Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1036020 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26678302_1.fastq.gz | Fastqsanger.gz | |||
| SRR26678302_2.fastq.gz | Fastqsanger.gz | |||
| SRR26678303_1.fastq.gz | Fastqsanger.gz | |||
| SRR26678303_2.fastq.gz | Fastqsanger.gz | |||
| SRR26678304_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 42 |
Similar Datasets
Project description:To make the human liver accessible to metabolic treatments, we employed a liver-specific humanized mouse model in which approximately 50% of the mouse hepatocytes were replaced by human ones. For the dietary treatment, the humanized mice were allowed free access to food (AL, n=4 for donor1, n=3 for donor2) or subjected to a twenty-four hours food withdrawal (Fast, n=4 for donor1, n=3 for donor2). For the transcription factor agonist treatments, the humanized mice were injected with DMSO (n=4), fenofibrate (n=4, 50mg/kg, Sigma-Aldrich, Cat. F6020), rosiglitazone (n=4,10mg/kg, Sigma-Aldrich, Cat. R2408) and GW4064 (n=4, 30mg/kg, Sigma-Aldrich, Cat. G5172) by i.p. injection. The livers were collected after 6 hours fasting and stored in liquid nitrogen immediately after mice sacrificed.
2024-01-23 | GSE224277 | GEO
Project description:Total RNA was isolated from liver samples of C57/BL6 mice over a circadian time course, 3 biological replicate samples per time point were collected and processed individually. RNA from each individual biological replicate sample was extracted using RNeasy mini kit (Qiagen Cat# 74106) and hybridized on an Affymetrix mouse Gene ST1.0 microarray. Examination of mouse liver tissue at 4 time-points around the clock in free-running, continuous conditions (constant darkness, temperature and food available ad libitum).
2013-01-01 | E-GEOD-37387 | biostudies-arrayexpress
Project description:Food web analysis of spider comunity using DNA meta-barcoding
| PRJDB12701 | ENA
Project description:Light-controlled in situ synthesis of DNA microarrays (Affymetrix GeneChip® Mouse Genome 430 2.0) were performed to determine the altered gene expression. Affymetrix algorithm and multiple analysis comparison software were used for assessing gene expression differences, and mRNAs that increased or decreased in the brains of NP(α-M)-treated mice relative to that in the brains of Blank-NP-treated mice were identified. For the assay, total RNA was extracted using Takara RNAiso Plus Kit (Cat#9109, Takara, DaLian, LiaoNing, CN) following the manufacturer’s instructions and checked for a RIN number to inspect RNA integrity by an Agilent Bioanalyzer 2100 (Agilent technologies, Santa Clara, CA, US). Qualified total RNA was further purified by RNeasy mini kit (Cat#74106, QIAGEN, GmBH, Germany) and RNase-Free DNase Set (Cat#79254, QIAGEN, GmBH, Germany). Array hybridization and wash was performed using GeneChip® Hybridization, Wash and Stain Kit (Cat#900720, Affymetrix, Santa Clara, CA, US) in Hybridization Oven 645 (Cat#00-0331-220V, Affymetrix, Santa Clara, CA, US) and Fluidics Station 450 (Cat#00-0079, Affymetrix, Santa Clara, CA, US) followed the manufacturer’s instructions. Slides were scanned by GeneChip® Scanner 3000 (Cat#00-00212, Affymetrix, Santa Clara, CA, US) and Command Console Software 4.0 (Affymetrix, Santa Clara, CA, US) with default settings. Raw data were normalized by MAS 5.0 algorithm, Gene Spring Software12.6.1 (Agilent technologies, Santa Clara, CA, US).
2018-09-14 | GSE119904 | GEO
Project description:Primary mMSCs were cultured in control medium (Con), containing DMEM and 15% FBS, or were subjeucted to osteogenic induction (OI) for 2 days. RNA was isolated using RNeasy Mini Kit (Qiagen, Cat#74104) from three biological replicates of primary MSCs from Prx1Cre;Kdm4bf/f mice and control mice. Total RNA was then purified with Dynabeads™ mRNA Purification Kit (Invitrogen, Cat#61006). RNA-seq libraries were constructed using Stranded RNA-Seq Library Preparation Kit (Kapa Biosystems, Cat#KK8400), and sequenced using an illumina HiSeq 3000 sequencer at the Technology Center for Genomics & Bioinformatics (TCGB) core at UCLA.
2021-02-10 | GSE104258 | GEO
Project description:miRNA was extracted from a range of Oesophageal Adenocarcinoma cell lines using the miRNeasy Mini Kit (Qiagen, #217004, Chadstone, Australia) and RNase-free DNase Set (Qiagen, #79254, Chadstone, Australia). miRNA was reverse transcribed using a Custom OpenArray® miRNA RT pool (Life Technologies cat # A25630) and the TaqMan® microRNA Reverse Transcription Kit (Life Technologies cat # 4366596). cDNA Pre-amplifications were carried out with a Custom OpenArray® PreAmp pool (Life Technologies cat # 4485255) and TaqMan PreAmp Master Mix (Life Technologies cat # 4488593). PCR runs were performed using a QuantStudio™ 12K Flex Real-Time PCR System. Baseline qPCR expression profiling of miRNAs from 8 oesophageal Adenocarcinoma cell lines, prior to treating the cell lines with either 2Gy ionising radiation, 20 µM Cisplatin, or 50 µM 5-fluorouracil (5-FU).
2020-12-15 | GSE161585 | GEO
Project description:The goal of this study was to identify the key functions of the six main symbionts that are hosted in gills of the marine bivalve, Idas modiolaeformis, which lives at deep-sea hydrocarbon seeps and wood falls in the Eastern Atlantic Ocean and the Mediterranean Sea. These symbionts include the main autotrophic methane- and sulfur-oxidizing lineages (Methyloprofundus, Thioglobus, Thiodubillierella), as well as a Methylophagaceae methylotrophic autotroph, a flavobacterial degrader of complex polysaccharides Urechidicola and a Nitrincolaceae heterotroph that specializes in degradation of nitrogen-rich compounds such as peptides and nucleosides. Four I. modiolaeformis individuals were preserved in RNAlater following retrieval from a brine pool habitat in the Eastern Mediterranean at 1,150 m water depth (32° 13.4' N 34° 10.7' E), using a remotely-operated vehicle. RNAlater was discarded after 24 hours, and the specimens were kept at -80°C until DNA/RNA/protein co-extraction using the AllPrep DNA/RNA/Protein Mini Kit (Cat. No. 80004, Qiagen).
2023-07-20 | PXD040273 | Pride
Project description:<p><strong>BACKGROUND:</strong> In all living organisms, DNA replication is exquisitely regulated in a wide range of growth conditions to achieve timely and accurate genome duplication prior to cell division. Failures in this regulation cause DNA damage with potentially disastrous consequences for cell viability and human health, including cancer. To cope with these threats, cells tightly control replication initiation using well-known mechanisms. They also couple DNA synthesis to nutrient richness and growth rate through a poorly understood process thought to involve central carbon metabolism. One such process may involve the cross-species conserved pyruvate kinase (PykA) which catalyzes the last reaction of glycolysis. Here we have investigated the role of PykA in regulating DNA replication in the model system <em>Bacillus subtilis.</em></p><p><strong>RESULTS: </strong>On analysing mutants of the catalytic (Cat) and C-terminal (PEPut) domains of <em>B. subtilis</em> PykA we found replication phenotypes in conditions where PykA is dispensable for growth. These phenotypes are independent from the effect of mutations on PykA catalytic activity and are not associated with significant changes in the metabolome. PEPut operates as a nutrient-dependent inhibitor of initiation while Cat acts as a stimulator of replication fork speed. Disruption of either PEPut or Cat replication function dramatically impacted the cell cycle and replication timing even in cells fully proficient in known replication control functions. <em>In vitro</em>, PykA modulates activities of enzymes essential for replication initiation and elongation via functional interactions. Additional experiments showed that PEPut regulates PykA activity and that Cat and PEPut determinants important for PykA catalytic activity regulation are also important for PykA-driven replication functions.</p><p><strong>CONCLUSIONS:</strong> We infer from our findings that PykA typifies a new family of cross-species replication control regulators that drive the metabolic control of replication through a mechanism involving regulatory determinants of PykA catalytic activity. As disruption of PykA replication functions causes dramatic replication defects, we suggest that dysfunctions in this new family of universal replication regulators may pave the path to genetic instability and carcinogenesis.</p>
2022-04-19 | MTBLS4415 | MetaboLights