| TNF Alpha Induced Protein 3 | |
|---|---|
| Gene Symbol | TNFAIP3 |
| Full Name | TNF alpha induced protein 3 (A20) |
| Chromosome | 6q23.3 |
| NCBI Gene ID | 7128 |
| OMIM | 191163 |
| Ensembl ID | ENSG00000118503 |
| UniProt ID | P21579 |
| Associated Diseases | Alzheimer's Disease, Parkinson's Disease, ALS, Neuroinflammation |
TNFAIP3 (TNF Alpha Induced Protein 3), also known as A20, is a critical gene involved in the negative regulation of inflammation and cell survival. Located on chromosome 6q23.3, this gene encodes a zinc finger protein that plays a essential role in dampening NF-κB signaling and protecting cells from TNF-α-induced cell death. A20 has emerged as an important regulator of neuroinflammation in the central nervous system, with dysfunction implicated in various neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS). The gene's products act as a deubiquitinating enzyme, removing ubiquitin chains from key signaling molecules such as TRAF6 and RIPK1, thereby preventing excessive inflammatory responses. Given its central role in controlling inflammation, TNFAIP3 represents a promising therapeutic target for modulating neuroinflammatory processes in neurodegenerative conditions.
TNFAIP3 encodes A20, a zinc finger protein that functions as a key negative regulator of NF-κB signaling and inflammation. A20 is rapidly induced by TNF-α and other inflammatory stimuli, and it deubiquitinates key signaling molecules (TRAF6, RIPK1) to dampen NF-κB activation. In the brain, TNFAIP3/A20 helps control neuroinflammatory responses and protects against excessive microglial activation.
Expressed in various tissues including brain, particularly in microglia, astrocytes, and neurons. Induced by inflammatory stimuli.
| Disease | Variants | Inheritance | Mechanism |
|---|---|---|---|
| Alzheimer's Disease | Various | Risk factor | Dysregulated neuroinflammation, NF-κB signaling |
| Parkinson's Disease | Various | Risk factor | Impaired inflammatory response control |
| ALS | Various | Risk factor | Microglial activation, NF-κB dysregulation |
| Multiple Sclerosis | Various | Risk factor | Autoimmune neuroinflammation |