| DGKQ — Diacylglycerol Kinase Theta | |
|---|---|
| Gene Symbol | DGKQ |
| Full Name | Diacylglycerol Kinase Theta |
| Chromosome | 19p13.3 |
| NCBI Gene ID | [17185](https://www.ncbi.nlm.nih.gov/gene/17185) |
| OMIM | 604017 |
| Ensembl ID | ENSG00000145214 |
| UniProt ID | [Q86XR1](https://www.uniprot.org/uniprot/Q86XR1) |
| Protein Name | Diacylglycerol kinase theta |
| Associated Diseases | [Parkinson's Disease](/diseases/parkinsons-disease), [Alzheimer's Disease](/diseases/alzheimers-disease), Neurodegeneration |
DGKQ is a human gene whose product dGKQ (Diacylglycerol Kinase Theta) is a member of the diacylglycerol kinase family that catalyzes the phosphorylation of diacylglycerol (DAG) to phosphatidic acid (PA), a critical lipid signaling reaction [1]. This conversion regulates the balance between two important second messengers: DAG, which activates protein kinase C (PKC) and other DAG-responsive proteins, and PA, which has distinct signaling properties and is involved in membrane trafficking, actin cytoskeleton reorganization, and mTOR signaling [2]. DGKQ variants have been implicated in Parkinson's Disease, Neurodegeneration. This page covers the gene's normal function, disease associations, expression patterns, and key research findings relevant to neurodegeneration.
DGKQ (Diacylglycerol Kinase Theta) is a member of the diacylglycerol kinase family that catalyzes the phosphorylation of diacylglycerol (DAG) to phosphatidic acid (PA), a critical lipid signaling reaction [1]. This conversion regulates the balance between two important second messengers: DAG, which activates protein kinase C (PKC) and other DAG-responsive proteins, and PA, which has distinct signaling properties and is involved in membrane trafficking, actin cytoskeleton reorganization, and mTOR signaling [2].
In neurons, DGKQ plays important roles in synaptic plasticity, neurotransmitter release, and neuronal survival. By regulating DAG and PA levels, it modulates PKC activation, which is essential for long-term potentiation (LTP) and memory formation [3].
Dysregulation of DGKQ has been implicated in Parkinson's disease pathogenesis. DAG metabolism is altered in dopaminergic neurons in PD, and DGKQ activity affects mitochondrial function and neuronal survival [4].
Alterations in lipid signaling pathways, including DGKQ-mediated DAG metabolism, are increasingly recognized as contributors to neurodegenerative processes.
DGKQ is widely expressed in the brain, with high expression in the cortex, hippocampus, basal ganglia, and cerebellum. It is localized to the cytoplasm and synaptic vesicles in neurons.
DGKQ interacts with several key proteins involved in neuronal signaling:
| Protein | Interaction | Function |
|---|---|---|
| PKC (Protein Kinase C) | Substrate/regulator | DGKQ regulates DAG levels to modulate PKC activity |
| mTOR | Regulation | PA production influences mTORC1 signaling [1] |
| PSD-95 | Synaptic localization | Localized to postsynaptic densities |
| Synapsin | Vesicle association | Regulates neurotransmitter release |
Emerging evidence suggests DGKQ may play a role in AD pathogenesis through:
Dysregulation of DGKQ has been implicated in Parkinson's disease pathogenesis. DAG metabolism is altered in dopaminergic neurons in PD, and DGKQ activity affects mitochondrial function and neuronal survival [4].
Alterations in lipid signaling pathways, including DGKQ-mediated DAG metabolism, are increasingly recognized as contributors to neurodegenerative processes.
Targeting DGKQ may offer therapeutic benefits:
Shulga et al. DGKQ regulates mTOR signaling and autophagy (2019). 2019. ↩︎
Lopez et al. DGK isoforms in neurodegeneration (2019). 2019. ↩︎