Project description:This experiment describes the quantitative proteomic profiling of whole-cell, soma, and neuronal projection fractions from day 35 induced neurons (iN) derived from control and ASAH1 knockout human embryonic stem cells. Soma and projection compartments were physically separated using Transwell culture inserts, and triplicate biological replicates were processed using TMTpro 18-plex labeling and high-resolution Orbitrap mass spectrometry with FAIMS. Data were searched against the human proteome with stringent FDR control and reporter ion quantification, enabling compartment-resolved analysis of proteome alterations associated with ASAH1 deficiency.
Project description:The transcriptional response of normal and glioblastoma-derived neural (GNS) cells was profiled in self-renewing conditions and over a time course of differentiation in the presence of bone morphogenic protein (BMP).
Project description:Glioblastoma-derived neural stem (GNS) cells were reprogrammed to induced pluripotent stem (iPS) cells by transgenic expression of OCT4 and KLF4. Genome-wide DNA methylation status was profiled at 27,578 CpG sites to assess epigenetic erasure and restoration due to reprogramming and redifferentiation to the neural stem (NS) cell state.
Project description:Glioblastoma-derived neural stem (GNS) cells were reprogrammed to induced pluripotent stem (iPS) cells by transgenic expression of OCT4 and KLF4. Genome-wide DNA methylation status was profiled at 485,000 loci to assess epigenetic erasure and restoration due to reprogramming and redifferentiation to the neural stem (NS) cell state.
Project description:Glioblastoma-derived neural stem (GNS) cells were reprogrammed to induced pluripotent stem (iPS) cells by transgenic expression of OCT4 and KLF4. Genome-wide DNA methylation status was profiled at 485,000 loci to assess epigenetic erasure and restoration due to reprogramming and redifferentiation to the neural stem (NS) cell state.
Project description:Chromatin accessibility was profiled by ATAC-seq in normal and glioblastoma-derived neural stem (GNS) cells, in self-renewing conditions and in response to differentiation stimulus with bone morphogenic protein (BMP).
Project description:BRD4 is an important epigenetic reader implicated in the pathogenesis of a number of different cancers and other diseases. Brd4-null mouse embryos die shortly after implantation and are compromised in their ability to maintain the inner cell mass (ICM), which gives rise to embryonic stem cells (ESCs). We investigated the functions of Brd4 in the ESCs in the present study. To determine the Brd4 target genes in embryonic stem cells. TL1 ESCs were transfected with control siRNA, or Brd4 siRNA. At 48 h post-transfection, total RNAs were isolated using the RNeasy minikit (Qiagen). Expression microarray analyses were performed on mRNA samples isolated from three independent experiments using a mouse Gene 2.0ST array (Affymetrix) at the University of Pennsylvania Microarray Core Facility. RMA from Affymetrix package was applied to the data for preprocessing and normalization. Limma was used for detection of differentially expressed genes. Benjamini & Hochberg correction was applied for the multiple comparisons.