Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15860439_1.fastq.gz | Fastqsanger.gz | |||
| SRR15860439_2.fastq.gz | Fastqsanger.gz | |||
| SRR15860440_1.fastq.gz | Fastqsanger.gz | |||
| SRR15860440_2.fastq.gz | Fastqsanger.gz | |||
| SRR15860441_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:2-Dodecyl-6-Methoxycyclohexa-2, 5 -Diene-1,4-Dione (DMDD) was purified from the roots of Averrhoa carambola L. Previous research demonstrated that DMDD is a small molecular compound with significant therapeutic potential for diabetes. However, the efficacy of DMDD to ameliorate diabetic cognitive impairment in type 2 diabetes mice has not been reported. In present study, we detected gene expression profiles in the hippocampi of diabetic db/db mice after DMDD treatment. 9-week-old male db/db mice were treated with DMDD (50 mg/kg) for 28 days followed by Y maze and novel object recognition test for behavioral evaluation. Our results showed that DMDD attenuated the spatial working memory and object recognition memory impairment in db/db mice. Using mouse lncRNA array analysis, 11 lncRNAs and 4 mRNAs with significant differential expression were identified after DMDD treatment. Among these, Hif3a expression was significantly increased in the hippocampi of diabetic db/db mice compared with db/m control mice and then decreased after DMDD treatment. Besides, DMDD treatment reduced tau protein expression, the formation of a-synuclein oligomers and high glucose-induced apoptosis in the hippocampi of db/db mice and high glucose-treated HT22 cells. DMDD protected neural cells from apoptosis by repression of Hif3a. These data suggest that DMDD can alleviate cognitive impairment by regulating apoptosis through the pro-apoptotic protein Hif3a. In conclusion, our study suggests that DMDD has great potential to be a new preventive and therapeutic compound for diabetic cognitive impairment.
2021-12-31 | GSE174378 | GEO
Project description:modENCODE_submission_5986 This submission comes from a modENCODE project of Jason Lieb. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: The focus of our analysis will be elements that specify nucleosome positioning and occupancy, control domains of gene expression, induce repression of the X chromosome, guide mitotic segregation and genome duplication, govern homolog pairing and recombination during meiosis, and organize chromosome positioning within the nucleus. Our 126 strategically selected targets include RNA polymerase II isoforms, dosage-compensation proteins, centromere components, homolog-pairing facilitators, recombination markers, and nuclear-envelope constituents. We will integrate information generated with existing knowledge on the biology of the targets and perform ChIP-seq analysis on mutant and RNAi extracts lacking selected target proteins. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: N2; Developmental Stage: L3 Larva; Genotype: wild type; Sex: mixed Male and Hermaphrodite population; EXPERIMENTAL FACTORS: Developmental Stage L3 Larva; temp (temperature) 20 degree celsius; Strain N2; Antibody NURF-1 SDQ3525 (target is NURF-1)
2013-08-28 | E-GEOD-50296 | biostudies-arrayexpress