IlArePhra
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB89312 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR14986917_1.fastq.gz | Fastqsanger.gz | |||
| ERR14986917_2.fastq.gz | Fastqsanger.gz | |||
| ERR14986746_1.fastq.gz | Fastqsanger.gz | |||
| ERR14986746_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
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Project description:Arenostola phragmitidis (fen wainscot), genomic and transcriptomic data
| PRJEB89311 | ENA
Project description:We proposed that DNA recombination/repair processes play a role in memory formation. Here, we used microarray analysis of rat amygdala genes to identify possible DNA recombination/repair factors involved in memory consolidation of conditioned taste aversion (CTA). Among the genes that showed statistically significant differential expression, we identified fen-1, encoding a flap-structure specific DNA endonuclease. Amygdalar fen-1 mRNA induction was associated to the illness component of CTA, since it could be observed by the pairing of a flavor and gastrointestinal illness, by the illness itself, but not by the presentation of the flavor alone. No CTA related induction of fen-1 expression was observed in the insular cortex. Importantly, functional validation studies demonstrated that amygdalar suppression of fen-1 expression impaired memory consolidation of CTA. Overall, our studies helped identify a new DNA recombination/repair candidate factor involved in memory formation of aversive experiences.
2009-12-30 | GSE11520 | GEO
Project description:Bruton’s tyrosine kinase (BTK) is an intracellular signaling enzyme that regulates B cell and myeloid cell functions. Due to its involvement in both innate and adaptive immune compartments, inhibitors of BTK have emerged as a therapeutic option in autoimmune disorders such as multiple sclerosis (MS). Brain penetrant small molecule BTK inhibitors may also help to address compartmentalized neuroinflammation which is proposed to underlie MS disease progression. BTK is expressed by microglia, the resident innate immune cells of the brain, however the precise roles of microglial BTK and the impact of BTK inhibitors on microglial functions is still being elucidated. Much research to date has also focused on the effects of BTK inhibitors using rodent disease models. Here we characterize the pharmacological and functional properties of fenebrutinib (FEN), a potent, highly selective, noncovalent, reversible BTK inhibitor, in human microglia and complex human brain cell systems including brain organoids. We find that FEN blocks the effects of microglial FcγR activation including cytokine and chemokine release, microglial clustering and neurite damage in diverse human brain cell systems. Gene expression analyses identified pathways linked to inflammation, matrix metalloproteinase production and cholesterol metabolism that were modulated by FEN treatment. In contrast, FEN had no significant impact on human microglial pathways linked to TLR4 or NLRP3 signaling nor myelin phagocytosis. Our study increases the understanding of BTK functions in human microglial signaling relevant to MS pathogenesis and suggests that FEN could attenuate detrimental microglial activity associated with FcγR activation in MS patients.
2024-10-28 | GSE276803 | GEO
Project description:We proposed that DNA recombination/repair processes play a role in memory formation. Here, we used microarray analysis of rat amygdala genes to identify possible DNA recombination/repair factors involved in memory consolidation of conditioned taste aversion (CTA). Among the genes that showed statistically significant differential expression, we identified fen-1, encoding a flap-structure specific DNA endonuclease. Amygdalar fen-1 mRNA induction was associated to the illness component of CTA, since it could be observed by the pairing of a flavor and gastrointestinal illness, by the illness itself, but not by the presentation of the flavor alone. No CTA related induction of fen-1 expression was observed in the insular cortex. Importantly, functional validation studies demonstrated that amygdalar suppression of fen-1 expression impaired memory consolidation of CTA. Overall, our studies helped identify a new DNA recombination/repair candidate factor involved in memory formation of aversive experiences. Two comparisons were established between the cRNA samples: CTA versus Flavor-only and CTA versus Toxin-only. For each comparison, the microarray experiment was repeated four times using new biological samples, each consisting of a sample pool from 3 animals. Two of the four biological replicates were performed as dye-swaps in order to correct for dye bias effects.
2009-12-30 | E-GEOD-11520 | biostudies-arrayexpress
Project description:The aim of this study was to explore the possible action mechanism of fenofibrate in treating non-alcoholic fatty liver disease (NAFLD) through bioinformatic analysis. Statistical and bioinformatic analyses were conducted through Gene Ontology, Gene Set Enrichment Analysis (GSEA), and Kyoto Encyclopedia of Genes and Genomes (KEGG). The control, high-fat diet (HFD), and HFD + fenofibrate (HFD + Fen) groups were analyzed for differentially expressed genes (DEGs). In the HFD versus control dataset analysis, 493 DEGs were identified, of which 200 were upregulated and 293 were downregulated. In the HFD + Fen versus HFD dataset, 449 DEGs, comprising 376 upregulated and 73 downregulated genes, were observed. Two KEGG pathways and one key gene were identified. The key gene mup family appeared to mediate the mechanism underlying NAFLD. Treatment of NAFLD with fenofibrate may occur through the core gene mup.
2023-05-01 | GSE205021 | GEO
Project description:Ypsolopha scabrella (wainscot smudge) genome assembly, ilYpsScab1
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Project description:Mythimna impura (smoky wainscot) genome assembly, ilMytImpu1
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