Heterotopic cardiac transplants were constructed in male Wistar Furth (allograft donor) and ACI (host) rats. Rats were divided into three groups consisting of no treatment, treatment with a sub-therapeutic dose of cyclosporin A, and treated with combination of a sub-therapeutic dose of cyclosporin A and allochimeric peptide. The allografts were harvested at defined periods post-transplantation and RNA was harvested to monitor gene expression changes resulting from the various treatments in T-cells and in heart cells.
Intragraft gene expression profile associated with the induction of tolerance by allochimeric MHC I in the rat heart transplantation model.
Sex, Specimen part
View SamplesPurpose:The goals of this study are to evaluate the effect of OX40 ligation on transcriptome profiling of in vitro polarized T helper 17 cell (RNA-seq). Methods: mRNA profiles of CD4+ T cells cultured in vitro under Th17-polarizing conditions for 48hrs (both Ctrl and OX40L treated groups) were generated by deep sequencing, using Illumina RapidRun. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays Results: Among the 398 genes that were significantly affected by OX40, only about 11% were previously identified as ROR?t target genes in Th17 cells. Conclusions: Our study suggests that OX40 unlikely affects Th17 commitment, but most likely impairs their effector differentiation. As IL-17A and IL-17F are Th17-defining cytokines, their suppression suggests that OX40 may inhibits effector functions of Th17 cells. Overall design: mRNA profiles of CD4+ T cells cultured in vitro under Th17 differentiation conditions for 48 hours in the presence of WT-APCs or OX40L-TG APCs were generated by deep sequencing using Illumina RapidRun.
The Costimulatory Receptor OX40 Inhibits Interleukin-17 Expression through Activation of Repressive Chromatin Remodeling Pathways.
Specimen part, Cell line, Subject
View SamplesMM1S cells have been cultured under normoxic and hypoxic conditions, and gene expression profiling has been performed using the Affymetrix Human Genome U133 Plus 2.0 array.
Metabolic signature identifies novel targets for drug resistance in multiple myeloma.
Cell line
View SamplesThe role of chronic hepatitis C virus (HCV) in the pathogenesis of HCV-associated hepatocellular carcinoma (HCC) is not completely understood, particularly at the molecular level.
Genes involved in viral carcinogenesis and tumor initiation in hepatitis C virus-induced hepatocellular carcinoma.
Specimen part
View SamplesPodocytes are highly specialised cells within the glomeruli of the kidney that maintain the filtration barrier by forming interdigitating foot processes and slit-diaphragms. Disruption to these features result in proteinuria and glomerulosclerosis. Studies into podocyte biology and disease have previously relied on conditionally immortalised cell lines due to the non- proliferative nature of this cell type. Here we describe an advanced model to study both podocyte and glomerular biology using isolated glomeruli from kidney organoids derived from human pluripotent stem cells. Overall design: Gene expression profiling of day three 17, 21 and 26 day kidney organoid derived glomeruli respectively with heterzygous genotype for BFP tagged MAFB; gene expression profiling of three day 25 kidney organoid derived glomeruli; gene expression profiling of three organoid-derived podocytes grown out for 3 days from day 25 kidney organoid derived glomeruli.
3D organoid-derived human glomeruli for personalised podocyte disease modelling and drug screening.
Specimen part, Subject
View SamplesC1013G/CXCR4 variant has been inserted into BCWM.1 cells, and gene expression profile has been performed on the mutated cells and on the parental cells.
C1013G/CXCR4 acts as a driver mutation of tumor progression and modulator of drug resistance in lymphoplasmacytic lymphoma.
Cell line
View SamplesMYC is a major oncogenic driver of Multiple Myeloma (MM) and yet almost no therapeutic agents exist that target MYC in MM. Here we report that the let-7 biogenesis inhibitor LIN28B correlates with MYC expression in MM and is associated with adverse outcome. We also demonstrate that the LIN28B/let-7 axis modulates the expression of MYC, itself a let-7 target. Further, perturbation of the axis regulates the proliferation of MM cells in vivo in a xenograft tumor model. RNA sequencing and gene set enrichment analyses of CRISPR-engineered cells further suggest that the LIN28/let-7 axis regulates MYC and cell cycle pathways in MM. We provide proof-of-principle for therapeutic regulation of MYC through let-7 with an LNA-GapmeR containing a let-7b mimic in vivo, demonstrating that high levels of let-7 expression repress tumor growth by regulating MYC expression. These findings reveal a novel mechanism of therapeutic targeting of MYC through the LIN28B/let-7 axis in MM that may impact other MYC dependent cancers as well. Overall design: RNA sequencing of MOLP-8 cells transduced with lentiCRISPRv2 scrambled control or containing a sgRNA against LIN28B. Both control and LIN28B KO cells were sequenced in triplicate.
The LIN28B/let-7 axis is a novel therapeutic pathway in multiple myeloma.
No sample metadata fields
View SamplesmicroRNA-155 acts as an oncogenic miRNA in B-cell lymphoproliferative disorders including Waldenstrom Macroglobulinemia (WM) and Chronic Lymphocytic Leukemia (CLL).
LNA-mediated anti-miR-155 silencing in low-grade B-cell lymphomas.
Cell line
View SamplesMM.1S orthotopic tumors were analyzed fro their gene expression upon tumor outgrowth. In contorl/bortezomib/elesclmol and combo treatments. Overall design: examination of three tumors for each condition.
Mitochondrial metabolism promotes adaptation to proteotoxic stress.
Cell line, Subject
View SamplesWe transiently induce the Lo19S state with a dox inducible shRNa targeting PSMD2 and explore the gene expression in the presence and absence of bortezomib Overall design: one cell type (T47D), two states (Control and Lo19S) with and without treatment with 20nM bortezomib , all in triplicates
Mitochondrial metabolism promotes adaptation to proteotoxic stress.
Cell line, Subject
View Samples