We evaluated the transcriptome changes induced by infection with Salmonella (20 hpi, MOI 100). Overall design: Transcriptmic profiles of HeLa cells infected with Salmonella Typhimurium were generated by deep sequencing, using Illumina HiSeq 2000.
Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection.
No sample metadata fields
View SamplesWe identified miRNAs differentially regulated upon Salmonella infection by comparative deep-sequencing analysis of cDNA libraries prepared from the small RNA population (10–29 nt) of HeLa cells infected with Salmonella (20 hpi) and mock-treated cells. Considering that at a MOI of 25 Salmonella is internalized in only 10-15% of the HeLa cells, we separated the fraction of cells which had internalized Salmonella (Salmonella+) from the bystander fraction (Salmonella-) by fluorescence-activated cell sorting (FACS), and extended the analysis of miRNA changes to these samples. Interestingly, we observed that Salmonella infection induces a significant decrease in the expression of all the detected members of the miR-15 family Overall design: miRNA profiles of HeLa cells infected with Salmonella Typhimurium were generated by deep sequencing, using Illumina HiSeq2000.
Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection.
No sample metadata fields
View SamplesTo have a global picture of the targets of the miR-15 family, we assessed transcriptome changes, by deep-sequencing, of HeLa cells transfected with 3 members of the miR-15 family (miR-15a, miR-16 or miR-503) or a control miRNA (cel-miR-231). We observed a very extensive overlap between the genes down-regulated by these 3 miRNAs, as expected for miRNAs belonging to the same family. Overall design: transcriptmic profiles of HeLa cells treated miR-15a, miR-16, miR-503 and control-miR were generated by deep sequencing, using Illumina HiSeq2000.
Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection.
No sample metadata fields
View SamplesWe evaluated the transcriptome changes induced by infection of Hela 229 cells with Shigella flexneri. The sample set consists of a control (mock), total population of infected sample and infected sample sorted into Shigella positive and Shigella negative population. Overall design: Transcriptmic profiles of HeLa cells infected with Shigella were generated by high throughput sequencing using Illumina HiSeq2000.
Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia.
No sample metadata fields
View SamplesTo have a global picture of the targets of the mir-29b-2-5p, we assessed transcriptome changes, by deep-sequencing, of HeLa cells transfected with this miRNA or a control miRNA (cel-miR-231). Overall design: Transcriptmic profiles of HeLa cells treated miR-29b-2-5p and control-miR were generated by deep sequencing, using Illumina HiSeq2000.
Analysis of host microRNA function uncovers a role for miR-29b-2-5p in Shigella capture by filopodia.
No sample metadata fields
View SamplesRNA was isolated from siCTRL, siNSUN2 and ALYREF-RIP HeLa cells, and multiple mouse tissues using the TRIzol (Invitrogen) reagent by following the company manual. Approximately 2.5 µg of total RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq3000 (Illumina) or HiSeq2500 in paired-read mode, creating reads with a length of 101 or 125 bp. Sequencing chemistry v2 or v4 (Illumina) was used. Overall design: Examination of gene expressive levels in siCTRL, siNSUN2 and ALYREF-RIP HeLa cells, and multiple mouse tissues
5-methylcytosine promotes mRNA export - NSUN2 as the methyltransferase and ALYREF as an m<sup>5</sup>C reader.
No sample metadata fields
View SamplesBrown adipose tissue (BAT) is a thermogenic organ that dissipates stored energy as heat to maintain body temperature in infants and small mammals. This process may also provide protection from development of diet-induced obesity. We found that the bioactive lipid mediator lysophosphatidic acid (LPA) markedly decreases differentiation of cultured primary brown adipocyte precursors, while potent selective inhibitors of the LPA-generating enzyme autotaxin (ATX) promote differentiation. Transgenic mice overexpressing ATX exhibited reduced expression of BAT-related genes in peripheral white adipose tissue and accumulated significantly more fat than wild-type controls when fed a high fat diet. Our results indicate that ATX and its product LPA are physiologically relevant negative regulators of brown fat adipogenesis and suggest that a decrease in peripheral brown adipose tissue results in increased susceptibility to diet-induced obesity in mice.
Autotaxin and its product lysophosphatidic acid suppress brown adipose differentiation and promote diet-induced obesity in mice.
Sex, Age, Specimen part, Treatment
View SamplesApplied de novo assembly, both protein coding and non-coding RNAs were profiled in AFB1 induced HCC and AFB1 resistant liver sample. Compared with normal liver, the perturbation on transcriptome was revealed in multiple aspects, implying the potential mechanism of toxic resistance. Overall design: All rats were randomly divided into control and treated groups according to their weight. Then AFB1 was injected intraperitoneally to treated group in customized schedule. Biopsy was applied every 10 weeks on both groups. Tissues from rats died of HCC were reserved. All rats were sacrificed at 70th week. According to whether tumor formed, liver tissues from animals in treated group were further divided into AFB1 induced tumor sample and AFB1 resistant sample. Both samples were stored for later transcriptome analysis, as well as the normal sample from control group. RNA profiles of all 3 samples were generated by deep sequencing, using Illumina HiSeq2000 platform.
Distinct response of the hepatic transcriptome to Aflatoxin B1 induced hepatocellular carcinogenesis and resistance in rats.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Integrated genetic approaches identify the molecular mechanisms of Sox4 in early B-cell development: intricate roles for RAG1/2 and CK1ε.
Specimen part
View SamplesOne of the main objective of this study is to identify Sox4 controlled gene networks and their roles in progenitor B cells.
Integrated genetic approaches identify the molecular mechanisms of Sox4 in early B-cell development: intricate roles for RAG1/2 and CK1ε.
Specimen part
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