Ero-specific loxP in single cell-stage VEGF-AA Protein site embryos (zygotes) (50). Our tetO-SHP2E76K transgene is flanked by the enhanced L3/L2 loxP web sites placed in opposite orientation to let effective Cre-RMCE (41). The multiple lines of inducible tetO-SHP2E76K transgenic mice that we derived and characterized right here are a potential resource for generating new transgenic mice by Cre-RMCE as mouse models for studying other genetic lesions identified in human lung cancer. Supplementary material Supplementary Materials and Techniques, Table 1 and Figures 1? could be identified at carcin.oxfordjournals.org/ Funding Florida Biomedical Research Program (2KB04 and 3KB06); National Institutes of Well being (R56CA077467, R01CA178456, R21CA175603 and P50CA119997); Dr Tsai-fan Yu Cancer Study Fund. AcknowledgementsWe thank J.A.Whitset for the CCSP-rtTA transgenic mice, D.C.Radisky as well as a.P.Fields for assistance and assistance, K.Politi and G.Felsenfeld for reagents, and E.Ruiz, A.Lopez as well as the Moffitt Animal, Tissue, and Microscopy Core staffs for help. Conflict of Interest Statement: None declared.
Ling et al. BMC Genomics 2014, 15:624 biomedcentral/1471-2164/15/RESEARCH ARTICLEOpen AccessFunctional transcriptome analysis from the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals international disruption of interferon-related molecular networksKing-Hwa Ling1,two,three, Chelsee A Hewitt2,four, Kai-Leng Tan1,five, Pike-See Cheah1,five, Sharmili Vidyadaran1,6, Mei-I Lai1,six, Han-Chung Lee1, Ken Simpson2, Lavinia Hyde2, Melanie A Pritchard7, Gordon K Smyth2, Tim Thomas2 and Hamish S Scott2,8,9AbstractBackground: The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16 (MMU16), that is partially homologous to human chromosome 21. These mice develop several neuropathological capabilities identified in DS men and women. We analysed the impact of partial triplication from the MMU16 segment on international gene expression in the cerebral cortex, cerebellum and hippocampus of Ts1Cje mice at 4 time-points: postnatal day (P)1, P15, P30 and P84. Final results: Gene expression profiling identified a total of 317 differentially expressed genes (DEGs), chosen from various spatiotemporal comparisons, amongst Ts1Cje and disomic mice. A total of 201 DEGs have been identified from the cerebellum, 129 from the hippocampus and 40 in the cerebral cortex. Of those, only 18 DEGs had been identified as frequent to all 3 brain regions and 15 were located inside the triplicated segment. We validated 8 chosen DEGs in the cerebral cortex (Brwd1, Donson, Erdr1, Ifnar1, Itgb8, Itsn1, Mrps6 and Tmem50b), 18 DEGs in the cerebellum (Atp5o, Brwd1, Donson, Dopey2, Erdr1, Hmgn1, Ifnar1, Ifnar2, gp140, HIV-1 (627a.a, HEK293, Fc) Ifngr2, Itgb8, Itsn1, Mrps6, Paxbp1, Son, Stat1, Tbata, Tmem50b and Wrb) and 11 DEGs from the hippocampus (Atp5o, Brwd1, Cbr1, Donson, Erdr1, Itgb8, Itsn1, Morc3, Son, Tmem50b and Wrb). Functional clustering evaluation of your 317 DEGs identified interferon-related signal transduction because the most significantly dysregulated pathway in Ts1Cje postnatal brain development. RT-qPCR and western blotting analysis showed each Ifnar1 and Stat1 had been over-expressed in P84 Ts1Cje cerebral cortex and cerebellum as compared to wild type littermates. Conclusions: These findings suggest over-expression of interferon receptor may well cause over-stimulation of Jak-Stat signaling pathway which could contribute to the neuropathology in Ts1Cje or DS brain. The role of interferon mediated activation or inhibition of signal transduction inclu.
