Similar Datasets
Project description:Selective neuronal vulnerability is a common, yet poorly understood characteristic of neurodegenerative diseases and is particularly prominent in familial prion diseases, such as Creutzfeldt-Jakob disease (CJD) and fatal familial insomnia (FFI), where different mutations in the prion protein manifest as neuropathologically distinct diseases. To determine how presence of mutant prion protein influences gene expression at pre-symptomatic stages, we used RiboTag to isolate cell type-specific, translating RNA from GABAergic, glutamatergic, somatostatin- (SST) and parvalbumin-expressing neurons of 9-month-old knock-in mice of CJD and FFI.
2022-09-21 | GSE198063 | GEO
Project description:Fatal familial insomnia (FFI) is a special subtype of genetic human prion diseases that is caused by the D178N mutation of the prion protein gene (PRNP). In this study, global expression patterns of the thalamus and parietal cortex from three patients with FFI were analyzed by Affymetrix Human Genome U133+ 2.0 chip. We used microarrays to detail the global gene expression in tissues from normal human and FFI patients thalamus, or parietal lobe. Tissues from normal human and FFI patients' thalamus, or parietal lobe were for RNA extraction and hybridization on Affymetrix microarrays.
2015-08-30 | E-GEOD-40562 | biostudies-arrayexpress
Project description:Fatal familial insomnia (FFI) is a special subtype of genetic human prion diseases that is caused by the D178N mutation of the prion protein gene (PRNP). In this study, global expression patterns of the thalamus and parietal cortex from three patients with FFI were analyzed by Affymetrix Human Genome U133+ 2.0 chip. We used microarrays to detail the global gene expression in tissues from normal human and FFI patients thalamus, or parietal lobe.
2015-08-30 | GSE40562 | GEO
Project description:Translational profiling of neuronal subtypes reveals early vulnerability of somatostatin-expressing neurons in pre-symptomatic fatal familial insomnia
| PRJNA813557 | ENA
Project description:Cytoplasmic RNA granules have emerged as important elements of posttranscriptional and translational regulation. Stress, germinal and neuronal granules contain RNA-binding proteins capable of self-assembly due to prion-like domains. Hyperassembly mediated by these prion-like domains causes several neurodegenerative diseases. Here, we report a subset of the mammalian prion protein (PrP), also prone to self-assembly, propagation and to cause devastating diseases, is a component of naturally occurring messenger ribonucleoproteins (mRNPs) in adult mouse brains. Biomolecules co-purified with PrP revealed a multitude of diverse RNA granule associated proteins and mRNAs encoding members of the translation machinery, indicating a role in a specialized translation process. Importantly, PrP mutations linked to Creutzfeldt-Jakob disease (CJD) or fatal familial insomnia (FFI) severely impaired recovery of mRNPs from preclinical mice, possibly representing a very early pathological process. Thus, mutant PrP may cause dysfunction in RNA regulation, thereby joining the constantly expanding ranks of disease associated RNP granule proteins. The file Enrichment_analysis.xlsx contains mRNAs (FDR < 0.01) co-purified with PrP in both WT sample pools as identified by DESeq2 and the respective gene counts and log2 fold changes for CJD and FFI PrP:IP sample pools.
2015-11-01 | GSE57233 | GEO
Project description:Genome-wide transcriptional profiling results were used to systematically assess the extent to which transcriptomes of older adults with insomnia show expression of genes that are different from those without insomnia
2022-07-22 | GSE208668 | GEO
Project description:Cytoplasmic RNA granules have emerged as important elements of posttranscriptional and translational regulation. Stress, germinal and neuronal granules contain RNA-binding proteins capable of self-assembly due to prion-like domains. Hyperassembly mediated by these prion-like domains causes several neurodegenerative diseases. Here, we report a subset of the mammalian prion protein (PrP), also prone to self-assembly, propagation and to cause devastating diseases, is a component of naturally occurring messenger ribonucleoproteins (mRNPs) in adult mouse brains. Biomolecules co-purified with PrP revealed a multitude of diverse RNA granule associated proteins and mRNAs encoding members of the translation machinery, indicating a role in a specialized translation process. Importantly, PrP mutations linked to Creutzfeldt-Jakob disease (CJD) or fatal familial insomnia (FFI) severely impaired recovery of mRNPs from preclinical mice, possibly representing a very early pathological process. Thus, mutant PrP may cause dysfunction in RNA regulation, thereby joining the constantly expanding ranks of disease associated RNP granule proteins. The file Enrichment_analysis.xlsx contains mRNAs (FDR < 0.01) co-purified with PrP in both WT sample pools as identified by DESeq2 and the respective gene counts and log2 fold changes for CJD and FFI PrP:IP sample pools. RIP-Seq analysis of mRNAs co-purified with PrP from murine brain cytoplasmic fractions in wild-type (WT), CJD and FFI mice. Each RIP-Seq and control (input) library represents a pool of 12 to 16 co-immunoprecipitation samples out of 3 to 4 mice. To control for post-homogenization artifacts, we conducted an experiment in which we prepared homogenates from WT and PrP-KO (Prnp-/-) mice of different genetic backgrounds (C57BL/6 and 129S4) and identified SNPs in RIP-Seq and control libraries to finally identify specifically co-purified mRNAs.
2015-11-01 | E-GEOD-57233 | biostudies-arrayexpress
Project description:Insomnia is an economic burden and public health problem. This study aimed to explore potential biological pathways and protein networks for insomnia characterized by wakefulness after sleep. Proteomics analysis was performed in the insomnia group with wakefulness and the control group. The differentially expressed proteins (DEPs) were enriched, then hub proteins were identified by protein-protein interaction (PPI) network and verified by parallel reaction monitoring (PRM). Compared with the control group, the sleep time and efficiency of insomnia patients were decreased, awakening time and numbers after sleep onset were significantly increased (P < 0.001).
2022-10-14 | PXD026610 | Pride
Project description:Insomnia is an economic burden and public health problem. This study aimed to explore potential biological pathways and protein networks for insomnia characterized by wakefulness after sleep. Proteomics analysis was performed in the insomnia group with wakefulness and the control group. The differentially expressed proteins (DEPs) were enriched, then hub proteins were identified by protein-protein interaction (PPI) network and verified by parallel reaction monitoring (PRM). Compared with the control group, the sleep time and efficiency of insomnia patients were decreased, awakening time and numbers after sleep onset were significantly increased (P < 0.001). The results of proteomic sequencing found 68 DEPs in serum under 1.2-fold changed standard. These DEPs were significantly enriched in humoral immune response, complement and coagulation cascades, cholesterol metabolism. Through PPI network, we identified 10 proteins with the highest connectivity as hub proteins. Among them, differential expression of 9 proteins was verified by PRM.We identified the hub proteins and molecular mechanisms of insomnia patients characterized by wakefulness after sleep. It provided potential molecular targets for the clinical diagnosis and treatment of these patients, and indicated the immune and metabolic systems may be closely related to insomnia characterized by wakefulness after sleep.
2021-09-09 | PXD023246 | Pride