Insulin resistance is a sine qua non of Type 2 diabetes (T2D) and a frequent complication of multiple clinical conditions, including obesity, aging, and steroid use, among others. How such a panoply of insults can result in a common phenotype is incompletely understood. Furthermore, very little is known about the transcriptional and epigenetic basis of this disorder, despite evidence that such pathways are likely to play a fundamental role. Here, we compare cell autonomous models of insulin resistance induced by the cytokine tumor necrosis factor-a (TNF) or by the steroid dexamethasone (Dex) to construct detailed transcriptional profiles associated with cellular insulin resistance.
Identification of nuclear hormone receptor pathways causing insulin resistance by transcriptional and epigenomic analysis.
Specimen part, Cell line, Treatment, Time
View Samplesgene expression data from mouse adipocyte, with and without Ebf1 knock-down
Early B-cell factor-1 (EBF1) is a key regulator of metabolic and inflammatory signaling pathways in mature adipocytes.
Specimen part
View SamplesMind-body practices that elicit the relaxation response (RR) have been used worldwide for millennia to prevent and treat disease. The RR is believed to be the counterpart to stress response and is characterized by decreased oxygen consumption, increased exhaled nitric oxide, and reduced psychological distress. Individuals experiencing chronic psychological stress have the opposite pattern of physiology and a characteristic transcriptional profile. We hypothesized that consistent, long-term practice of RR techniques results in characteristic changes in gene expression. We tested this hypothesis by assessing the transcriptional profile of whole blood in healthy, long-term practitioners of daily RR practice (group M) in comparison to healthy controls (group N1). The signature obtained has been validated on new subject data.
Genomic counter-stress changes induced by the relaxation response.
No sample metadata fields
View SamplesPatients with chronic illnesses such as Irritable Bowel Syndrome (IBS) or Inflammatory Bowel Disease (IBD) often have reduced quality of life. IBS is characterized by abdominal pain/discomfort associated with altered bowel function, such as diarrhea or constipation, without gross structural changes or inflammation [1]; IBD is characterized by gross inflammation in the gastrointestinal (GI) tract which can result in symptoms such as abdominal pain, cramping, diarrhea and bloody stools. IBS and IBD can profoundly affect quality of life and are influenced by stress and resiliency.The impact of mind-body interventions (MBIs) on IBS and IBD patients has not previously been examined. In this study IBS and IBD patients were enrolled in a 9-week relaxation response based mind-body group intervention (RR-MBI), focusing on elicitation of the RR and cognitive skill building. We performed Peripheral blood transcriptome analysis to identify genomic correlates of the RR-MBI.
Genomic and clinical effects associated with a relaxation response mind-body intervention in patients with irritable bowel syndrome and inflammatory bowel disease.
Specimen part, Disease, Disease stage, Subject, Time
View SamplesPURPOSE:
Unique gene expression profile based on pathologic response in epithelial ovarian cancer.
No sample metadata fields
View SamplesWe compared 22 primary Pca (hormone-dependent) versus 29 metastatic Pca (CRPC). The expression of genes related to cell cycle, proliferation, DNA synthesis, and androgen metablism are significantly increased in CRPC group. The expression of AR-stimulated genes were partially reactivated.
ERG induces androgen receptor-mediated regulation of SOX9 in prostate cancer.
No sample metadata fields
View SamplesGene expression profiling of HUVEC (human umbilical vein EC cell; Lonza), HAEC (human aortic EC cells), HCAEC (human coronary artery EC cells), HPAEC (human pulmonary artery EC cells), HMVEC (human microvascular (dermal) , HASMC ( Human Aortic Smooth Muscle Cells), T cells and Bcells.
No associated publication
Specimen part
View SamplesThis study was performed to understand the gene expression changes that accompany treatment of renal cell carcinoma (RCC) with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy. Human RCC cell lines were implanted into the flanks of nude beige mice, allowed to reach 12mm in long axis, and then treated with TKIs (sunitinib or sorafenib). Tumors were excised at 2 timepoints (prior to any therapy and at the 20mm endpoint of the study) and gene expression analysis was performed.
Anti-S1P Antibody as a Novel Therapeutic Strategy for VEGFR TKI-Resistant Renal Cancer.
Specimen part, Cell line, Treatment
View Samples8 week-old male C57BL6J mice were given Gram-negative endotoxin (LPS O111:B4, 10 mg/kg) intraperitoneally at time 0. 18 hrs thereafter, they were administered 10 ml/kg 0.9% saline. Mice were sacrificed at 0, 18, or 42 hrs after LPS challenge. Kidneys were immediately collected into TRIzol for RNA preparation. Renal function was measured on blood collected at the time of tissue harvest
PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice.
Sex, Age, Specimen part
View SamplesWe profiled genome-wide gene expression of human prostate benign and malignant tissue to identify potential biomarkers and immunotherapy targets.
Identification of the transcription factor single-minded homologue 2 as a potential biomarker and immunotherapy target in prostate cancer.
Specimen part
View Samples