Sox3 has been shown to be expressed within neural progenitors of the developing mouse central nervous system. However, identification of Sox3 targets within neural progenitors has remained elusive.
Dbx1 is a direct target of SOX3 in the spinal cord.
Specimen part, Cell line
View SamplesStatus Epilepticus (SE) is an abnormally prolonged seizure that results from either a failure of mechanisms that terminate seizures or from initiating mechanisms that inherently lead to prolonged seizures.
Induction of Type 2 Iodothyronine Deiodinase After Status Epilepticus Modifies Hippocampal Gene Expression in Male Mice.
Specimen part
View SamplesZinc is an essential micronutrient in pregnancy and zinc deficiency impairs fetal growth. We used a mouse model of moderate zinc deficiency to determine how zinc is important to placental morphogenesis.
Zinc is a critical regulator of placental morphogenesis and maternal hemodynamics during pregnancy in mice.
Specimen part
View SamplesMicroarray analysis obtained from RNA of AML12 cells stably expresing Zfp125 or empty vector (EV)
The Foxo1-Inducible Transcriptional Repressor Zfp125 Causes Hepatic Steatosis and Hypercholesterolemia.
Specimen part, Cell line
View SamplesExpression data from different brain regions of mice
Type 2 deiodinase polymorphism causes ER stress and hypothyroidism in the brain.
Specimen part
View SamplesDU145 prostate cancer cells were treated with 50 ng/ml FGF19 and 50 ug/ml heparin, or 10 ng/ml TNFalpha, or both
The receptor tyrosine kinase FGFR4 negatively regulates NF-kappaB signaling.
Cell line
View SamplesGenomic instability predisposes cells to malignant transformation, however the molecular mechanisms that allow for the propagation of cells with a high-degree of genomic instability remains unclear. Here we report that miR-181a is able to transform fallopian tube secretory epithelial cells- the precursor cell type for the majority of high-grade serous ovarian cancers- through the inhibition of RB1 and simultaneously drives a cell protective inhibition of the stimulator-of-interferon-genes (STING) in order to maintain a microenvironment conducive to the propagation of cells with a high-degree of genomic instability. We found that miR-181a inhibition of RB1 leads to profound nuclear defects, genomic instability, and nuclear rupture resulting in a persistence of genomic material in the cytoplasm. While normally, this persistence of genomic material in the cytoplasm induces interferon response through STING to drive cell death, miR-181a directly downregulates STING and prevents apoptosis. The most common mechanism by which oncogenic miRNAs promote tumorigenesis is through the direct inhibition of tumor suppressor genes, however our studies highlight a new mechanism of oncomiR transformation through the combination of tumor suppressor gene inhibition and abrogation of immune surveillance that initiates and propagates tumor cell survival. Importantly, we found that miR-181a induction in ovarian patient tumors is tightly associated with decreased IFNg response and downregulation of lymphocyte infiltration amd leukocyte fraction. To date, DNA oncoviruses are the only known inhibitors of STING that allow for cellular transformation thus, our findings are the first to identify a genetic factor, miR-181a, that can downregulate STING expression, suppress activation of the immunosurveillance machinery, and impair signaling in cancer cells creating a survival advantage. Our studies support the notion that the induction of STING-mediated signaling in cancer cells could lead directly to cancer cell death however these effects are abrogated by miR-181a. Given the recent interest in the development of STING agonists as a strategy to harness the immune system to treat cancer, this study introduces novel patient selective biomarker as well as potent therapeutic target for development of the most effective combination treatments.
miR-181a initiates and perpetuates oncogenic transformation through the regulation of innate immune signaling.
No sample metadata fields
View SamplesContractile and highly synthetic myofibroblasts are the key effector cells involved in excessive extracellular matrix (ECM) deposition in multiple fibrotic conditions, including idiopathic pulmonary fibrosis (IPF). In order to define the key drivers of the fibrotic response, we used laser capture microdissection to isolate RNA from myofibroblasts within fibroblastic foci and performed microarray analysis in combination with a novel eigengene approach to identify functional clusters of genes which associate with collagen gene expression.
Transcriptome analysis of IPF fibroblastic foci identifies key pathways involved in fibrogenesis.
Specimen part, Disease, Subject
View SamplesIn this study Panc-1 cells and BxPC-3 cells were cultured. The cells were harvested (untreated control 'cont') for RNA extraction, or treated for 3 hours with various exosomes preparations. The exosomes were collected from BJ human foreskin fibroblast culture supernatant without further processing (control exosomes or 'CE'), or engineered to contain scrambled siRNA ('scr') or KRASG12D siRNA ('iExo). Two or three distinct wells of cells were evaluated per treatment condition and assigned a well number (well -1, -2 or 3).
Generation and testing of clinical-grade exosomes for pancreatic cancer.
Cell line, Treatment
View SamplesAE-expressing murine BM cells treated with all-trans retinoic acid (ATRA) in semi-solid methycellulose-based cultures show an increase in self-renewal capacity whilst treatment with a specific RARa agonist NRX195183 reduces their clonogenicity. Gene expression analysis was performed to further investigate the molecular mechanisms underlying these observations. Upregulated gene sets were identified in the ATRA-treated AE BM cells.
ATRA and the specific RARα agonist, NRX195183, have opposing effects on the clonogenicity of pre-leukemic murine AML1-ETO bone marrow cells.
Specimen part, Treatment
View Samples