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Identifying microRNAs that bind to cytoplasmic TDP43

ABSTRACT: Identifying microRNAs that bind to cytoplasmic TDP43

PROVIDER: PRJNA606339 | ENA |

REPOSITORIES: ENA

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Identifying microRNAs that bind to cytoplasmic TDP43

Project description:TDP43 is involved in microRNA biogenesis and found in cytoplasmic aggregates in amyotrophic lateral sclerosis (ALS), and microRNAs are important for regulation of gene expression and represent potential biomarkers and therapeutic targets. Therefore, we examined microRNAs that preferentially bind cytoplasmic TDP43 using cellular models expressing TDP43 variants and NanoString miRNA profiling analyses. We identified cytoplasmic TDP43-associated miRNAs and predicted genes and pathways to gain insights into potentially relevant disease pathways, biomarkers, and reversible therapeutic targets for ALS.

2020-04-23 | GSE145214 | GEO

An intramolecular salt bridge linking TDP43’s RNA recognition motifs dictates RNA binding, protein stability and TDP43-dependent neurodegeneration

Project description:The majority of individuals with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) exhibit neuronal cytoplasmic inclusions rich in the RNA binding protein TDP43. Even so, the relationship between TDP43’s RNA binding properties and neurodegeneration remain obscure. Here we show that engineered mutations disrupting a salt bridge between TDP43’s RNA recognition motifs interfere with nucleic acid binding and eliminate recognition of native TDP43 substrates. The accumulation of WT TDP43, but not RNA binding-deficient variants, disproportionately affected the abundance and splicing of encoding ribosome and oxidative phosphorylation components.

2019-03-22 | GSE128647 | GEO

Cytoplasmic TDP43 Binds microRNAs: New Disease Targets in Amyotrophic Lateral Sclerosis.

Project description:Amyotrophic lateral sclerosis (ALS) is a progressive, fatal, and incurable neurodegenerative disease. Recent studies suggest that dysregulation of gene expression by microRNAs (miRNAs) may play an important role in ALS pathogenesis. The reversible nature of this dysregulation makes miRNAs attractive pharmacological targets and a potential therapeutic avenue. Under physiological conditions, miRNA biogenesis, which begins in the nucleus and includes further maturation in the cytoplasm, involves trans-activation response element DNA/RNA-binding protein of 43 kDa (TDP43). However, TDP43 mutations or stress trigger TDP43 mislocalization and inclusion formation, a hallmark of most ALS cases, that may lead to aberrant protein/miRNA interactions in the cytoplasm. Herein, we demonstrated that TDP43 exhibits differential binding affinity for select miRNAs, which prompted us to profile miRNAs that preferentially bind cytoplasmic TDP43. Using cellular models expressing TDP43 variants and miRNA profiling analyses, we identified differential levels of 65 cytoplasmic TDP43-associated miRNAs. Of these, approximately 30% exhibited levels that differed by more than 3-fold in the cytoplasmic TDP43 models relative to our control model. The hits included both novel miRNAs and miRNAs previously associated with ALS that potentially regulate several predicted genes and pathways that may be important for pathogenesis. Accordingly, these findings highlight specific miRNAs that may shed light on relevant disease pathways and could represent potential biomarkers and reversible treatment targets for ALS.

| S-EPMC7235295 | biostudies-literature

Identifying and targeting angiogenesis-related microRNAs in ovarian cancer

Project description:Identifying and targeting angiogenesis-related microRNAs in ovarian cancer

| PRJNA493637 | ENA

Identifying microRNAs and their editing sites in Macaca mulatta

Project description:Identifying microRNAs and their editing sites in Macaca mulatta

| PRJNA511985 | ENA

TDP43 proteinopathy exhibits disease, tissue, and context-specific cryptic splicing signatures

Project description:Mislocalization of the nuclear protein TDP43 is a hallmark of ALS and FTD and leads to de-repression and inclusion of cryptic exons, which represent promising biomarkers of TDP43 pathology. However, most cryptic exons to date have been identified from in vitro models, limiting our understanding of any tissue and/or cell-specific splices. We meta-analyzed published bulk RNA-Seq datasets representing 1,778 RNAseq profiles of ALS and FTD post mortem tissue, and in vitro models with experimentally depleted TDP43. We identified novel cryptic splices and mapped out their tissue-specificity, demonstrating subsets with distinct cortical and spinal cord enrichment. Novel events were validated by RNA-Seq and RT-qPCR in a new spinal cord cohort, and analysis of single-nucleus datasets localized cortical splices to layer-specific neuronal populations. This catalog of cryptic splices is the first step towards the development of biomarkers for cell type-specific TDP43 pathology.

2024-03-28 | GSE255683 | GEO

Rapid and Inducible Mislocalization of Endogenous TDP43 in a Novel Human Model of Amyotrophic Lateral Sclerosis [Nanopore]

Project description:In this study, we describe the development of a new model of TDP43 proteinopathy using human induced pluripotent stem cell (iPSC)-derived neurons. Utilizing a genome engineering approach, we induced the mislocalization of endogenous TDP43 from the nucleus to the cytoplasm without mutating the TDP43 gene or using chemical stressors

2025-03-07 | GSE290441 | GEO

Rapid and Inducible Mislocalization of Endogenous TDP43 in a Novel Human Model of Amyotrophic Lateral Sclerosis [miRNA-seq]

2025-03-07 | GSE290437 | GEO

Rapid and Inducible Mislocalization of Endogenous TDP43 in a Novel Human Model of Amyotrophic Lateral Sclerosis [RNA-seq]

2025-03-07 | GSE290436 | GEO

Transcriptome analysis on TDP43 and SRSF3 downstream genes and binding RNAs in MDA-MB231 cells by Next Generation Sequencing

Project description:TDP43 and SRSF3 has been reported to be RNA-binding proteins; however their roles in breast cancer progression has not been examined previously. Here, we performed RNA-seq on MDA-MB231 cells stably expressed sh-control, shTDP43, shSRSF3 or sh-TDP43 and sh-SRSF3 using lentivirus in duplicates. In addition, MDA-MB231 cells with stable expression of flag-TDP43 or flag-SRSF3 were also generated by using lentivirus. RIP-seq was also applied to identify binding RNA against Flag antibodies.

2018-12-31 | GSE98016 | GEO

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