Individual olfactory sensory neurons express a single odorant receptor (OR) gene from either class I genes residing in a single cluster on a single chromosome or class II genes spread over multiple clusters on multiple chromosomes.
A long-range cis-regulatory element for class I odorant receptor genes.
Sex, Specimen part
View Samplesgenes regualted by LPS or LPS+cAMP stimulation in BMDCs
Cyclic adenosine monophosphate suppresses the transcription of proinflammatory cytokines via the phosphorylated c-Fos protein.
Specimen part
View SamplesSevere acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes an immune-mediated disease. We have recently shown that SARS-CoV-induced epithelial Calu-3 cytokines could exacerbate and dampen host inflammatory and T cell responses, respectively, through modulating the functions of macrophages and dendritic cells, thereby suggesting that not only are lung epithelial cells the primary cells of SARS-CoV infection, but they also involve in initiating and orchestrating the host innate and adaptive immunity. Comprehensive evaluation of the complex epithelial signaling to SARS-CoV is, thus, crucial for paving the way to better understand SARS pathogenesis and develop the innovative therapeutics against SARS. Here, based on the microarray-based functional genomics, we reported that 2B4 cells, a clonal derivative of Calu-3 cells, elicited a temporal and spatial activation of nuclear factor (NF)kappaB, activator protein (AP)-1 (ATF2/c-Jun), and interferon regulatory factor (IRF)-3/-7 at 12-, 24-, and 48-hrs post infection (p.i.), respectively, resulting in the activation of many antiviral genes, including interferon (IFN)-, -s, SARS-related inflammatory mediators, and various IFN-stimulated genes (ISGs). While elevated responses of IFN- and IFN-s were not detected until 48-hrs p.i., as a consequence of a delayed IRF-3/-7 activation, we showed, for the first time, that both types of IFNs exerted previously under-described non-redundant, complementary, and/or synergistic effects on the epithelial defense against SARS-CoV. Collectively, our results highlight the molecular mechanisms of the sequential activation of virus- and IFN-dependent signaling of lung epithelial cells against SARS-CoV and identify novel cellular targets for future studies, aiming at advancing strategies against SARS.
Dynamic innate immune responses of human bronchial epithelial cells to severe acute respiratory syndrome-associated coronavirus infection.
Cell line, Time
View SamplesAnalysis of gene expressions in human microvascular endothelial cells (HMVEC)s following co-cultured with mouse dorsal root ganglion cells. Results provide insight into a role for responses of neurovascular interaction in endothelial cell in angiogenesis and vascular remodeling.
JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin.
Specimen part
View SamplesAnalysis of gene expression in immortalized human microvascular endothelial cells (TIME cells) following forced expression of the JunB. Results provide insight into a role for the JunB signaling pathway in endothelial cell.
JunB regulates angiogenesis and neurovascular parallel alignment in mouse embryonic skin.
Specimen part
View SamplesEstrogen-related receptor ? (ERR?) signaling increases during the neonatal to adult transition in pancreatic islet ß-cells. We show that ß-cell-specific ERR?-deficient (ßERR?KO) mice exhibit glucose intolerance with reduced glucose-stimulated insulin secretion (GSIS) and ßERR?KO islets have defective GSIS function accompanied by changes in genes that regulate ATP biosynthesis, oxidative phosphorylation, and the electron transport chain. ERR? overexpression enhances genes involved in mitochondrial metabolism, resulting in transformation of ß-like-cells into metabolically functional ß-cells that can ameliorate STZ-induced hyperglycemia in NOD-SCID mice. These results suggest that ERR? signaling is essential for the metabolic maturation of ß-like-cells and thus represents a novel therapeutic target in the treatment of diabetes.
ERRγ Is Required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells.
No sample metadata fields
View SamplesWe characterized the effect of loss of ERR expression in mouse pancreatic islets using adenoviral constructs.
ERRγ Is Required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells.
Specimen part
View SamplesWe show that ERR? overexpression in ß-like-cells differentiated from human iPSCs enhances genes involved in mitochondrial metabolism, resulting in transformation of these cells into metabolically functional ß-cells that can ameliorate STZ-induced hyperglycemia in NOD-SCID mice. These results suggest that ERR? signaling is essential for the metabolic maturation of ß-like-cells and thus represents a novel therapeutic target in the treatment of diabetes.
ERRγ Is Required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells.
No sample metadata fields
View SamplesASCL1 is a master transcription factor for neuroendocrine differentiation. RNA-sequencing analysis on VMRC-LCD cells following ASCL1 knockdown revealed a subset of genes possibly regulated by ASCL1. Overall design: VMRC-LCD cells were transfected with siRNAs for ASCL1, and RNA-sequencing was performed using Illumina HiSeq.
An Integrative Analysis of Transcriptome and Epigenome Features of ASCL1-Positive Lung Adenocarcinomas.
Cell line, Subject
View SamplesWe report the expression profiles of the nuclear receptor family of transcription factors, known regulators of metabolism, during iPSC generation. Unique but overlapping expression patterns were found in iPSCs derived from adipose derived stem cells (ADSCs) and embryonic fibroblasts (human and mouse) that correlate with developmental transitions in the cell.
ERRs Mediate a Metabolic Switch Required for Somatic Cell Reprogramming to Pluripotency.
Specimen part, Cell line, Time
View Samples