Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR13333503.fastq.gz | Fastqsanger.gz | |||
| ERR13333479.fastq.gz | Fastqsanger.gz |
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Project description:Single Cell RNA sequencing using 10x Genomics 3' v2 chemistry assessing the consequence of Bax/Atoh7 loss of function on retinal ganglion cell development and retinal development
2021-03-17 | GSE148814 | GEO
Project description:This clinical trial studies the effectiveness of a web-based cancer education tool called Helping Oncology Patients Explore Genomics (HOPE-Genomics) in improving patient knowledge of personal genomic testing results and cancer and genomics in general. HOPE-Genomics is a web-based education tool that teaches cancer/leukemia patients, and patients who may be at high-risk for developing cancer, about genomic testing and provide patients with information about their own genomic test results. The HOPE-Genomics tool may improve patient’s genomic knowledge and quality of patient-centered care. In addition, it may also improve education and care quality for future patients.
| 2378933 | ecrin-mdr-crc
Project description:To investigate the diversity of gene contents of Candida albicans strain by array-based comparative genomic hybridization (array CGH; aCGH). the srd1 null mutant Candida albicans strain CaLY202 was selected to carry out the comparative genomics microarray. Two-condition experiment, CaLY202 vs.SN152. Biological replicates: 2 control, 2 transfected, independently grown and harvested. One replicate per array.
2014-06-24 | E-GEOD-48530 | biostudies-arrayexpress
Project description:Targeted mutant models are common in mechanistic toxicology experiments investigating the absorption, metabolism, distribution, or elimination (ADME) of chemicals from individuals. Key models include those for xenosensing transcription factors and cytochrome P450s (CYP). Here we investigated changes in transcript levels, protein expression, and steroid hydroxylation of several xenobiotic detoxifying CYPs in constitutive androstane receptor (CAR)-null and two CYP-null mouse models that have subfamily members regulated by CAR; the Cyp3a-null and a newly described Cyp2b9/10/13-null mouse model. Compensatory changes in CYP expression that occur in these models may also occur in polymorphic humans, or may complicate interpretation of ADME studies performed using these models. The loss of CAR causes significant changes in several CYPs probably due to loss of CAR-mediated constitutive regulation of these CYPs. Expression and activity changes include significant repression of Cyp2a and Cyp2b members with corresponding drops in 6α- and 16β-testosterone hydroxylase activity. Further, the ratio of 6α-/15α-hydroxylase activity, a biomarker of sexual dimorphism in the liver, indicates masculinization of female CAR-null mice, suggesting a role for CAR in the regulation of sexually dimorphic liver CYP profiles. The loss of Cyp3a causes fewer changes than CAR. Nevertheless, there are compensatory changes including gender-specific increases in Cyp2a and Cyp2b. Cyp2a and Cyp2b were down-regulated in CAR-null mice, suggesting activation of CAR and potentially PXR following loss of the Cyp3a members. However, the loss of Cyp2b causes few changes in hepatic CYP transcript levels and almost no significant compensatory changes in protein expression or activity with the possible exception of 6α-hydroxylase activity. This lack of a compensatory response in the Cyp2b9/10/13-null mice is probably due to low CYP2B hepatic expression, especially in male mice. Overall, compensatory and regulatory CYP changes followed the order CAR-null > Cyp3a-null > Cyp2b-null mice.
| S-EPMC5370058 | biostudies-literature
Project description:TNF ligand ectodysplasin-A1 contributes to embryonic mammary gland development. We searched for target genes of the Eda pathway using profiling of genes differentially expressed in Eda-null mammary buds after a short exposure to recombinant Fc-Eda-A1 protein. Microdissected E13.5 Eda-/- epithelial mammary buds from 5-6 embryos were pooled together. Other half of an embryo was used as a control and the other half as a treated sample. Littermates from 3 litters of B6CBA background were used for the analysis. Array and data analysis were performed in the Biomedicum Functional Genomics Unit (University of Helsinki, Finland).
2015-11-01 | E-GEOD-69781 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from the knockout of Hira in undifferentiated mouse embryonic stem cells (mESCs) and in day 15 differentiated cardiomyocytes.Methods: RNA extraction was done in duplicate from WT and Hira-null mESCs at day0 and day15 using TRIzol reagent. RNAseq was done onIllumina Nextseq500 and processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R2 package. Gene lists were filtered using adjusted p-value ≤ 0.05 and absolute fold change ≥ 2. Results:We identified 1680 transcripts changed in the absence of HIRA in day 15 differentiated cardiomyocytes. GO term cardiovascular system development was the most downregulated gene set(p-value ≤ 0.01 and FDR ≤0.1. Conclusion: this study analysis the role of HIRA in early cardiac mesoderm development usinf an invitro mESCs model.
2019-04-01 | GSE111910 | GEO
Project description:Foxi3 is a transcription factor expressed in the hair follicle epithelium during development and postnatally. In this study we used a microarray analysis to indentify differentially expressed genes in Foxi3 null epithelium compared to Foxi3 wt epithelium. We used E15.5 stage as the earliest time point when the Foxi3 null hair phenotype bacame obvious, to find out the most early consequences of Foxi3 ablation. Dispase-dissociated back skin epithelia of 4 Foxi3 total null and 4 wild-type E15.5 mouse embryos, littermates from 4 litters of C57/Bl6 background, were used for the analysis. Array and data analysis were performed in the Biomedicum Functional Genomics Unit (University of Helsinki, Finland).
2016-03-01 | E-GEOD-68985 | biostudies-arrayexpress
Project description:Preventing the ototoxicity caused by cisplatin is a major issue yet to be overcome. Useful preventive treatments will soon be available. Consequently, the next step is to filter out those patients who are more prone to develop ototoxicity. The aim of this study was to prospectively evaluate potential predictive markers of acute ototoxicity as determined by measures of distortion product otoacoustic emissions (DPOAEs). A total of 118 patients from our previous DPOAE analysis were put under evaluation. Ototoxic cases were divided according to unilateral (n = 45) or bilateral (n = 23) involvement. The clinicopathological characteristics, hearing test results, germline GSTT1, GSTM1, and GSTP1 polymorphisms, and common laboratory parameters were included in the new analysis. Univariate and multivariate statistical tests were applied. According to multivariate logistic regression, the only independent predictor of unilateral ototoxicity (vs. non-affected) was a GSTM1 null genotype (OR = 4.52; 95%CI = 1.3-16.3), while for bilateral damage, the GSTT1 null genotype (OR = 4.76; 1.4-16) was a predictor. The higher starting serum urea level was characteristic of bilateral ototoxicity; however, the only independent marker of bilateral (vs. unilateral) ototoxicity was the presence of GSTT1 null genotype (OR = 2.44; 1.23-4.85). Different processes, involving the GSTM1 and GSTT1 genotypes, respectively, govern the development of acute unilateral and bilateral ototoxicities. Further research is needed to clarify these processes. Based on the above findings, patients whom are at risk may be selected for otoprotective therapies. KEY MESSAGES: The acute ototoxicity was determined by DPOAE in 118 testicular cancer patients. GSTM1 null was the only marker of unilateral ototoxicity (vs. non-affected). The only marker of bilateral hearing loss (vs. non-affected) was the GSTT1 null. GSTT1 null was also the marker of bilateral vs. unilateral ototoxicity. A high-risk group may be selected for new, individualized otoprotective treatment.
| S-EPMC7343745 | biostudies-literature
Project description:The dinucleotide sequence 5'CG acts as a signalling module that can influence the epigenome and modulate chromosome function. CG exists in three chemically distinct forms that differ due to the modification status of the cytosine base: unmethylated, methylated or hydroxymethylated. The Cfp1 protein binds to unmethylated CG clusters in vivo and is required for the coincident trimethylation of lysine 4 in histone H3 by the Setd1 complex. On the other hand, the methyl-CG binding protein MeCP2 can direct deacetylation of histones. These findings align with evidence that nonmethylated CpG islands mark promoters, whereas CG methylation leads to gene silencing. Interfering with Cfp1 or Mecp2 function will therefore impact chromatin structure, possibly resulting in alteration of transcription. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ Abstract: This project aims to assess effects of Cfp1- and Mecp2-deficiency on transcription using RNA-seq of nascent RNA. This involves in vitro run-on transcription with isolated nuclei using BrU as a substrate to permit purification of nascent RNA. This technique shows where active polymerases are loaded on chromatin, unlike conventional RNA-seq, which only detects stable cytoplasmic RNAs.
2012-06-21 | E-ERAD-80 | biostudies-arrayexpress