Camk1A 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.
Calcium/Calmodulin-Dependent Protein Kinase 1 Alpha
| Protein Name | Calcium/Calmodulin-Dependent Protein Kinase 1 Alpha |
| Gene Symbol | CAMK1A |
| UniProt ID | Q9UQB8 |
| PDB ID | 2EXR |
| Molecular Weight | 41 kDa |
| Subcellular Localization | Cytoplasm, Nucleus |
| Protein Family | CaMK1 (calcium/calmodulin-dependent protein kinase) |
| Associated Diseases | Alzheimer's Disease, Parkinson's Disease, Cognitive Impairment |
Calcium/Calmodulin-Dependent Protein Kinase 1 Alpha (CAMK1A encoded) is a CaMK1 (calcium/calmodulin-dependent protein kinase) that plays critical roles in Downstream kinase in calcium signaling pathways. This protein is implicated in the pathogenesis of several neurodegenerative diseases through its involvement in neuronal signaling, synaptic plasticity, gene transcription.
CaMK1A has a kinase domain at the N-terminus followed by a regulatory segment containing the calmodulin-binding site.
CaMK1A is a serine/threonine protein kinase activated by calcium/calmodulin. It phosphorylates various downstream targets including transcription factors (CREB).
In Alzheimer's disease, CaMK1A signaling may be disrupted due to amyloid-beta-induced calcium dysregulation.
| Disease | Pathogenic Mechanism |
|---|---|
| Alzheimer's Disease | Pathogenic variants |
| Parkinson's Disease | Pathogenic variants |
| Cognitive Impairment | Pathogenic variants |
Disrupted CaMK1A-CREB signaling contributes to memory deficits in Alzheimer's disease.
Small molecule activators of CaMK1A signaling are being explored.
The study of Camk1A 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.