Ontology highlight
ABSTRACT:
PROVIDER: PRJNA744518 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15064580.fastq.gz | Fastqsanger.gz | |||
| SRR15064581.fastq.gz | Fastqsanger.gz | |||
| SRR15064582.fastq.gz | Fastqsanger.gz | |||
| SRR15064583.fastq.gz | Fastqsanger.gz | |||
| SRR15064584.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:Poly(A)-ClickSeq is a new methodology for the sequencing of the 3'UTR/poly(A) tail junction of RNA. We analysed both wild-type and CF25Im knock-down HeLa cells in culture using Poly(A)-ClickSeq to find the distribution of poly(A) sites in these samples and determine the role of CF25Im in poly(A) site selection (alternative poly-adenylation, APA).
2017-05-02 | GSE94950 | GEO
Project description:Poly(A)-ClickSeq: click-chemistry for next-generation 3'-end sequencing without RNA enrichment or fragmentation enabling simultaneous genomewide poly(A)-site identification and differential expression analysis
2023-01-12 | GSE169140 | GEO
Project description:Poly(A)-ClickSeq resolves CF25-mediated alternative poly-adenylation, HeLa
| PRJNA374982 | ENA
Project description:Purpose: Overexpression of tau isoforms has been linked to neurodegenerative diseases, and abnormal tau expression is correlated with genomic instability. The purpose of this study is to use RNA-sequencing and molecular biological techniques to determine if there are any unique genomic consequences associated with overexpression of one or more tau isoforms. Methods: SHSY-5Y cells were infected in triplicate with lentiviruses to induce overexpression of 3R and 4R tau isoforms, were treated with amyloid-beta oligomers or DMSO, and were differentiated into neurons using retinoic acid. After RNA collection via TRIzol, poly(A)-selected, 100 bp, paired-end library preparation and sequencing were completed by the IGM Genomics Center, University of California, San Diego, La Jolla, CA, using an Illumina NovaSeq 6000 that was purchased with funding from a National Institutes of Health SIG grant (#S10 OD026929). Trimmed FASTQ files were aligned to GRCH38 using STAR and differential expression of genes and transposable elements was determined using DESeq2 and software from TEToolkit (available from the Hammell Lab at Cold Spring Harbor Laboratory). Results: Our RNA-seq analysis revealed similar gene and transposable element expression patterns between cells overexpressing tau isoforms and patients with Alzheimer's disease or progressive supranuclear palsy. We found widespread differential expression particularly in L1 and Alu transposable elements and upregulation of genes related to extracellular matrix organization, focal adhesions, and cell junctions, among other biological processes. Conclusions: Our study is the first to our knowledge to examine locus-specific transposable element expression in the context of tauopathies, and to our knowledge is the first to specifically examine transposable element expression stemming from overexpression of tau isoforms. Our study provides additional evidence that transposable elements may play a role in tauopathies and provides further insight into the locations of transposable element expression in the genome in the context of neurodegenerative diseases.
2021-09-12 | GSE163150 | GEO
Project description:There is accumulating evidence that amyloid beta and tau proteins may act synergistically to cause synapse and neural circuit degeneration in Alzheimer’s disease. In order to study this, we designed a new mouse model which lacks endogenous mouse tau, but expresses both the APP/PS1 transgene, which causes well-characterised plaque-associated synapse loss, and also reversibly expresses wild-type human tau (which can be suppressed with doxycycline). We examined the transcriptional changes in the frontal cortex of this mouse model, along with behaviour, pathology, synaptic plasticity, synapse degeneration and accumulation of amyloid beta and tau at synapses, and compared with littermate control genotypes: those lacking endogenous mouse tau, those lacking endogenous mouse tau but expressing the APP/PS1 transgene only, and those lacking endogenous mouse tau but reversibly expressing wild-type human tau only.
2019-11-12 | E-MTAB-7856 | biostudies-arrayexpress
Project description:We performed snRNA-seq using 10xgenomics platform to study the role of MAIT cells in regulating neuroinflammation in mice with neurodegenerative tau pathology. MAIT cells are a type of innate-like T cells that are present in the meninges of mice carrying neurodgenerative human tau mutant transgene. This is the first study to examine single nucleus transcriptome profiles of human tau mice lacking MAIT cells.
2025-03-26 | GSE285822 | GEO
Project description:Tau aggregates lead to progressive neurodegeneration in Alzheimer’s disease (AD) (ref). Neuron death is one of the hallmarks of neurodegeneration (ref). However, the pathological influence of neuronal death is undetermined, and the connection between Tau aggregates and neuronal death remains elusive. Here we demonstrated the essential role of neuron death in Tau-related neurodegeneration. Tau-neurons died in necroptosis, dependent on ZBP1 sensitized by Z-RNAs (an unusual left-handed conformation). Those endogenous Z-RNAs were transcripts of reactivated transposable elements (TEs) originally silenced in heterochromatin.
2023-11-22 | GSE248068 | GEO