eScholarship
metadata only
CC BY
Loss of TDP-43 function contributes to genomic instability in amyotrophic lateral sclerosis
A common pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the cytoplasmic mislocalization and aggregation of the DNA/RNA-binding protein TDP-43, but how loss of nuclear TDP-43 function contributes to ALS and FTD pathogenesis remains largely unknown. H
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- DCPS modulates TDP-43-linked neurodegeneration through P-body-mediated RNA decay#261809
- Molecular signatures and biomarker development for limbic-predominant age-related TDP-43 encephalopathy (LATE).#193328
- Recurrent patterns of TOP1-mediated neuronal genomic damage shared by major neurodegenerative disorders.#351564
- Inhibition of RNA lariat debranching enzyme suppresses TDP-43 toxicity in ALS disease models#1311449
- Recurrent patterns of TOP1-mediated neuronal genomic damage shared by major neurodegenerative disorders#1311977
Record · ID 1358109
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive