Analysis of human natural killer cells following stimulation with immobilized IgG1 for 4 and 24 hours. Results identified significantly differentially expressed genes in natural killer cells stimulated with immobilized IgG1 providing insight into how antibodies modulate the transcriptome in way that may contribute to cell activation and immune tolerance
No associated publication
Specimen part, Treatment, Time
View SamplesWe asked what genes are significantly differentially regulated in the spinal cord of SCI trkB.T1 WT and trkB.T1 KO mice. TrkB.T1 is upregulated shortly after SCI although the precise mechanisms underyling this upregulation are poorly understood. In the trkB.T1 null, we show less mechanical allodynia and better locomotor recovery following SCI. The microarray studies helped us to elucidate a signaling pathway that is differently regulated in the WT versus KO mice at 1 day after SCI.
No associated publication
Specimen part, Time
View SamplesWe profiled spinal cord tissue at the site of a moderate contusion injury at the level of the thoracic spinal cord
TrkB.T1 contributes to neuropathic pain after spinal cord injury through regulation of cell cycle pathways.
Age, Specimen part, Time
View Samplesgene expression data is from RNA extracted from muscle biopsy samples taken from boys with Duchenne muscular dystrophy (DMD) or pathologically normal controls (CTRL). Each muscle biospy was examined in detail histologically by Dr. Eric P. Hoffman at Children's National Medical Center to determine stage of disease. In addition, the absence or presence of dystrophin was determined via western blot analyses.
No associated publication
Specimen part, Disease
View SamplesAnalysis of human, adult, dermal fibroblasts following treatment with 100nM or 1 uM of erlotinib, a tryrosine kinase inhibitor (TKI) that targets the epidermal growth factor receptor (EGFR) inhibiting EGFR activation and signaling. Erlotinib is widely used to effectively treat patients with advanced non-small cell lung cancer but treatment with erlotinib and other EGFR TKIs are associated with a painful skin rash. Results identified significantly differentially expressed genes in fibroblasts treated with erlotinib providing insight into how the drug alters the transcriptome in ways that may contribute to the TKI-related rash.
No associated publication
Specimen part, Treatment
View SamplesIn this study, we examined C57BL/6J and AJ mice who received either sham surgery or cholestatic intestinal injury.
CANDIDATE GENES FOR LIMITING CHOLESTATIC INTESTINAL INJURY IDENTIFIED BY GENE EXPRESSION PROFILING.
Sex, Age, Specimen part, Treatment
View SamplesRNA was harvested from T-bet deficient MEP cells versus "wild type" C57BL/6 control MEP cells freshly harvested from bone marrow.
No associated publication
Specimen part
View SamplesBackground: The ErbB3 binding protein-1 (Ebp1) belongs to a family of DNA/RNA binding proteins implicated in cell growth, apoptosis and differentiation. However, the physiological role of Ebp1 in the whole organism is not known. Therefore, we generated Ebp1-deficient mice carrying a gene trap insertion in intron 2 of the Ebp1 (pa2g4) gene.
No associated publication
No sample metadata fields
View SamplesTherapies targeting the androgen receptor are critical for treatment of hormone refractory prostate cancer. We have previously demonstrated that Ebp1, a protein isolated by its ability to bind ErbB3, is a downstream effector of heregulin activated pathways and an AR corepressor. As Ebp1 is decreased in preclinical models of hormone refractory prostate cancer, we studied the ability of Ebp1 to mitigate the hormone refractory phenotype. As we previously found that Ebp1 affected the expression of some androgen receptor target genes, we sought to determine a full spectrum of genes changed using an unbiased appraoch by microarry analysis.
EBP1, an ErbB3-binding protein, is decreased in prostate cancer and implicated in hormone resistance.
No sample metadata fields
View SamplesThis data was used to determine levels of BRCA1 and BRCA2 in primary human leukemia samples. Samples were determined to be high BRCA1 and/or BRCA2 or low BRCA1 and/or BRAC2.
Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile.
No sample metadata fields
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