| PPID — Peptidylprolyl Isomerase D | |
|---|---|
| Symbol | PPID |
| Full Name | Peptidylprolyl Isomerase D (Cyclophilin D) |
| Chromosome | 4q31.3 |
| NCBI Gene | 54840 |
| Ensembl | ENSG00000117595 |
| UniProt | Q8WWC6 |
| Diseases | Alzheimer's Disease, Parkinson's Disease |
| Expression | Brain, Heart, Muscle, Liver |
| Key Information | |
| Mitochondrial cyclophilin, mPTP regulator | |
Ppid — Peptidylprolyl Isomerase D is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
PPID (Peptidylprolyl Isomerase D), also known as Cyclopin D (CypD), is a gene located on chromosome 4q31.3 that encodes a mitochondrial cyclophilin protein. PPID is a key regulator of the mitochondrial permeability transition pore (mPTP) and plays a critical role in mitochondrial cell death pathways.
PPID encodes peptidylprolyl isomerase D, a member of the cyclophilin family that catalyzes the cis-trans isomerization of proline residues in target proteins. In mitochondria, PPID/CypD is primarily localized to the matrix and regulates the opening of the mitochondrial permeability transition pore (mPTP).
PPID is ubiquitously expressed, with high levels in brain, heart, skeletal muscle, and liver. In the brain, it is expressed in neurons throughout the cortex, hippocampus, basal ganglia, and cerebellum.
Expression data is available from the Allen Human Brain Atlas.
PPID/CypD is implicated in AD pathogenesis through its role in mitochondrial dysfunction and apoptosis. Increased CypD expression and its interaction with amyloid-beta have been reported in AD. CypD inhibitors have shown neuroprotective effects in AD models.
In PD, PPID contributes to mitochondrial dysfunction in dopaminergic neurons. The protein is involved in mPTP opening triggered by oxidative stress, a key pathogenic mechanism in PD.
PPID/CypD is a therapeutic target for neurodegeneration:
The study of Ppid — Peptidylprolyl Isomerase D 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.