Project description:Using chromatin immunoprecipitation and next-generation sequencing (ChIP-seq), we assessed the effects of acute exposure to oligomeric amyloid-beta on 82-kDa ChAT and SATB1 genome association in human SH-SY5Y neural cells, finding that Aβ-exposure increased 82-kDa ChAT and SATB1 association with gene promoters, introns and matrix attachment regions. We found that both SATB1 and 82-kDa ChAT associate with synapse and cell stress related genes after amyloid-beta exposure.
Project description:The goal of this study was to look at genes that were affected by 69-kDa and/or 82-kDa ChAT proteins in IMR32 cells Experiment Overall Design: The gene expression changes of IMR32 cells stably expressing either 69-kDa or 82-kDa ChAT proteins were anaylzed and compared to control IMR32 wild type cells. 3 biological replicates were anaylzed per condition (69-kDa ChAT expressing cells, 82-kDa ChAT expressing cells, or wild type IMR32 cells) for a total of 9 samples altogether.
Project description:The goal of this study was to look at genes that were affected by 69-kDa and/or 82-kDa ChAT proteins in IMR32 cells Keywords: comparative
Project description:ATP6V1A plays a unique role in synapse function in neurons and we found decreased neuronal activity in ATP6V1A-deficient neurons. To characterize the molecular pathways regulated by ATP6V1A under both normal and stressed conditions, we generated hiPSC-derived NGN2-neurons with reduced ATP6V1A expression by CRISPRi knock-down (KD) and performed RNA-seq analysis on the wild-type and KD neurons which were subject to amyloid-beta or vehicle treatment. A number of gene ontology (GO)/pathways were identified in KD neurons without amyloid-beta treatment (proton transporting V-ATPase complex, phagosome acidification and trivalent inorganic cation transport were down-regulated, and mitochondrial protein complex up-regulated), while KD in amyloid-beta treated cells specifically resulted in down-regulation of cell adhesion, synapse assembly and structure/activity and up-regulation of UPR and ER stress response.
Project description:To test Pbodies (anibodies screened from PETAL) for more applications, we performed ChIP-seq with selected Pbodies. ChIP-seq assays in HepG2 for Pbodies against SMRC1, SATB1 and NFIC were carried out.
Project description:SATB1 is a genetic master regulator in dopaminergic neurons. We try to identify the downstream regulated genes and pathways of SATB1 in human dopaminergic and CTX neurons. The RNA-Seq experiment was performed to investigate the role of the genetic master regulator SATB1 in human dopaminergic neurons in comparison to cortical neurons. We generated a human embryonic stem cell knockout clone for SATB1 and differentiated this clone into either dopaminergic or cortical neurons. Immature dopaminergic (day 30 of differentiation), mature dopaminergic (day 50 of differentiation) and mature cortical neurons (day 30 of differentiation) were subsequently subjected to RNA-Seq. We compared wild type and SATB1-KO neurons at the afore mentioned time points, to characterize the regulatory role of SATB1 in the different neuron subtypes.
Project description:Complement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection. Immature rat cortical primary neurons are treated with fibrillar amyloid-beta peptides and/or C1q for 3h before RNA extraction and hybridization on rat Affymetrix microarrays. Supplementary file: Processed/normalized, probe-level signal intensities from neurons treated with amyloid-beta or C1q. Median signal intensity used as global normalization method, done with JMP genomics (v5.0) software.
