The effect of Tlr4P712H mutation (rendering TLR4 non-functional), or gut-sterilization by antbiotics, on the induction of tumorgenesis by CCl4 and diethylnitrosamine (DEN) was characterized. Affymetrix Mouse 430 2.0 gene expression measurements were used to characterize the transcriptomic basis of the effects of the above treatments and genotypes on tumorgenesis.
Promotion of hepatocellular carcinoma by the intestinal microbiota and TLR4.
Sex, Age, Specimen part
View SamplesThe gene expression of mice with osteoblast-specific beta-catenin activation or FoxO1 deactivation are each compared to that of Wt.
Leukaemogenesis induced by an activating β-catenin mutation in osteoblasts.
Sex, Specimen part
View SamplesWhile skeletal myogenesis is tightly coordinated by myogenic regulatory factors including MyoD and myogenin, chromatin modifications have emerged as vital mechanisms of myogenic regulation. We have previously established that bexarotene, a clinically approved agonist of retinoid X receptor, promotes the specification and differentiation of skeletal muscle lineage. Here, we examine a genome-wide impact of rexinoids on myogenic differentiation through integral RNA-seq and ChIP-seq analyses. We found that bexarotene promotes myoblast differentiation through the coordination of exit from the cell cycle and the activation of muscle-related genes. We uncovered a new mechanism of rexinoid action which is mediated by the nuclear receptor and largely reconciled through a direct regulation of MyoD gene expression. In addition, we determined a rexinoid-responsive residue-specific histone acetylation at a distinct chromatin state associated to MyoD and myogenin. Thus, we provide novel molecular insights into the interplay between retinoid X receptor signaling and chromatin states pertinent to myogenic programs in early myoblast differentiation. Overall design: We have profiled the global effect of bexarotene, a selective agonist of retinoid X receptor on myoblast gene expression by RNA-seq analysis using RNA isolated from C2C12 myoblasts following 12 or 24 hours of differentiation in the presence and absence of 50 nM bexarotene, with 2 biological replicates. Proliferating myoblasts were used as controls.
Insights into interplay between rexinoid signaling and myogenic regulatory factor-associated chromatin state in myogenic differentiation.
Cell line, Subject
View SamplesThe CCCTC-binding factor (CTCF) is a versatile transcriptional regulator required for embryogenesis, but its function in vascular development or in diseases with a vascular component is poorly understood. Here, we found that endothelial Ctcf is essential for mouse vascular development and limits accumulation of reactive oxygen species (ROS). Conditional knockout of Ctcf in endothelial progenitors and their descendants affected embryonic growth, and caused lethality at embryonic day 10.5 owing to defective yolk sac and placental vascular development. Analysis of global gene expression revealed Frataxin (Fxn), the gene mutated in Friedreich's ataxia (FRDA), as the most strongly downregulated gene in Ctcfdeficient placental endothelial cells. Moreover, in vitro reporter assays showed that Ctcf activates the Fxn promoter in endothelial cells. Reactive oxygen species (ROS) are known to accumulate in the endothelium of FRDA patients. Importantly, Ctcf deficiency induced ROS-mediated DNA damage in endothelial cells in vitro, and in placental endothelium in vivo. Taken together, our findings indicate that, Ctcf promotes vascular development, and limits oxidative stress in endothelial cells, perhaps through activation of Fxn transcription. These results reveal a function for a Ctcf–Fxn transcriptional pathway in vascular development, and also suggest a potential mechanism for endothelial dysfunction in FRDA. Overall design: Examination of transcriptome profiles of placental endothelial cells isolated from wildtype or ctcf defecient endothelial cells at E9.5
The transcriptional regulator CCCTC-binding factor limits oxidative stress in endothelial cells.
Specimen part, Subject
View SamplesComparison between cell lines from 9 different cancer tissue of origin types (Breast, Central Nervous System, Colon, Leukemia, Melanoma, Non-Small Cell Lung, Ovarian, Prostate, Renal) from NCI-60 panel.
Topoisomerase I levels in the NCI-60 cancer cell line panel determined by validated ELISA and microarray analysis and correlation with indenoisoquinoline sensitivity.
Sex, Age, Specimen part, Cell line
View SamplesWe compared gene expression profiles of ALS patients with normal patients and with multifocal motor neuropathy (MMN) patients.
Differential gene expression in patients with amyotrophic lateral sclerosis.
Specimen part, Disease, Disease stage
View SamplesThis scRNA-seq experiment is an integral part of a manuscript with the above title. Our analysis of the scRNA-seq data suggests that activated CARD11 promotes immunoglobulin class-switching in germinal center B cells and generation of IgG1-secreting plasma cells. Overall design: Single-cell suspensions were prepared from spleens harvested from mice 5 days post immunization with sheep red blood cells. B cells were enriched using an immunomagnetic negative selection kit. scRNA-seq was performed using the Chromium product suite by 10x Genomics.
Activated CARD11 accelerates germinal center kinetics, promoting mTORC1 and terminal differentiation.
Cell line, Subject
View SamplesGenome-wide profiling of RNA differential expression in v-Abl transformed 220-8 pro-B mouse cell line Overall design: Expression profiles generated for 220-8 cell lines with and without hLIN28A retroviral transduction
Enhancement of LIN28B-induced hematopoietic reprogramming by IGF2BP3.
Cell line, Subject
View SamplesGene expression profiles of 75 tissue samples were analyzed representing the stepwise carcinogenic process from pre-neoplastic lesions (cirrhosis and dysplasia) to HCC, including four neoplastic stages (very early HCC to metastatic tumors) from patients with HCV infection. Gene signatures that accurately reflect the pathological progression of disease at each stage were identified and potential molecular markers for early diagnosis uncovered. Pathway analysis revealed dysregulation of the Notch and Toll-like receptor pathways in cirrhosis, followed by deregulation of several components of the Jak/STAT pathway in early carcinogenesis, then up-regulation of genes involved in DNA replication and repair and cell cycle in late cancerous stages.
Genome-wide molecular profiles of HCV-induced dysplasia and hepatocellular carcinoma.
No sample metadata fields
View SamplesThis sample is part of a study that compares small sample amplification technologies. The analysis looks at differential gene expression when compared to one round of T7 amplification. A tumor cell line was used in comparison to a human reference RNA in this study.
Big results from small samples: evaluation of amplification protocols for gene expression profiling.
No sample metadata fields
View Samples