Mouse model of neurodegeneration: atrophy of basal forebrain cholinergic neurons in trisomy 16 transplants. Holtzman, D.M., Li, Y.W., DeArmond, S.J., McKinley, M.P., Gage, F.H., Epstein, C.J., Mobley, W.C. Proc. Natl. Acad. Sci. U.S.A. (1992) [Pubmed]
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