| JUP — Junction Plakoglobin (Gamma-Catenin) | |
|---|---|
| Protein Name | Junction Plakoglobin |
| Gene | JUP |
| UniProt ID | P14923 |
| PDB IDs | 1L7W, 3L7X |
| Molecular Weight | 81.7 kDa |
| Subcellular Localization | Plasma membrane, Cell junctions, Cytoplasm |
| Protein Family | Catenin family |
JUP (junction plakoglobin), also known as gamma-catenin, is a member of the catenin protein family. It is a key component of desmosomes and adherens junctions, where it mediates cell-cell adhesion. While primarily studied in the context of cell adhesion and cardiac function, emerging research suggests roles for JUP in neuronal function and neurodegenerative diseases.
JUP contains:
JUP undergoes various PTMs including:
These modifications regulate its localization, protein interactions, and signaling functions.
JUP is a core component of desmosomes, specialized cell-cell junctions that provide strong mechanical adhesion between cells. In neurons, JUP may contribute to:
Beyond structural roles, JUP participates in several signaling pathways:
While JUP is not a primary disease-causing gene in most neurodegenerative disorders, several connections have been identified:
Alzheimer's Disease: Altered JUP expression has been reported in AD brain tissue. JUP may interact with amyloid precursor protein processing and affect neuronal survival pathways.
Parkinson's Disease: Studies suggest JUP may be involved in dopaminergic neuron survival and protein quality control mechanisms.
Amyotrophic Lateral Sclerosis: JUP has been detected in some protein aggregates in ALS, though its role remains to be fully characterized.
JUP is more extensively studied in cancer biology where it functions as a tumor suppressor. Loss of JUP expression promotes tumor invasion and metastasis.
Current therapeutic approaches targeting JUP are primarily in the context of cancer. However, understanding JUP's roles in neuronal survival may lead to: