HAL (France)
open access
Microtubule stability, Golgi organization, and transport flux require dystonin-a2–MAP1B interaction
Loss of function of dystonin cytoskeletal linker proteins causes neurodegeneration in dystonia musculorum (dt) mutant mice. Although much investigation has focused on understanding dt pathology, the diverse cellular functions of dystonin isoforms remain poorly characterized. In this paper, we highli
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
- Endomysial Fibrosis, Muscular Inflammatory Response and Calcium Homeostasis Dysfunction in Duchenne Muscular Dystrophy#872955
- Dystrophin expression in muscle stem cells regulates their polarity and asymmetric division#781256
- CAR-T cells targeting fibroblast activation protein eliminate pathological fibroblasts and preserve cardiac function in a Duchenne Muscular Dystrophy murine model#1313010
- Functional and structural pathologies in skeletal muscle of a rat model of Duchenne muscular dystrophy#1250687
- Generation and characterization of three human induced pluripotent stem cell lines from patients with Duchenne muscular dystrophy#1235405
Record · ID 1312692
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