To characterize the potential molecular pathway(s) affected by iron treatment and identify the one(s) responsible for C3 induction, we performed a whole genome microarray on untreated ARPE-19 cells and cells treated with 250 M FAC for 48h/2d.
Iron-induced Local Complement Component 3 (C3) Up-regulation via Non-canonical Transforming Growth Factor (TGF)-β Signaling in the Retinal Pigment Epithelium.
Cell line, TreatmentView Samples
Microarray analysis of murine retinal light damage reveals changes in iron regulatory, complement, and antioxidant genes in the neurosensory retina and isolated retinal pigment epithelium (RPE). With the advent of microarrays representing most of the transcriptome and techniques to obtain RNA from the isolated RPE monolayer, we have probed the response of the RPE and neurosensory retina (NSR) to light damage.
Microarray analysis of murine retinal light damage reveals changes in iron regulatory, complement, and antioxidant genes in the neurosensory retina and isolated RPE.
Sex, Specimen part, TreatmentView Samples
Total RNA extracted from prostate cancer LNCaP cells transfected with siRNA against CTCF(siCTCF), or negative control siRNA (si-)were processed, and sequenced by two different companies using Illumina Hi-seq 2000 platform to generate RNA sequencing with two output sequences: paired-end 50bp and 101bp in read length. Nearly 100 million and 50 million raw reads were yielded from each sample respectively. We used FastQC to confirm the quality of raw fastq sequencing data, and SOAPfuse software to detect fusion transcripts. Overall design: Discovering fusion genes from siCTCF and si- in LNCaP cells.
Discovery of CTCF-sensitive Cis-spliced fusion RNAs between adjacent genes in human prostate cells.
No sample metadata fieldsView Samples
Here, we focused on the intermediate stages of SCR by comparing the somatic cell line induced by OCT4, SOX2, and KLF4 (OSK) for 7 days with mouse embryonic fibroblasts (MEFs), iPSCs, and embryonic stem cells (ESCs). Transcriptional profiles of these four cell lines were analyzed by microarray, and we found that the transition process from day 7 to the formation of iPSCs is crucial for SCR and that the reverse expression patterns can provide more candidate markers to distinguish ESCs and somatic cells iPSC. Data confirmed that the viral infection results in defense innate immunity, DNA damage, and apoptosis in MEFs, which slows down cell proliferation and immortalization to inhibit SCR. Although SCR is initiated by OSK, the p53 signaling pathway can affect the transcriptional regulatory networks through cell cycle and genomic instability as a powerful core node.
Global transcriptional analysis of nuclear reprogramming in the transition from MEFs to iPSCs.
Sex, Specimen partView Samples
Transcriptome dynamics of nucellus in early maize seed
High Temporal-Resolution Transcriptome Landscape of Early Maize Seed Development.
Age, Specimen partView Samples
Proteosome inhibitors such as bortezomib (BTZ) have been used to treat muscle wasting in animal models. However, direct effect of BTZ on skeletal muscle cells has not been reported. In the present study, our data showed that C2C12 cells exhibited a dose-dependent decrease in cell viability in response to increasing concentrations of BTZ.
Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway.
Specimen partView Samples
Analysis of gene expression change of normal cells, human fore skin fibroblast (HFFs) upon over-expression of c-Myc
Oncogene-induced senescence mediated by c-Myc requires USP10 dependent deubiquitination and stabilization of p14ARF.
Cell lineView Samples
UBE2O is localized in the 17q25 locus, which is known to be amplified in human cancers, but its role in tumorigenesis remains undefined. Here we show that Ube2o deletion in MMTV-PyVT or TRAMP mice profoundly impairs tumor initiation, growth and metastasis, while switching off the metabolic reprogramming of tumor cells. Mechanistically, UBE2O specifically targets AMPK2 for ubiquitination and degradation, and thereby promotes activation of the mTOR-HIF1 pathway. Notably, inactivation of AMPK2, but not AMPK1, abrogates the tumor attenuation caused by UBE2O-loss, while treatment with rapamycin or inhibition of HIF1 ablates UBE2O-dependent tumor biology. Finally, pharmacological blockade of UBE2O inhibits tumorigenesis through the restoration of AMPK2, suggesting the UBE2O-AMPK2 axis as a potential cancer therapeutic target.
A UBE2O-AMPKα2 Axis that Promotes Tumor Initiation and Progression Offers Opportunities for Therapy.
Specimen partView Samples
In previous studies, it was observed that survivors who received stem cell transplantation and whole body irradiation showed development of NAFLD as a chronic effect.
Decreased Hepatic Lactotransferrin Induces Hepatic Steatosis in Chronic Non-Alcoholic Fatty Liver Disease Model.
Sex, Age, Specimen partView Samples