| PI3K Protein | |
|---|---|
| Gene | [PIK3CA](/genes/PIK3CA) (p110α), [PIK3CB](/genes/PIK3CB) (p110β) |
| UniProt | P42336 (p110α) |
| PDB | 4OVU, 3ZMS |
| Mol. Weight | 110 kDa (catalytic subunit) |
| Localization | Plasma membrane, cytoplasm |
| Family | PI3K family, lipid kinases |
| Diseases | [Alzheimer's Disease](/diseases/alzheimers), [Parkinson's Disease](/diseases/parkinsons-disease), [Cancer](/diseases/cancer) |
Pi3K 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.
PI3K (Phosphoinositide 3-kinase) is a key signaling enzyme that generates phosphatidylinositol (3,4,5)-trisphosphate (PIP3), a critical second messenger that regulates cell survival, growth, proliferation, and metabolism[1]. In neurons, PI3K signaling is essential for development, synaptic plasticity, and neuroprotection against various stresses[2].
There are multiple PI3K classes, with Class I PI3Ks being most relevant to signaling:
Each has distinct cellular functions and expression patterns[3].
Class I PI3Ks have a characteristic structure:
The regulatory subunit contains:
The catalytic subunit contains:
PI3K is recruited to the membrane via:
PI3K is activated by:
PI3K activates multiple downstream effectors:
In neurons, PI3K regulates:
PI3K/Akt signaling is implicated in AD:
In PD:
PI3K is frequently mutated/activated:
Therapeutic strategies include:
The study of Pi3K 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.
Cantley, PI3K signaling (2002). 2002. ↩︎
Th� et al. PI3K in neurodegeneration (2019). 2019. ↩︎
Zhang et al. PI3K/Akt in neuronal survival (2017). 2017. ↩︎