| GSTT1 | |
|---|---|
| Gene Symbol | GSTT1 |
| Full Name | Glutathione S-Transferase Theta 1 |
| Chromosomal Location | 22q11.23 |
| NCBI Gene ID | [2952](https://www.ncbi.nlm.nih.gov/gene/2952) |
| OMIM | [600436](https://www.omim.org/entry/600436) |
| Ensembl ID | ENSG00000120708 |
| UniProt ID | [P30711](https://www.uniprot.org/uniprot/P30711) |
| Associated Diseases | Alzheimer's Disease, Parkinson's Disease, ALS, Cancer, Stroke |
## is a human gene whose product gSTT1 (Glutathione S-Transferase Theta 1)** encodes a member of the theta class of glutathione S-transferase enzymes. GSTT1 plays important roles in cellular detoxification, oxidative stress protection, and metabolism of xenobiotic compounds 1. Variants in ## have been implicated in Alzheimer's Disease, Parkinson's Disease, ALS. This page covers the gene's normal function, disease associations, expression patterns, and key research findings relevant to neurodegeneration.
GSTT1 (Glutathione S-Transferase Theta 1) encodes a member of the theta class of glutathione S-transferase enzymes. GSTT1 plays important roles in cellular detoxification, oxidative stress protection, and metabolism of xenobiotic compounds 1.
GSTT1 has distinct substrate specificity compared to other GST classes, with activity toward certain halogenated compounds, epoxides, and organic hydroperoxides. The enzyme is polymorphic in humans, with a common null allele resulting in complete lack of enzyme activity in approximately 20% of Caucasians 2.
Key functions in neuronal cells:
GSTT1 null genotype may increase AD risk through reduced detoxification capacity. The enzyme contributes to clearance of neurotoxic compounds 4.
GSTT1 polymorphisms influence PD susceptibility. Combined GSTM1 and GSTT1 null genotypes show additive risk effects 5.
Oxidative stress is a key contributor to ALS pathogenesis. GSTT1 variants may modify disease risk and progression 6.
GSTT1 is expressed in most tissues, with high expression in liver and moderate expression in brain. In the brain, GSTT1 is expressed in neurons and glial cells. Expression is inducible by oxidative stress through Nrf2-mediated transcription 7.
Nrf2 activators that induce GST expression represent potential neuroprotective strategies for neurodegenerative diseases 8.