Anxa11 Protein — Annexin A11 is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| Protein Name | Annexin A11 |
|---|---|
| Gene | [ANXA11](/genes/anxa11) |
| UniProt ID | P50995 |
| Protein Size | 505 amino acids (~54 kDa) |
| Subcellular Localization | Cytoplasm; nucleus; plasma membrane; cytoskeleton |
| Protein Family | Annexin family (calcium-dependent phospholipid-binding proteins) |
| PDB Structures | 1HMH, 1XJL |
Annexin A11 (ANXA11) is a calcium-dependent phospholipid-binding protein that plays important roles in membrane organization, vesicle trafficking, and more recently has been implicated in the pathogenesis of ALS and other neurodegenerative diseases.
ANXA11 has a characteristic annexin domain structure:
The protein forms a convex surface with the convex face being the membrane-binding surface.
In normal cells, ANXA11 functions in:
Membrane Organization: Binds to phospholipid membranes in a calcium-dependent manner, helping organize membrane domains.
Vesicle Trafficking: Participates in endocytic and exocytic vesicle transport.
Cytoskeletal Interactions: Associates with actin cytoskeleton to regulate membrane-cytoskeleton dynamics.
Nuclear Functions: Can translocate to the nucleus where it may regulate gene expression.
Phagocytosis: Involved in macrophage phagocytosis of apoptotic cells.
ANXA11 was identified as an ALS susceptibility gene through GWAS[1]. Pathogenic mutations (e.g., D40G, R235C, G38R) disrupt the normal function of ANXA11 in several ways:
ANXA11 mutations have also been reported in FTD cases, suggesting a shared pathomechanism with ALS.
ANXA11 is upregulated in AD brains and may contribute to altered membrane dynamics and inflammation.
No specific ANXA11-targeted therapies exist yet, but strategies under investigation include:
ANXA11 interacts with:
The study of Anxa11 Protein — Annexin A11 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.