Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Involvement of autophagy in mesaconitine-induced neurotoxicity in HT22 cells revealed through integrated transcriptomic, proteomic, and m6A epitranscriptomic profiling

ABSTRACT: Involvement of autophagy in mesaconitine-induced neurotoxicity in HT22 cells revealed through integrated transcriptomic, proteomic, and m6A epitranscriptomic profiling

PROVIDER: PRJNA1086484 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28291205_1.fastq.gz	Fastqsanger.gz
	SRR28291205_2.fastq.gz	Fastqsanger.gz
	SRR28291206_1.fastq.gz	Fastqsanger.gz
	SRR28291206_2.fastq.gz	Fastqsanger.gz
	SRR28291207_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

The involvement of autophagy in mesaconitine-induced neurotoxicity in HT22 cells revealed through integrated transcriptomic, proteomic, and m6A epitranscriptomic profiling

Project description:In order to investigate the effects of mesaconitine treatment on protein expression, we carried out quantitative proteomic analysis to elucidate comprehensive protein changes in HT22 cells with or without mesaconitine treatment.

2024-05-03 | PXD052001 |

Involvement of autophagy in mesaconitine-induced neurotoxicity in HT22 cells revealed through integrated transcriptomic, proteomic, and m6A epitranscriptomic profiling

Project description:Our study provided a comprehensive mechanistic understanding of the neurotoxic effects induced by MA at multi-omics resolution, and offered valuable insights for enhancing the rational application of traditional Chinese medicine containing aconitum in clinical practice.

2024-07-03 | GSE261320 | GEO

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

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

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 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.

2013-03-28 | GSE45534 | GEO

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

Neuronal Nsun2 deficiency is associated with codon-specific epitranscriptomic dysregulation of Gly-tRNAs and corresponding proteomic shift impacting synaptic signaling and behavior

Project description:Epitranscriptomic mechanisms linking the brain proteome to cognition and complex behaviors essentially remain unexplored. Here, we describe bi-directional changes in depression-related behaviors after genetic disruption of neuronal tRNA cytosine methylation, including conditional ablation and transgene-derived overexpression of NOL1/NOP2/SUN domain 2 (Nsun2) in the prefrontal cortex (PFC). Neuronal Nsun2-deficiency was associated with a sharp drop in tRNA m5C levels, resulting in significant deficits in expression of 70% (7/10) of tRNAGlyGCC, GlyCCC GlyTCC isodecoders, while expression changes in non-glycinergic tRNAs were minimal (4/152). Altogether, 1488/5820 proteins were sensitive to neuronal Nsun2-deficiency, in conjunction with GCC and CCC codon-specific defects in translational efficiencies and loss of Gly-rich proteins critical for glutamatergic neurotransmission, resulting in impaired synaptic signaling at PFC pyramidal neurons and impairments in contextual fear memory. These distortions in the neuronal translatome were associated with an adaptive, 2.46-fold up-regulation in PFC glycine levels with increased expression of multiple enzymes in the glycine biosynthetic pathway. These findings highlight the methylation sensitivity of glycinergic tRNAs in the adult PFC and link synaptic plasticity and complex behaviors to epitranscriptomic regulation of cognate tRNAs and the proteomic homeostasis associated with specific amino acids.

2021-07-01 | GSE165202 | 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

| PRJNA521221 | ENA

A quantitative proteomic analysis to reveal effects of N-acetylcystein on H2O2-induced neurotoxicity

Project description:SK-N-MC cell was used to evaluate effects of N-acetylcystein on H2O2-induced neurotoxicity. Proteomic analysis was conducted in three groups: control, H2O2-treatment (disease group), and NAC pretreatment followed by H2O2-treatment (NAC group).

2020-10-13 | PXD018177 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data