ABSTRACT: Expression data from primary osteoblasts isolated from calvaria of Gnptab(c.3082insC) knock-in mice compared with osteoblasts isolated from wild-type littermates
Project description:Mucolipidosis type II (MLII) is a severe inherited multisystemic disorder caused by mutations in the GNPTAB gene. Skeletal abnormalities are a predominant feature of MLII. Here we investigate the gene expression in a knock-in mouse model for mucolipidosis type II, generated by the insertion of a cytosine in the murine Gnptab gene (c.3082insC) that is homologous to a homozygous mutation in an MLII patient. Since osteoblasts are critically involved in regulating bone development and remodeling, a genome-wide expression analysis was performed with RNA isolated from primary cultures of osteoblasts originating from MLII knock-in mice (KI) compared to RNA from wild-type (WT) osteoblasts to identify dysregulated genes involved in pathogenic mechanisms. Primary osteoblasts were isolated from calvaria of 5-day-old wild-type (WT) and MLII knock-in littermates (KI). RNA was extracted at day 10 of differentiation induced by ascorbic acid and beta-glycerophosphate and hybridization on Affymetrix microarrays. We used preparations of RNA from two individual primary cultures of osteoblasts for every genotype (WT_OB_I, WT_OB_II, KI_OB_I, KI_OB_II) and compared WT vs KI samples.
Project description:Mucolipidosis type II (MLII) is a severe inherited multisystemic disorder caused by mutations in the GNPTAB gene. Skeletal abnormalities are a predominant feature of MLII. Here we investigate the gene expression in a knock-in mouse model for mucolipidosis type II, generated by the insertion of a cytosine in the murine Gnptab gene (c.3082insC) that is homologous to a homozygous mutation in an MLII patient. Since osteoblasts are critically involved in regulating bone development and remodeling, a genome-wide expression analysis was performed with RNA isolated from primary cultures of osteoblasts originating from MLII knock-in mice (KI) compared to RNA from wild-type (WT) osteoblasts to identify dysregulated genes involved in pathogenic mechanisms.
Project description:Investigation of whole genome gene expression level changes in OASIS KO calvaria compared to wild-type calvaria. To gain further insight into the potential mechanisms underlying the defective bone formation in OASIS KO mice, we compared the gene expression in calvaria between WT and OASIS KO mice using a microarray.
Project description:Mouse retinal proteome for LFQ. The retinal samples of CCT2-LCA model of R516H/R516H (RH/RH) knock-in mice and its wild type littermates (WT/WT) were analyzed for LFQ.
Project description:The purpose of this project was to investigate whole genome expression in primary microglia cultured from homozygous Trem2 R47H knock-in mice versus wild type littermates under basal conditions and in response to IL-4 treatment. The primary phenotype of microglia from Trem2 R47H knock-in mice was decreased expression levels of Trem2. IL-4 induced the expression of an anti-inflammatory programme of genes in microglia, which was attenuated when Trem2 expression was decreased.
Project description:Gene expression from livers of knock-out, hemizygous and wild-type mice at the age of , 8 and 12 months. Including tumor and non-tumor tissue of the same animals. AlbCre negative littermates were used as wild type controls. The hepatic gene expression of mice carrying a hepatocyte specific deletion of the anti-apoptotic protein Mcl-1 was analyzed at various age. Expression was compared between knock-out, hemizygous and wild-type littermates as well as between tumor and corresponding non-tumor tissue.
Project description:Gene expression data from CD22+B220+ FACS-purified splenocytes of adult Sca1-HGAL knock-in CBAxC57BL/6J mice or wild-type littermates.
Project description:Gene expression from livers of knock-out, hemizygous and wild-type mice at the age of , 8 and 12 months. Including tumor and non-tumor tissue of the same animals. AlbCre negative littermates were used as wild type controls.
Project description:ChIP-Seq analysis of the potential accumulated binding sites on whole genome by wild-type tnni2 and tnni2 del175k mutant The primary osteoblasts from Tnni2del175k/175k mice and wild-type littermates (n=3) were cultured for ChIP-Seq. ChIP and construct libraries were performed using the antibody against tnni2 (Santa Cluz Biotechnology) and conducted as previously described above. Illumina HiSeq 2000 is used for sequencing. Raw reads were aligned with the mouse reference 8 using Bowtie software and viewed with the IGV browser.
