Streptococcus agalactiae breed:Long-Evans Rat
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA342556 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MJHP01.dat.gz | Other | |||
| MJHP01.fasta.gz | Fasta.gz | |||
| MJHP01.master.dat | Other | |||
| MJHQ01.dat.gz | Other | |||
| MJHQ01.fasta.gz | Fasta.gz |
Items per page: 5 1 - 5 of 35 |
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Project description:Rattus norvegicus breed:Long Evans Raw sequence reads
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Project description:Rattus norvegicus Long Evans transcriptome project
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Project description:To determine whether immortalized cells derived from the rat SCN (SCN 2.2) retain intrinsic rhythm-generating properties characteristic of the SCN, oscillatory properties of the SCN2.2 transcriptome were analyzed and compared to those found in the rat SCN in vivo using rat U34A Affymetrix GeneChips. In this comparison, adult male Long-Evans rats (175-200g; N=45) were housed under a standard 12h light:12h dark photoperiod (LD 12:12; lights-on at 0600 hr). At 1800 hr (circadian time [CT] 12), animals were exposed to constant darkness (DD) and 12 hours later (0600 hr or CT 0), sacrificed under isoflurane anesthesia at 6-hr intervals (N=5) for 48 hours by decapitation using an infrared viewer. After the eyes were removed in the dark, SCN tissue was immediately dissected under dim light, frozen in liquid nitrogen, and stored at â??800C. SCN tissue from individual animals was separately homogenized in TRIzol reagent by aspiration through a 25-gauge needle and then extracted cellular RNA for all animals at each timepoint was pooled into a single sample. RNA samples were subjected to on-column treatment with DNAse-1 to digest genomic DNA and then were stored at â??80°C before routine processing for GeneChip analysis.
2008-06-11 | E-GEOD-1673 | biostudies-arrayexpress
Project description:To determine whether immortalized cells derived from the rat SCN (SCN 2.2) retain intrinsic rhythm-generating properties characteristic of the SCN, oscillatory properties of the SCN2.2 transcriptome were analyzed and compared to those found in the rat SCN in vivo using rat U34A Affymetrix GeneChips. In this comparison, adult male Long-Evans rats (175-200g; N=45) were housed under a standard 12h light:12h dark photoperiod (LD 12:12; lights-on at 0600 hr). At 1800 hr (circadian time [CT] 12), animals were exposed to constant darkness (DD) and 12 hours later (0600 hr or CT 0), sacrificed under isoflurane anesthesia at 6-hr intervals (N=5) for 48 hours by decapitation using an infrared viewer. After the eyes were removed in the dark, SCN tissue was immediately dissected under dim light, frozen in liquid nitrogen, and stored at –800C. SCN tissue from individual animals was separately homogenized in TRIzol reagent by aspiration through a 25-gauge needle and then extracted cellular RNA for all animals at each timepoint was pooled into a single sample. RNA samples were subjected to on-column treatment with DNAse-1 to digest genomic DNA and then were stored at –80°C before routine processing for GeneChip analysis. Keywords: other
2004-10-09 | GSE1673 | GEO
Project description:Hippocampal gene expression profiles in aged memory-impaired and aged memoryunimpaired Long-Evans rats
2006-03-30 | E-MEXP-553 | biostudies-arrayexpress
Project description:Dioxin-like chemicals are well-known for their ability to upregulate expression of numerous genes via the AH receptor (AHR). However, recent transcriptomic analyses in several laboratories indicate that dioxin-like chemicals or AHR genotype itself also can downregulate levels of mRNAs encoded by numerous genes. The mechanism responsible for such downregulation is unknown. We hypothesized that microRNAs (miRNAs), which have emerged as powerful negative regulators of mRNA levels in several systems, might be responsible for mRNA downregulation in dioxin/AHR pathways. We used the Exiqon miRNA array platform as well as quantitative RT-PCR to measure miRNA levels in dioxin-sensitive Long-Evans (Turku/AB; L-E) rats. Treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 96 hr in vivo caused few changes in miRNA levels in rat livers and those changes that were statistically significant were of modest magnitude. Feed-restricted-control L-E rats were included to ensure that changes in miRNA levels were due to TCDD-treatment per se and not the result of the decreased feed intake which occurs in dioxin-sensitive strains within 96 h after TCDD exposure. Manuscript Submitted: Moffat ID, Boutros PC, Celius T, Pohjanvirta R & Okey AB. Micro-RNAs in rodent liver are refractory to dioxin treatment. Toxicological Sciences May, 2007. Keywords: miRNA expression, response to xenobiotics, feed restriction response
2007-08-15 | GSE8469 | GEO
Project description:Copy number variations (CNVs) of the human 16p11.2 locus are associated with several developmental/neurocognitive syndromes. Particularly, deletion and duplication of this genetic interval are found in patients with autism spectrum disorders, intellectual disability and other psychiatric traits. The high gene density associated with the region and the strong phenotypic variability of incomplete penetrance, make the study of the 16p11.2 syndromes extremely complex. To systematically study the effect of 16p11.2 CNVs and identify candidate genes and molecular mechanisms involved in the pathophysiology, mouse models were generated previously and showed learning and memory, and to some extent social deficits. To go further in understanding the social deficits caused by 16p11.2 syndromes, we engineered deletion and duplication of the homologous region to the human 16p11.2 genetic interval in two rat outbred strains, Sprague Dawley (SD) and Long Evans (LE). The 16p11.2 rat models displayed convergent defects in social behaviour and only a few cognitive defects. Interestingly major pathways affecting MAPK3 and CUL3 were found altered in the rat 16p11.2 models with additional changes in males compared to females. Altogether, the consequences of the 16p11.2 genetic region dosage on social behaviour are now found in three different species: humans, mice and rats. In addition, the rat models pointed to sexual dimorphism, with lower severity of phenotypes in rat females compared to male mutants. This phenomenon is also observed in humans. We are convinced that the two rat models will be key to further investigating social behaviour and understanding the brain mechanisms and specific brain regions that are key to controlling social behaviour.
2023-02-18 | GSE225112 | GEO
Project description:Dioxin-like chemicals are well-known for their ability to upregulate expression of numerous genes via the AH receptor (AHR). However, recent transcriptomic analyses in several laboratories indicate that dioxin-like chemicals or AHR genotype itself also can downregulate levels of mRNAs encoded by numerous genes. The mechanism responsible for such downregulation is unknown. We hypothesized that microRNAs (miRNAs), which have emerged as powerful negative regulators of mRNA levels in several systems, might be responsible for mRNA downregulation in dioxin/AHR pathways. We used the Exiqon miRNA array platform as well as quantitative RT-PCR to measure miRNA levels in dioxin-sensitive Long-Evans (Turku/AB; L-E) rats. Treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 96 hr in vivo caused few changes in miRNA levels in rat livers and those changes that were statistically significant were of modest magnitude. Feed-restricted-control L-E rats were included to ensure that changes in miRNA levels were due to TCDD-treatment per se and not the result of the decreased feed intake which occurs in dioxin-sensitive strains within 96 h after TCDD exposure. Manuscript Submitted: Moffat ID, Boutros PC, Celius T, Pohjanvirta R & Okey AB. Micro-RNAs in rodent liver are refractory to dioxin treatment. Toxicological Sciences May, 2007. Keywords: miRNA expression, response to xenobiotics, feed restriction response A loop design used to profile miRNA levels from dioxin-sensitive L-E AHRWT/WT vehicle-control rats (LC96), those exposed to TCDD for 96 h (LT96), and feed-restricted (LF96) rats.
2007-08-14 | E-GEOD-8469 | biostudies-arrayexpress
Project description:We performed very deep small RNA sequencing on one sample of medial entorhinal cortex of a Long Evans rat aged P23 to see which small RNAs could be detected in this brain area.
2017-08-01 | GSE85788 | GEO
Project description:Rodents exposed to the environmental contaminant, TCDD, suffer from a number of acute and chronic toxicities, including lethality and a wasting syndrome. Hypothesizing that the wasting syndrome may be caused by changes in neural control of energy flux and metabolism, we profiled the transcriptional response of rat hypothalamus to TCDD. We employed two separate rat strains: the Long-Evans strain is sensitive to TCDD toxicities while the Han/Wistar strain is over four orders of magnitude more resistant. Surprisingly, few transcriptional changes were induced by TCDD in either strain. Only four genes were altered in Long-Evans rats, including three classic TCDD-responsive genes: Cyp1a1, Cyp1b1, and Nqo1. These three genes were also altered in Han/Wistar rats, along with 133 additional genes. However, the magnitudes of alteration of these additional genes was very modest, with most changes well below two-fold in magnitude. We therefore concluded that rat hypothalamus is mostly refractory to TCDD exposure, at least at the doses and time-points surveyed here.
2009-11-24 | GSE18257 | GEO