Calcineurin A Alpha Protein 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 Phosphatase 3 Catalytic Subunit Alpha (Calcineurin A)
| Protein Name | Protein Phosphatase 3 Catalytic Subunit Alpha (Calcineurin A) |
| Gene Symbol | PPP3CA |
| UniProt ID | P48431 |
| PDB ID | 1TCO, 2JGI |
| Molecular Weight | 59 kDa |
| Subcellular Localization | Cytoplasm |
| Protein Family | Calcineurin (calcium/calmodulin-dependent protein phosphatase) |
| Associated Diseases | Alzheimer's Disease, Parkinson's Disease, Amyotrophic Lateral Sclerosis, Immune Disorders |
Protein Phosphatase 3 Catalytic Subunit Alpha (Calcineurin A) (PPP3CA encoded) is a Calcineurin (calcium/calmodulin-dependent protein phosphatase) that plays critical roles in Dephosphorylates NFAT and other substrates. This protein is implicated in the pathogenesis of several neurodegenerative diseases through its involvement in NFAT activation, immune response, synaptic plasticity.
Calcineurin A has a phosphatase domain at the N-terminus followed by a calmodulin-binding regulatory domain.
Calcineurin is a calcium/calmodulin-dependent protein phosphatase that dephosphorylates NFAT, AMPA receptor subunits, and various signaling proteins.
In Alzheimer's disease, calcineurin activity is dysregulated and may contribute to synaptic dysfunction.
| Disease | Pathogenic Mechanism |
|---|---|
| Alzheimer's Disease | Pathogenic variants |
| Parkinson's Disease | Pathogenic variants |
| Amyotrophic Lateral Sclerosis | Pathogenic variants |
| Immune Disorders | Pathogenic variants |
Altered calcineurin activity contributes to synaptic plasticity deficits in AD.
Calcineurin inhibitors are immunosuppressants but have neurotoxic side effects.
The study of Calcineurin A Alpha Protein 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.