We analysed the combined effects of exposure to maternal diabetes and disrupted HIF-1 signaling on the transcriptom in cardiac left ventricles of 12 weeks old male mice. This approach provides the information about the long term changes originating in utero due to maternal diabetes and inefficient response to hypoxia which develops as a result of hyperglycemia. The majority of changes were detected in Hif1a insufficient mice exposed to maternal diabetes. Overall design: Streptozotocin induced diabetic FVB females were mated with non-diabetic males with global heterozygous deletion of Hif1a (Hif1a+/-). Total RNA was extracted from the LV of the hearts of 12-week-old male offspring in biological triplicates per each group (wt, non-diabetic pregnancy; wt, diabetic pregnancy; Hif1a+/-, non-diabetic pregnancy; Hif1a+/-, diabetic pregnancy). RNA profiles were generated by deep sequencing using Illumina NextSeq.
Adverse effects of Hif1a mutation and maternal diabetes on the offspring heart.
Sex, Age, Specimen part, Subject
View SamplesWe sequenced mRNA from Left Ventricles of Streptozotocin induced Type I diabetic mouse hearts or mock treated controls at 4 weeks post-treatment in order to assess alternative splicing changes. Overall design: Heart mRNA profiles of Control and Diabetic (STZ:T1D) mice were generated by deep sequencing using Illumina HiSeq 1000.
Dysregulation of RBFOX2 Is an Early Event in Cardiac Pathogenesis of Diabetes.
Age, Specimen part, Cell line, Treatment, Subject
View SamplesThe response of the nematode C. elegans to Y. pestis infection was evaluated by gene expression profiling. A synchronized population of nematodes were exposed to Y. pestis KIM5 for 24h. Transcript levels from Y. pestis-treated animals were compared with animals maintained on relatively nonpathogenic E. coli OP50 for 24h.
A conserved PMK-1/p38 MAPK is required in caenorhabditis elegans tissue-specific immune response to Yersinia pestis infection.
Specimen part
View SamplesTo provide insights into the mechanism underlying the enhanced immunity of tag-24/octr-1 animals, we used genome microarrays to find clusters of genes commonly misregulated in tag-24 relative to wild-type animals grown on live P. aeruginosa.
Neuronal GPCR controls innate immunity by regulating noncanonical unfolded protein response genes.
Specimen part
View SamplesTo investigate the role of NKX3.1 in prostate differentiation, we employed transcriptome analysis of mouse seminal vesicle (from 15-month-old Nkx3.1+/+ mice); mouse prostate (from 4-month-old Nkx3.1+/+ and Nkx3.1-/- mice); human prostate cells (RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression); and tissue recombinants (generated from combining engineered mouse epithelial cells (seminal vesicle epithelial cells or prostate epithelial cells from 2-month-old mice) and rat UGS mesenchymal cells). Mouse tissue or human cells were snap frozen for subsequent molecular analysis.
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Disease, Disease stage, Treatment
View SamplesAnalysis of the transcriptome of mouse models of prostate cancer after treatment with rapamycin and PD0325901 combination therapy or standard of care docetaxel. The Nkx3.1CreERT2/+; Ptenflox/flox; KrasLSL-G12D/+ (NPK mice) was used in this study. Two months after tumor induction, mice were randomly assigned to vehicle (Veh) or treatments groups, such as rapamycin and PD0325901 (RAPPD) or docetaxel (Docetaxel). For the treatment groups mice were administered rapamycin (10 mg/kg) and PD0325901 (10 mg/kg) or docetaxel (10 mg/kg) for 5 days (SHORT) or for 1 month (LONG). At the end of the treatment, mice were euthanized, tumors harvested and snap frozen for subsequent molecular analysis.
Predicting Drug Response in Human Prostate Cancer from Preclinical Analysis of In Vivo Mouse Models.
Specimen part, Treatment
View SamplesAnalysis of transcriptome of tissue recombinants (mouse seminal vesicle epithelial [SVE] cells or prostate epithelial [PE] cells, and rat urogenital sinus [UGS] mesenchymal cells) grown under the kidney capsule in athymic nude mice for 3 months. Overall design: Total RNA obtained from tissue recombinants generated from combining engineered mouse epithelial cells (SVE or PE from 2-month-old C57Bl/6J mice) and rat UGS mesenchymal cells. Tissue recombinants were harvested and processed for RNA isolation and transcriptome analysis using the RNeasy kit (Qiagen).
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Subject
View SamplesAnalysis of transcriptome of human RWPE1 cells over-expressing wild type NKX3.1 and mutant NKX3.1 (T164A). Overall design: Total RNA obtained from RWPE1 cells engineered with empty vector (altered pTRIPZ), NKX3.1 wild type over-expression, and NKX3.1 (T164A) mutant over-expression. Engineered RWPE1 cells were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion).
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Cell line, Subject
View SamplesAnalysis of transcriptome of prostate tissue from 4-month-old Nkx3.1 +/+ and Nkx3.1 -/- mice. Overall design: Total RNA obtained from prostate tissues from 4-month-old Nkx3.1 +/+ and Nkx3.1 -/- mice. Prostate tissues were harvested and processed for RNA isolation and transcriptome analysis using the MagMAX RNA isolation kit (Ambion).
Identification of an NKX3.1-G9a-UTY transcriptional regulatory network that controls prostate differentiation.
Age, Specimen part, Subject
View Samples