Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1077985 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28006675_1.fastq.gz | Fastqsanger.gz | |||
| SRR28006675_2.fastq.gz | Fastqsanger.gz | |||
| SRR28006676_1.fastq.gz | Fastqsanger.gz | |||
| SRR28006676_2.fastq.gz | Fastqsanger.gz | |||
| SRR28006677_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 30 |
Similar Datasets
Project description:HSV G207 and polio:rhinovirus PVSRIPO are two different viral immunotherapies used to treat malignant brain tumors in children. While some patients experience durable survival with these viral immunotherapies, many children have no response. The purpose of this work is to explore these viral immunotherapies in pediatric high grade glioma (pHGG) and medulloblastoma in order to elucidate how tumor response to treatment and to identify putative biomarkers of response and therapeutic targets.
2024-01-31 | GSE233949 | GEO
Project description:Zika virus (ZIKV) is an emerging, mosquito-borne pathogen associated with a widespread 2015–2016 epidemic in the Western Hemisphere and a proven cause of microcephaly and other fetal brain defects in infants born to infected mothers. ZIKV infections have been also linked to other neurological illnesses in infected adults and children, including Guillain-Barré syndrome (GBS), acute flaccid paralysis (AFP) and meningoencephalitis, but the viral pathophysiology behind those conditions remains poorly understood. Here we investigated ZIKV infectivity in neuroblastoma SH-SY5Y cells, both undifferentiated and following differentiation with retinoic acid. We perform RNA seq, and global trancriptome analysis to corroborate the effect of retinoic acid in SH-SY5Y cells. Then we analyze the virus infection in differentiated and undifferntiated cells. We found that multiple ZIKV strains, representing both the prototype African and contemporary Asian epidemic lineages, were able to replicate in SH-SY5Y cells. Differentiation with resultant expression of mature neuron markers increased infectivity in these cells, and the extent of infectivity correlated with degree of differentiation. Enhanced ZIKV infectivity in a neural cell line following differentiation may contribute to viral neuropathogenesis in the developing or mature central nervous system.
2018-10-20 | GSE121534 | GEO
Project description:Transcriptome analysis of RNA extracted from human induced pluripotent stem cell (hipsc)-derived neurons exposed to botulinum neurotoxin type A1 (BoNT/A1) and an atoxic derivative, BoNT/A ad. Botulinum neurotoxin type A1 (BoNT/A1) is a potent protein toxin responsible for the potentially fatal human illness botulism. Despite this, the long-lasting flaccid muscle paralysis caused by BoNT/A has led to its rise as a powerful and versatile bio-pharmaceutical. The flaccid paralysis is due to specific cleavage of SNAREs by BoNTs inside neurons. However, potential effects of BoNTs on intoxicated neurons besides the cleavage of SNAREs have not been studied in detail. In this study we investigated by microarray analysis the effects of BoNT/A and a catalytically inactive derivative (BoNT/A ad) on the transcriptome of human induced pluripotent stem cell (hiPSC)-derived neurons at 2 days and 2 weeks after exposure. While there were only minor changes in expression levels at 2 days post exposure, at 2 weeks post exposure 492 genes were differentially expressed more than 2-fold in BoNT/A1-exposed cells when compared to non-exposed populations, and 682 genes were differentially expressed in BoNT/A ad-exposed cells. The vast majority of genes were similarly regulated in BoNT/A1 and BoNT/A ad-exposed neurons, and the few genes differentially regulated between BoNT/A1 and BoNT/A ad-exposed neurons were regulated less than 3.5 fold. These data indicate a similar response of neurons to BoNT/A1 and BoNT/A ad exposure. The most highly regulated genes in cells exposed to either BoNT/A1 or BoNT/A ad are involved in neurite outgrowth and calcium channel sensitization.
2014-09-15 | GSE58149 | GEO
Project description:Transcriptome analysis of RNA extracted from human induced pluripotent stem cell (hipsc)-derived neurons exposed to botulinum neurotoxin type A1 (BoNT/A1) and an atoxic derivative, BoNT/A ad. Botulinum neurotoxin type A1 (BoNT/A1) is a potent protein toxin responsible for the potentially fatal human illness botulism. Despite this, the long-lasting flaccid muscle paralysis caused by BoNT/A has led to its rise as a powerful and versatile bio-pharmaceutical. The flaccid paralysis is due to specific cleavage of SNAREs by BoNTs inside neurons. However, potential effects of BoNTs on intoxicated neurons besides the cleavage of SNAREs have not been studied in detail. In this study we investigated by microarray analysis the effects of BoNT/A and a catalytically inactive derivative (BoNT/A ad) on the transcriptome of human induced pluripotent stem cell (hiPSC)-derived neurons at 2 days and 2 weeks after exposure. While there were only minor changes in expression levels at 2 days post exposure, at 2 weeks post exposure 492 genes were differentially expressed more than 2-fold in BoNT/A1-exposed cells when compared to non-exposed populations, and 682 genes were differentially expressed in BoNT/A ad-exposed cells. The vast majority of genes were similarly regulated in BoNT/A1 and BoNT/A ad-exposed neurons, and the few genes differentially regulated between BoNT/A1 and BoNT/A ad-exposed neurons were regulated less than 3.5 fold. These data indicate a similar response of neurons to BoNT/A1 and BoNT/A ad exposure. The most highly regulated genes in cells exposed to either BoNT/A1 or BoNT/A ad are involved in neurite outgrowth and calcium channel sensitization. 18 samples were used for this project: 6 populations were exposed to BoNT/A1, 6 to BoNT/A ad, and 6 were non-exposed. All exposures lasted for 48h, at which point 3 samples of each exposure group were harvested (2d condition), and the remaining 3 samples were grown for an additional 12d (2wk condition). Analysis was performed using the Affymetrix HG U133 Plus 2.0 array, and data was extracted using the Affymetrix Expression Console v 1.2.0.20 software
2014-09-15 | E-GEOD-58149 | biostudies-arrayexpress
Project description:Laboratory strain poliovirus was hybridized to the array as a control run and a proof of concept. Degree of cross hybridization between polio nucleic acid and non-polio probes was evaluated. Specificity of the probe design was determined. Keywords: control study: target detection and specificity
2008-02-28 | GSE10566 | GEO
Project description:Spinal cord injury leads to impaired motor and sensory functions. After spinal cord injury there is a an initial phase of hypo-reflexia followed by a developing hyper-reflexia, often termed spasticity. Previous studies have suggested a relationship between the reappearence of plateau potentials in motor neurons and the development of spasticity after spinalizaion. To understand the moleclar mechanism behind this pheneomona we examined the transcriptional response of the motor neurons after spinal cord injury as it progress over time. We used a rat tail injury model where a complete transection of the caudal (S2) rat spinal cord leads to an immidate flaccid paralysis of the tail and a subsequent appearence of spasticity 2-3 weeks post injury that develops into strong spasticity after 2 months. Gene expression changes were studied in motor neurones 0, 2, 7, 21 and 60 days after comlete spinal transection.
2010-05-01 | GSE19701 | GEO