Project description:In mouse models of PDGF-driven glioma where Notch is tumor-suppressive, we find that Notch activity shapes interferon-response in tumor cells and the local immune microenvironment early during tumor progression. Notch inhibition disturbs cytokine expression by tumor cells, altering recruitment and activation of immune cell populations and favoring hyper-proliferative "immune niche" independent growth. Genetic inactivation of Notch in glioma cells also attenuates their response to interferon-gamma, establishing a non-cell autonomous inhibitory feedback loop that further promotes immune evasion and aggressiveness. Hence, we propose that Notch signaling levels in tumor cells are key to orchestrate immune escape and microenvironment independency during brain tumor formation.
Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived neural cells to identify alterations in gene expression Methods: RNA were isolated from HD and control iPSC-derived neural cells. mRNAseq using Illumina Truseq mRNA PolyA+ v2 lib prep and Hiseq 2000. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis Results: mRNAseq and statistical analysis revealed 1869 differentially expressed genes between HD and control iPSC-derived neural cells. Conclusions: Our study shows 1869 differentially expressed genes between HD and control iPSC-derived neural cells, and reveals gene networks that relevant to the mechanism of HD pathogenesis.
Project description:Concomitant sRNA and mRNAseq was carried out to elucidate the reprogramming occurring during Magnaporthe oryzae - Brachypodium distachyon interaction in three different setups: biotrophic stage of leaf infection (Leaf 2 DPI), necrotrophic stage of leaf infection (Leaf 4 DPI) and finally root infection (Root).
Project description:Purpose: The goals of this study are to compare the transcriptomic profile (mRNA-seq) of HD and control patient iPSC-derived brain microvascular endotheial cells to identify alterations in gene expression. Methods: RNA were isolated from HD and control iPSC-derived brain microvascular endothelial cells. mRNAseq using Illumina TruSeq mRNA PolyA+ v2 lib prep and HiSeq 2500. Statistical difference in mRNA levels were calculated with subsequent GO and pathway analysis. Results: mRNAseq and statistical analysis revealed differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells. Conclusions: Our study shows differentially expressed genes between HD and control iPSC-derived brain microvascular endothelial cells, and reveals gene networks that are relevant to the mechanism of HD pathogenesis.
Project description:Single cell mRNAseq maps a global landscape of transcriptomes in uninjured tissue, showing clear transitions from neuronally fated progenitors to mature neurons and other mature cell types. Comparison with injured Neurog1-eGFP+ cells shows a dedifferentiation of cells towards a multipotent stem cell transcriptome.
Project description:Global gene expression (transcriptome) analysis was performed by messenger RNA sequencing (mRNAseq) on iPSC-derived MSCs produced in three separate lots to determine consistency in gene expression between lots.
Project description:This study demonstrated the effects of lncRNA HOTAIR knockdown on the glioma proteomics. An abnormally high expression of the lncRNA HOTAIR has been previously demonstrated in glioma cells. HOTAIR regulates genes by anchoring epigenetic modification proteins and causes abnormalities in multiple signaling pathways. We knocked down HOTAIR in glioma cells by siRNA with SILAC labeling, and then total protein was extracted for proteome mass spectrometry.
