Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA310786 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Huntington’s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the CAG repeat in exon 1 of the huntingtin gene. There is no cure for HD, existing pharmaceutical can only relieve its symptoms. Here, induced pluripotent stem cells were established from patients with low CAG repeat expansion in the huntingtin gene, and were then efficiently differentiated into GABA MS-like neurons under defined culture conditions. Analysis of differentially expressed genes between Huntington’s disease and wild type iPSCs derived GABA MS-like neurons has been performed.
2016-02-04 | GSE77558 | GEO
Project description:Compared the global gene expression profiles of HD- and CON-iPSC-derived neurons We used microarrays to detail the global programme of gene expression for comparing the global gene expression profiles of HD- and CON-iPSC-derived neurons and facilitating studies of medium spiny neurons (MSN)-degenerative processes of Huntington's Disease (HD). By using a step-wise in vitro differentiation protocol combining EB formation, neural induction by small molecules, treatment with inhibitors of the TGFß pathway (SB431542) and the BMP pathway (LDN193189), and mechanical isolation/purification of neural progenitors and neurons, we induced 60-70% of control iPSCs or HD-iPSCs to differentiate into GABA- and DARPP-32- double positive neurons.
2015-09-02 | E-GEOD-59051 | biostudies-arrayexpress
Project description:Fibroblasts from patients with Type I bipolar disorder (BPD) and their unaffected siblings were obtained from an Old Order Amish pedigree with a high incidence of BPD and reprogrammed to induced pluripotent stem cells (iPSCs). Established iPSCs were subsequently differentiated into neuroprogenitors (NPs) and then to neurons. Transcriptomic microarray analysis was conducted on RNA samples from iPSCs, NPs and neurons matured in culture for either 2 weeks (termed early neurons, E) or 4 weeks (termed late neurons, L). Global RNA profiling indicated that BPD and control iPSCs differentiated into NPs and neurons at a similar rate, enabling studies of differentially expressed genes in neurons from controls and BPD cases. Significant disease-associated differences in gene expression were observed only in L neurons. Specifically, 328 genes were differentially expressed between BPD and control L neurons including GAD1, glutamate decarboxylase 1 (2.5 fold) and SCN4B, the voltage gated type IV sodium channel beta subunit (-14.6 fold). Quantitative RT-PCR confirmed the up-regulation of GAD1 in BPD compared to control L neurons. Gene Ontology, GeneGo and Ingenuity Pathway Analysis of differentially regulated genes in L neurons suggest that alterations in RNA biosynthesis and metabolism, protein trafficking as well as receptor signaling pathways GSK3β signaling may play an important role in the pathophysiology of BPD. Samples for each of four iPSCs, NPs and neurons matured in culture for either 2 weeks (termed early neurons, E) or 4 weeks (termed late neurons, L) were analyzed
2015-10-26 | E-GEOD-74358 | biostudies-arrayexpress
Project description:Fibroblasts from patients with Type I bipolar disorder (BPD) and their unaffected siblings were obtained from an Old Order Amish pedigree with a high incidence of BPD and reprogrammed to induced pluripotent stem cells (iPSCs). Established iPSCs were subsequently differentiated into neuroprogenitors (NPs) and then to neurons. Transcriptomic microarray analysis was conducted on RNA samples from iPSCs, NPs and neurons matured in culture for either 2 weeks (termed early neurons, E) or 4 weeks (termed late neurons, L). Global RNA profiling indicated that BPD and control iPSCs differentiated into NPs and neurons at a similar rate, enabling studies of differentially expressed genes in neurons from controls and BPD cases. Significant disease-associated differences in gene expression were observed only in L neurons. Specifically, 328 genes were differentially expressed between BPD and control L neurons including GAD1, glutamate decarboxylase 1 (2.5 fold) and SCN4B, the voltage gated type IV sodium channel beta subunit (-14.6 fold). Quantitative RT-PCR confirmed the up-regulation of GAD1 in BPD compared to control L neurons. Gene Ontology, GeneGo and Ingenuity Pathway Analysis of differentially regulated genes in L neurons suggest that alterations in RNA biosynthesis and metabolism, protein trafficking as well as receptor signaling pathways GSK3β signaling may play an important role in the pathophysiology of BPD.
2015-10-26 | GSE74358 | GEO
Project description:This bulk RNAseq dataset is part of a dataset described in the manuscript titled "Fully defined NGN2 neuron protocol reveals diverse signatures of neuronal maturation". This dataset includes NPC derived neurons using a wild type iPSC line, and was used to validate a MS-117 maturation score which attempt to establish a socre system to assess neuronal maturation with iPSCs derived neurons.
2024-09-13 | GSE266359 | GEO
Project description:Huntington's disease is caused by an expanded CAG repeat in the huntingtin gene, yeilding a Huntingtin protein with an expanded polyglutamine tract. Patient-derived induced pluripotent stem cells (iPSCs) can help understand disease; however, defining pathological biomarkers in challanging. Here we used LC-MS/MS to determine differences in mitochondrial proteome between iPSC-derived neurons from healthy donors and Huntington's disease patients.
2023-02-10 | PXD037526 | Pride
Project description:Differentially expressed miRNAs between Alzheimer's disease and control mice's hippocampus
| PRJNA208725 | ENA
Project description:To define the interactome of huntingtin protein (HTT) in human neurons, we assessed interactors of HTT with coimmunoprecipitation experiments with huntingtin antibody or polyqlutamine antibody (it only recognizes mutant huntingtin protein with abnormal polyqlutamine expansion) in striatal neurons differentiated from control and patient-derived iPSC lines (HD-iPSCs). GFP antibody used as a negative control.
2022-12-02 | PXD037618 | Pride
Project description:A total of 36 postmortem brain samples (23 suicide completers, 13 control sudden death) were collected. We evaluated the proteome profile in the prefrontal cortex (Brodmann area 9, 10) with TMT-based quantification using LC-MS/MS. Several bioinformatics tools were used to elucidate biological mechanisms related to suicide. Subgroup analysis was conducted to find common differentially expressed proteins (DEPs) among various clinically different groups. Among the 9801 proteins identified in our dataset, 295 proteins were differentially expressed between suicide completers and sudden death subjects. Various bioinformatics analysis revealed that suicide completion is predominately enriched in synaptic functions and synaptogenesis especially in endocannabinoid and GABA signaling pathway. Our finding presents the largest protein pools related to suicide completion, and suggests that newly emerging neurotransmitter systems such as endocannabinoid system and synaptogenesis processes may have an impact upon the biological cascade leading to suicide.
2022-05-20 | PXD029845 | Pride
Project description:Differentially expressed genes between SPOPmut and control in mouse prostate organoids
| PRJNA374556 | ENA