This SuperSeries is composed of the SubSeries listed below.
Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells.
Specimen part, Treatment
View SamplesGene expression profiles of human embryonic stem cells, fibroblasts, and fibroblast-derived induced pluripotent stem cells
Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells.
Specimen part
View SampleslincRNA-ST8SIA3 was depleted using siRNAs and associated gene expression changes were profiled on Affymentrix arrays
Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A Distinct Gene Module for Dysfunction Uncoupled from Activation in Tumor-Infiltrating T Cells.
Specimen part
View SamplesWe measured the genome-wide expression changes induced by 29 compounds targeting HDACs, DNMTs, histone lysine methyltransferases (HKMTs), and protein arginine methyltransferases (PRMTs) in pancreatic - and -cell lines.
Chromatin-targeting small molecules cause class-specific transcriptional changes in pancreatic endocrine cells.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Musashi-2 regulates normal hematopoiesis and promotes aggressive myeloid leukemia.
Specimen part, Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reprogramming factor expression initiates widespread targeted chromatin remodeling.
Specimen part
View SamplesExpression data from treatment of actinomycin D (2.5uM) and triptolide (500 nM) on MCF7 cells for 2, 4 and 6 hours.
Chemical genomics identifies small-molecule MCL1 repressors and BCL-xL as a predictor of MCL1 dependency.
Cell line, Compound, Time
View SamplesReversing the dysfunctional T cell state that arises in cancer and chronic viral infections is the focus of therapeutic interventions; however, current therapies are effective in only some patients and some tumor types. To gain a deeper molecular understanding of the dysfunctional T cell state, we analyzed population and single-cell RNA profiles of CD8+ tumor-infiltrating lymphocytes (TILs) and used genetic perturbations to identify a distinct gene module for T cell dysfunction that can be uncoupled from T cell activation. This distinct dysfunction module is downstream of intracellular metallothioneins that regulate zinc metabolism and can be identified at single-cell resolution. We further identify Gata-3, a zinc-finger transcription factor in the dysfunctional module, as a regulator of dysfunction, and use CRISPR/Cas9 genome editing to show that it drives a dysfunctional phenotype in CD8+ TILs. Our results open novel avenues for targeting dysfunctional T cell states, while leaving activation programs intact.
A Distinct Gene Module for Dysfunction Uncoupled from Activation in Tumor-Infiltrating T Cells.
Specimen part
View SamplesRIP-chip-SRM : a New Combinatorial Large Scale Approach Identifies a Set of Translationally Regulated bantam/miR 58 Targets in C. elegans
RIP-chip-SRM--a new combinatorial large-scale approach identifies a set of translationally regulated bantam/miR-58 targets in C. elegans.
Specimen part
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