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SRP145098
Rattus norvegicus
9 Downloadable Samples
Illumina HiSeq 4000
Description
RNA seq analyses were performed in granulosa cells (GCs) collected from gonadotropin treated ESR2 mutant rats. Data obtained from a null mutant with Esr2 exon 3 deletion (?3) and another DNA binding domain (DBD) mutant with exon 4 deletion (?4) were compared to that of wildtype (WT) rats. The raw data were analyzed using CLC genomics workbench. High quality RNA-sequencing reads were aligned to the Rattus norvegicus genome. Differentially expressed genes in ?3 or ?4 Esr2-mutant GCs were identified based on the following criteria: FDR p-Value =0.05 and an absolute fold change of 2. Fewer differentially expressed genes were identified in ?3 compared to the ?4 mutant group. As both of the mutant groups demonstrated a common phenotype of ovulation failure, differentially expressed genes common to both in ?3 and ?4 mutant rats were emphasized and further analyzed in the companion article “ESR2 regulates granulosa cell genes essential for follicle maturation and ovulation” (Khristi et al., 2018).
Publication Title
ESR2 regulates granulosa cell genes essential for follicle maturation and ovulation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 4000
Description
The goal of this study was to perform RNA-seq on postnatal day 12 mouse oocytes to quantify gene expression.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line
View Samples- Rattus norvegicus
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
Estrogens are traditionally considered to be female sex steroid hormones and most of the studies examining estrogen regulation of metabolic function in the liver have been conducted in females. However, the liver expresses high levels of estrogen receptor alpha (ESR1) in both males and females, which mediates the hepatic response to estrogens. In this study, we investigated whether metabolic disorders in Esr1 knockout (Esr1-/-) male rats were linked with loss of transcriptional regulation by ESR1 in liver. To identify the ESR1 regulated genes in the mutant liver, RNA-sequencing was performed on liver RNAs purified from young male rats. The raw data were analyzed using the CLC Genomics Workbench and high-quality RNA-sequencing reads were aligned to the Rattus norvegicus genome. Transcriptome data obtained from Esr1-/- liver RNAs were compared to that of wild type rats. Based on an absolute fold change of 2 with a p-value = 0.05, a total of 618 differentially expressed genes were identified in the Esr1-/- male liver. Pathway analyses demonstrated that the majority of differentially expressed genes are regulators of carbohydrate and lipid metabolism in the liver.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 1500
Description
MDA-MB-231 and T47D human breast cancer cells were chronically treated with the novel STAT3/5 inhibitor SH-4-54 for 60 and 30 days, respectively. Surviving treatment-resistant individual clones were isolated and characterized for their phosphorylated STAT3 and phosphorylated STAT5 status. 3 biological replicates of mRNA from a representative resistant clone derived from both MDA-MB-231 and T47D cells, in parallel with mRNA from their respective wild-type counterparts, was subjected to NextGeneration Sequencing to analyze changes in gene expression between untreated and resistant cells.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
The impact of the transcriptome-wide alternative splicing on proteomic-wide protein subcellular localization was investigated by analyzing RNA-Seq data.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Disease, Cell line
View Samples- Homo sapiens
- 1 Downloadable Sample
- IonTorrentProton
Description
Cryptococcus neoformans infection and immune cell regulation on human monocytes
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 32 Downloadable Samples
- IlluminaHiSeq2000
Description
Transcriptome seqeunecing on 16 paired HCCs and non-tumorous livers to investigate the effect of HBV integration
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 24 Downloadable Samples
- NextSeq 500
Description
old and young human cardiac fibroblasts plus those treated with rapamycin and methionine restriction or a combination of both
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 17 Downloadable Samples
- IlluminaGenomeAnalyzerII
Description
No description.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 13 Downloadable Samples
- Illumina HiSeq 2000
Description
PTEN encodes a lipid phosphatase that is underexpressed in many cancers owing to deletions, mutations or gene silencing. PTEN dephosphorylates phosphatidylinositol 3,4,5-triphosphate (PIP3), thereby opposing the activity of class I phosphatidylinositol 3-kinases (PI3Ks) that mediate growth and survival factors signaling through PI3K effectors such as AKT and mTOR. To determine whether continued PTEN inactivation is required to maintain malignancy, we generated an RNAi-based transgenic mouse model that allows tetracycline-dependent regulation of PTEN in a time- and tissue-specific manner. Postnatal PTEN knockdown in the hematopoietic compartment produced highly disseminated T-cell leukemia (T-ALL). Surprisingly, reactivation of PTEN mainly reduced T-ALL dissemination but had little effect on tumor load in hematopoietic organs. Lymphoma infiltration into the intestine was dependent on CCR9 G-protein coupled receptor (GPCR) signaling, which was amplified by PTEN loss. Our results suggest that in the absence of PTEN, GPCRs may play an unanticipated role in driving tumor growth and invasion in an unsupportive environment. They further reveal that the role of PTEN loss in tumor maintenance is not invariant and can be influenced by the tissue microenvironment, thereby producing a form of intratumoral heterogeneity that is independent of cancer genotype.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples