ABSTRACT: 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:Transcriptome of 8 and 18 weeks old mice where fibrosis developed upon the full-body knocking-out gene Glmp (glycosylated lysosomal membrane protein) (Glmpgt/gt; Glmp KO) Glmp KO mice were compared to their wild-type (WT) littermates
Project description:Ventricular tissue of 8 week female PA mice (https://pubmed.ncbi.nlm.nih.gov/23648696/) and their female wild-type littermates were processed for phosphoproteomics
Project description:Olfaction is often deregulated in Alzheimer´s disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from aged Tg2576 mice (18 months of age) respect to age matched wild-type (WT) littermates.
Project description:In order to identify some lncRNA potentially involved in Rett syndrome we performed a mouse lncRNA expression microarray on whole brain samples coming from wild-type and MeCP2 Knock-out littermates. We found 2 lncRNAs directly bound by MeCP2 and upregulated in KO samples. We then focused on AK081227 because it overlaps with Gabrr2. The expression of this GABA receptor and the overlapping AK081227 are inversely correlated in thalamus, suggesting the long non-coding is regulating his own host. Whole brain total RNA was extracted from two Wild type mice (P60) and two MeCP2 KO littermates (P60)
Project description:We looked to find earlier molecular changes in 2-month-old transgenic P301S mice. S-nitrosylated (SNO) proteins were identified in two brain regions, cortex and hippocampus, in P301S and Wild Type (WT) littermate control mice.
Project description:The integrated stress response (ISR) is a conserved pathway in eukaryotic cells that is activated in response to multiple sources of cellular stress. Although acute activation of this pathway restores cellular homeostasis, intense or prolonged ISR activation perturbs cell function and may contribute to neurodegeneration. We have characterized an eIF2B loss of function (LOF) mouse model, carrying the homozygous Eif2b5[R191H] mutation that is homologous to the Vanishing White Matter Disease (VWMD)-causing human R195H variant. Characterization of previously reported transcript markers in animals 3-4 weeks of age confirmed ISR activation in the brain, but not in heterozygous or wild-type littermates.The robust elevation of ISR markers was further confirmed in bulk brain RNA sequencing analysis of a separate cohort of homozygous mutants and wild-type littermates. Known ATF4 targets feature prominently among the most strongly up-regulated genes in the eIF2B mutant compared to WT littermates.
Project description:Frataxin deficiency in human is the cause of Friedreich's ataxia (FA), a lethal neuro- and cardio-degenerative disease. Knock-out (KO) mice of this mouse model of FA exhibit classical cardiomyopathy of the patients. The onset of FA phenotypes in the KO mice is approximately 6-7 weeks of age. This genearray analysis was conducted to examine the changes in gene expression in the heart of KO mice relative to their wild-type (WT) littermates at 4- and 10-weeks of age. At 10-weeks of age, the KO mice begin to die from severe cardiomyopathy. RNA from the heart of four female 4-week-old MCK littermates (two WT and two KO) and four female 10-week-old MCK littermates (two WT and two KO) was extracted and hybridised to Affymetrix Mouse Genome 430 2.0 Array.
Project description:The purpose of this study was to determine the pathogenic changes that occur in myoepithelial cells (MECs) from lacrimal glands of a mouse model of Sjogren’s syndrome. MECs were cultured from lacrimal glands of C57BL/6J (wild type, WT), and thrombospondin 1 knockout null (TSP1 -/- ) mice. We used microarray to analyzed the differential expression of genes in cultured MECs of TSP1-/- and wild type (WT) mice.
Project description:Frataxin deficiency in human is the cause of Friedreich's ataxia (FA), a lethal neuro- and cardio-degenerative disease. Knock-out (KO) mice of this mouse model of FA exhibit classical cardiomyopathy of the patients. The onset of FA phenotypes in the KO mice is approximately 6-7 weeks of age. This genearray analysis was conducted to examine the changes in gene expression in the heart of KO mice relative to their wild-type (WT) littermates at 4- and 10-weeks of age. At 10-weeks of age, the KO mice begin to die from severe cardiomyopathy.