As a starting point for dissecting the cellular heterogeneity of gliomas, different subpopulations from a CRISPR mouse model of glioma were profiled for gene expression. Because we initially identified these astrocyte subpopulations in the mouse brain, we first sought to determine whether their malignant analogues are present in mouse models of glioma. Towards this, we recently developed a mouse model of malignant glioma, one that utilizes E16.5 IUE approaches in combination with CRISPR mediated gene editing, where we use IUE to introduce gRNA vectors to delete NFI, PTEN, and p53, CAS9, and a GFP reporter, resulting in the generation of malignant glioma at P70. Using the GFP label to distinguish tumor from normal brain tissue, along with FACS-based selection against the glioma stem cell (GSC) and endothelial cells (see methods), we screened our tumor models for the presence of these prospective astroglial populations in the non-GSC fractions of these tumors. Overall design: Gene expression profiles (by RNA-seq) were taken of mouse glioma cells of three different populations.
Identification of diverse astrocyte populations and their malignant analogs.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm.
Specimen part
View SamplesInactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To gain insights into the mechanisms by which Ezh2 deficiency promotes the development of MF in Jak2V617F knock-in mice, we performed microarray gene expression analysis on sorted LT-HSC from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.
Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm.
Specimen part
View SamplesThe Hippo pathway is an emerging signaling cascade involved in the regulation of organ size control. It consists of evolutionally conserved protein kinases that are sequentially phosphorylated and activated. The active Hippo pathway subsequently phosphorylates a transcription coactivator, YAP, which precludes its nuclear localization and transcriptional activation. Identification of transcriptional targets of YAP in diverse cellular contexts is therefore critical to the understanding of the molecular mechanisms in which the Hippo pathway restricts tissue growth.
Hippo signaling regulates microprocessor and links cell-density-dependent miRNA biogenesis to cancer.
Specimen part
View SamplesHere we harnessed the potential of RNA sequencing in 89 human pancreatic islet donors to identify genes and exons regulated in this relevant tissue for T2D. Overall design: mRNA profiles of 89 human pancreatic islet donors having different levels of blood glucose (HbA1c) with and without T2D. The data was generated by deep sequencing using Illumina HiSeq 2000.
Orphan G-protein coupled receptor 183 (GPR183) potentiates insulin secretion and prevents glucotoxicity-induced β-cell dysfunction.
Sex, Age, Specimen part, Subject
View SamplesThese patients proved resistant to docetaxel treatment, exhibiting residual tumor of 25% or greater remaining volume.
Gene expression profiling for the prediction of therapeutic response to docetaxel in patients with breast cancer.
No sample metadata fields
View SamplesThese patients were sensitive to docetaxel treatment, exhibiting less than 25% residual tumor.
Gene expression profiling for the prediction of therapeutic response to docetaxel in patients with breast cancer.
No sample metadata fields
View Samplesneuroblastoma cells derived from PDOX models were treated with the kinase inhibitor. Overall design: 5 repetitions of control and IBL-302 treated cells were harvest and submitted for RNAseq analysis
Anti-tumor effects of PIM/PI3K/mTOR triple kinase inhibitor IBL-302 in neuroblastoma.
Specimen part, Treatment, Subject
View SamplesAda3 (alteration/deficiency in activation) is a transcriptional adaptor that forms a core structural component of multiple HAT complexes. In order to gain insights into physiological roles of Ada3, we made a conditional knockout mouse for Ada3 which was early embryonic lethal. Deletion of Ada3 in MEFs by using Adenovirus-Cre showed changes in global histone acetylation.
Mammalian alteration/deficiency in activation 3 (Ada3) is essential for embryonic development and cell cycle progression.
Specimen part
View SamplesWe used PacBio data to identify more reliable transcripts from hESC, based on which we can estimate gene/transcript abundance better from Illumina data. Overall design: PacBio long reads and Illumina short reads were generated from the same hESC cell line H1. PacBio reads were error-corrected by Illumina reads to identify transcripts. rSeq is used to estimate gene/transcript abundance of the identified transcriptome.
Gaining comprehensive biological insight into the transcriptome by performing a broad-spectrum RNA-seq analysis.
No sample metadata fields
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