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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

ABSTRACT: The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChip® Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour.

ORGANISM(S): Mus musculus

PROVIDER: GSE45534 | GEO | 2013/03/28

SECONDARY ACCESSION(S): PRJNA194544

REPOSITORIES: GEO

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Expression data from J147-treated HT22 cells compared to untreated HT22 cells

Project description:The Neurotrophic Compound J147 Reverses Cognitive Impairment In Aged Alzheimer's Disease We used GeneChipM-BM-. Mouse Genome 430 2.0 Arrays to probe global gene expression changes when adding J147 compound to HT22 cells and compared to untreated cells. The hippocampal cell line HT22 were treated with the J147 compound for 1 hour and compared to HT22 treated only with vehicle (DMSO) for 1 hour. The gene expression profile from the J147-treated HT22 cells (1 hour exposure) was compared to HT22 cells treated with vehicle only (DMSO) for 1 hour. The DMSO/vehicle treated cells serve as the control and are referred to as untreated with drug.

2013-03-28 | E-GEOD-45534 | biostudies-arrayexpress

Identification of Klf9-regulated genes in HT22 tissue culture cells [RNA-Seq]

Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration. We used mouse hippocampus-derived HT22 cell line to identify genes differentially regulated by forced Klf9 expression. We stably transfected HT22 cells with pCDNA6:TR (encoding the Tet repressor) and pCDNA6:TO-Klf9 (encoding Klf9 downstream of the Tet operator), allowing doxycycline(dox)-inducible expression of Klf9. We chose a stably transfected clone with baseline Klf9 mRNA level similar to that of untransfected HT22 cells (parent line) and approximately 10-fold induction after dox treatment. We conducted RNA-seq on stably transfected HT22 cells treated with or without dox for 8 hours; we also conducted RNA-seq on parent cells subjected to the same dox treatment to separate nonspecific effects of dox from the effects of forced Klf9 expression. Analysis of RNA-seq data found 217 gene repressed and 21 upregulated by forced Klf9 expression (FDR-adjusted p<.005; because fold changes were small we used a stringent p value cutoff to ensure that we were studying genes likely to be bona fide targets), showing that Klf9 functions primarily as a transcriptional repressor. Gene ontology analysis showed that Klf9-repressed genes were enriched in cytoskeletal and Wnt signaling-related genes.

2019-09-19 | GSE87093 | GEO

Chromatin Immunoprecipitation analysis of mouse hippocampal neuron HT22 cells

Project description:We used H4K5bu and H4K5ac antibodies to specifically enrich mouse hippocampal neuronal cells (HT22) before and after BHBA administration. We found that the acetylation and butylation of histone H4K5 play a key role in the neuroprotection of BHBA.

2021-04-09 | GSE171743 | GEO

Chromatin profiling in HT22 hippocampal cells

Project description:Chromatin profiling in HT22 hippocampal cells

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Genome-wide analysis of gene expression in wild-type and KMT2D-deficient HT22 cells

Project description:We conducted genome wide transcription profiling by RNA-seq in a mouse hippocampal cell line (HT22), comparing cells with CRISPR-Cas9 mediated deletion of the KMT2D enzymatic SET methyltransferase domain to the parental cell line

2019-02-07 | GSE126165 | GEO

Identification of Klf9 genomic binding sites in HT22 tissue culture cells [ChIP-Seq]

Project description:Krueppel-like factor 9 (Klf9) is a DNA-binding transcription factor that has been implicated in neuronal development and regeneration, but none of its genomic targets are known in neurons. We used the mouse hippocampus-derived cell line HT22 to identify Klf9’s genomic binding sites in neurons. We stably transfected HT22 cells with the biotin ligase BirA with or without co-transfection of a Klf9 fusion protein with an n-terminal FLAG tag and a biotin ligase recognition peptide. This allowed us to precipitate Klf9 in chromatin using streptavidin. This permits the use of more stringent wash conditions, improving signal-to-noise ratio. We conducted high-throughput sequencing on DNA precipitated from these lines and identified 3,378 regions where Klf9 associated in chromatin. We found that Klf9 associated near transcription start sites and that its genomic targets were enriched for genes related to cytoskeletal regulation and apoptosis.

2019-09-19 | GSE87203 | GEO

Transcriptomic study of the HT22 cells after OGD treatment.

Project description:To investigate the key genes of ischemic stroke, the oxygen glucose deprivation model and RNA sequence of HT22 neuronal cells were performed. By comparing with each other, we identified 51 up-regulated and 119 down-regulated genes in 3H vs 0H, 229 up-regulated and 50 down-regulated genes in 6H-vs-3H, and 145 up-regulated and 121 down-regulated genes in 6H-vs-0H. The results indicate that c-Fos acts as the most key gene at 51 up-regulated genes in 3H vs 0H.

2021-06-28 | GSE178997 | GEO

Effects of NMDAR on mouse hippocampal neuron (HT22) mRNA and lncRNA expression during hypoxia/reoxygenation injury

Project description:To investigate the changes of the transcriptome in neuronal cells under the condition of NMDAR hypofunction and H/R injury, we compared the changes of mRNA and lncRNA expression levels in mouse hippocampal neuron HT22 cell with or without NMDAR knockdown and H/R stimulation by RNA sequencing.

2022-10-10 | GSE214716 | GEO

Astrocyte conditioned media-dependent Phosphatidylinositol 3-kinase interactome in mouse hippocampal neuron cell line Ht22

Project description:Astrocytes can support neuronal survival through a range of secreted signals that protect against neurotoxicity, oxidative stress, and apoptotic cascades. To identify proteins contributing to protective intracellular neuronal signalling originating from astrocytes, endogenous PI3K was immunoprecipitated from Ht22 cells exposed to primary astrocyte conditioned media (ACM) or cell free media (CFM), followed by iTRAQ-based quantitative proteomic analysis.

2021-09-09 | PXD022200 | Pride

The mRNAs alteration induced by Neat1 knockdown in HT22 cells

Project description:We knocked down the lncRNA-Neat1 by RNA interference in HT22 cells, which were immortalized from the mice hippocampal neurons. Then we measured the mRNA alteration induced by Neat1 knockdown through the next generation sequencing technique (RNA-seq). A total of 18,309 transcripts were detected in the current sequencing study, in which 593 transcripts were selected out according to the criteria: |log2(fold change)| > 1, P < 0.05 (22 up-regulated and 571 down-regulated). To explore whether the mRNA change induced by Neat1 knockdown in a stressed culture condition was different from that in normal condition, the cells were dealt with OGD and followed by RNA-seq. A total of 18,502 transcripts were detected, in which 121 transcripts were significantly up-regulated and 126 transcripts were significantly down-regulated according to the aforementioned filter rules.

2019-08-17 | GSE85749 | GEO

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