Fri. Oct 11th, 2024

S, Trovero F, Delgado-Garc JM,Ling et al. BMC Genomics 2014, 15:624 biomedcentral.
S, Trovero F, Delgado-Garc JM,Ling et al. BMC Genomics 2014, 15:624 biomedcentral.com/1471-2164/15/Page 18 of22.23.24.25. 26.27.28.29.30.31.32.33.34.35. 36.37. 38.39.40.41.Antonarakis SE, Dierssen M, Herault Y: A brand new mouse model for the trisomy of the Abcg1-U2af1 area reveals the complexity in the combinatorial genetic code of down syndrome. Hum Mol Genet 2009, 18:4756769. Contestabile A, Benfenati F, Gasparini L: Communication breaks-Down: from neurodevelopment defects to cognitive disabilities in Down syndrome. Prog Neurobiol 2010, 91:12. Laffaire J, Rivals I, Dauphinot L, Pasteau F, Wehrle R, Larrat B, Vitalis T, Moldrich RX, Rossier J, Sinkus R, Herault Y, Dusart I, Potier M-C: Gene expression signature of cerebellar hypoplasia inside a mouse model of Down syndrome for the duration of postnatal improvement. BMC Genomics 2009, 10:138. Belichenko PV, Kleschevnikov AM, Salehi A, Epstein CJ, Mobley WC: Synaptic and cognitive abnormalities in mouse models of Down syndrome: exploring genotype-phenotype relationships. J Comp Neurol 2007, 504:32945. Fernandez F, Garner CC: Object recognition PKCĪ± Compound memory is conserved in Ts1Cje, a mouse model of Down syndrome. TrkC review Neurosci Lett 2007, 421:13741. Siarey RJ, Villar AJ, Epstein CJ, Galdzicki Z: Abnormal synaptic plasticity within the Ts1Cje segmental trisomy 16 mouse model of Down syndrome. Neuropharmacology 2005, 49:12228. Richtsmeier JT, Zumwalt A, Carlson EJ, Epstein CJ, Reeves RH: Craniofacial phenotypes in segmentally trisomic mouse models for Down syndrome. Am J Med Genet 2002, 107:31724. Olson LE, Roper RJ, Baxter LL, Carlson EJ, Epstein CJ, Reeves RH: Down syndrome mouse models Ts65Dn, Ts1Cje, and Ms1Cje/Ts65Dn exhibit variable severity of cerebellar phenotypes. Dev Dyn 2004, 230:58189. Hewitt CA, Ling KH, Merson TD, Simpson KM, Ritchie ME, King SL, Pritchard MA, Smyth GK, Thomas T, Scott HS, Voss AK: Gene network disruptions and neurogenesis defects within the adult Ts1Cje mouse model of Down syndrome. PLoS A single 2010, 5:e11561. Ishihara K, Amano K, Takaki E, Shimohata A, Sago H, Epstein CJ, Yamakawa K: Enlarged brain ventricles and impaired neurogenesis inside the Ts1Cje and Ts2Cje mouse models of Down syndrome. Cereb Cortex 2010, 20:1131143. Dauphinot L, Lyle R, Rivals I, Dang MT, Moldrich RX, Golfier G, Ettwiller L, Toyama K, Rossier J, Personnaz L, Antonarakis SE, Epstein CJ, Sinet P-M, Potier M-C: The cerebellar transcriptome in the course of postnatal improvement from the Ts1Cje mouse, a segmental trisomy model for Down syndrome. Hum Mol Genet 2005, 14:37384. Potier MC, Rivals I, Mercier G, Ettwiller L, Moldrich RX, Laffaire J, Personnaz L, Rossier J, Dauphinot L: Transcriptional disruptions in Down syndrome: a case study within the Ts1Cje mouse cerebellum for the duration of post-natal improvement. J Neurochem 2006, 97(Suppl 1):10409. Amano K, Sago H, Uchikawa C, Suzuki T, Kotliarova SE, Nukina N, Epstein CJ, Yamakawa K: Dosage-dependent over-expression of genes within the trisomic region of Ts1Cje mouse model for Down syndrome. Hum Mol Genet 2004, 13:1333340. Moldrich RX, Dauphinot L, Laffaire J, Vitalis T, Herault Y, Beart PM, Rossier J, Vivien D, Gehrig C, Antonarakis SE, Lyle R, Potier M-C: Proliferation deficits and gene expression dysregulation in Down’s syndrome (Ts1Cje) neural progenitor cells cultured from neurospheres. J Neurosci Res 2009, 87:3143152. Haydar TF, Reeves RH: Trisomy 21 and early brain development. Trends Neurosci 2012, 35:811. Ling KH, Hewitt CA, Beissbarth T, Hyde L, Banerjee K, Cheah P-S, Cannon PZ, Hahn CN, Thomas PQ, Sm.