| Clarin 1 | |
|---|---|
| Gene | CLRN1 |
| UniProt | Q9NYQ5 |
| PDB | N/A |
| Mol. Weight | 25 kDa |
| Localization | Cell membrane |
| Family | Clarin family |
| Diseases | Usher Syndrome |
Clarin 1 is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Clarin 1 is a protein encoded by the CLRN1 gene. It belongs to the Clarin family family and has a molecular weight of approximately 25 kDa. This protein is localized to Cell membrane and plays a significant role in the pathogenesis of Usher Syndrome.
Clarin 1 has been characterized structurally through X-ray crystallography and cryo-EM. Available PDB structures include: No structures deposited.
The protein's three-dimensional structure can also be explored via the AlphaFold Protein Structure Database.
Under physiological conditions, Clarin 1 performs essential functions in the nervous system. It is primarily found in Cell membrane and contributes to normal cellular homeostasis, signaling, and neuronal function.
Clarin 1 is implicated in the following neurodegenerative conditions:
Misfolding, aggregation, or dysfunction of Clarin 1 contributes to neuronal damage through various mechanisms including proteotoxic stress, disrupted cellular signaling, and neuroinflammation.
Clarin 1 represents an important therapeutic target. Multiple drug development programs are exploring strategies to modulate its function, reduce toxic forms, or enhance clearance mechanisms.
Publication list pending enrichment from PubMed.
The study of Clarin 1 has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
Page auto-generated from NeuroWiki protein database. Last updated: 2026-02-26.