ArticleMolecular pharmacology2014
Overexpression of diacylglycerol kinase η enhances Gαq-coupled G protein-coupled receptor signaling.
Article in Molecular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- High glucose mediates diabetic peripheral neuropathy by inducing Schwann cells apoptosis through the Dgkh/PKC-α signaling pathway.Acta diabetologica · 2025Article
- High glucose induces tau hyperphosphorylation in hippocampal neurons via inhibition of ALKBH5-mediated Dgkh mCell death & disease · 2023Article
- Mania- and anxiety-like behavior and impaired maternal care in female diacylglycerol kinase eta and iota double knockout mice.Genes, brain, and behavior · 2020Article
- Article
- Role of Protein Kinase C in Bipolar Disorder: A Review of the Current Literature.Molecular neuropsychiatry · 2017Review
- Cloning and Characterization of Novel Testis-Specific Diacylglycerol Kinase η Splice Variants 3 and 4.PloS one · 2016Article
- Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Multiple genome-wide association studies have linked diacylglycerol kinase η (DGKη) to bipolar disorder (BPD). Moreover, DGKη expression is increased in tissue from patients with BPD. How increased levels of this lipid kinase might affect cellular functions is currently unclear. Here, we overexpressed mouse DGKη in human embryonic kidney 293 cells to examine substrate specificity and signaling downstream of endogenous G protein-coupled receptors (GPCRs). We found that DGKη can phosphorylate diacylglycerol (DAG) with different acyl side chains (8:0, 12:0, 18:1). In addition, overexpression of DGKη enhanced calcium mobilization after stimulating muscarinic receptors with carbachol and after stimulating purinergic receptors with ATP. This effect required DGKη catalytic activity, as assessed using a kinase-dead (G389D) mutant and multiple truncation constructs. DGKη was localized throughout the cytosol and did not translocate to the plasma membrane after stimulation with carbachol. Since protein kinase C (PKC) can be activated by DAG and promotes receptor desensitization, we also examined functional interactions between PKC and DGKη. We found that acute activation of PKC with phorbol 12-myristate 13-acetate shortened carbachol-evoked calcium responses and occluded the effect of overexpressed DGKη. Moreover, inhibition of PKC activity with bisindolylmaleimide I (BIM I) produced the same enhancing effect on carbachol-evoked calcium mobilization as overexpressed DGKη, and overexpression of DGKη produced no additional effect on calcium mobilization in the presence of BIM I. Taken together, our data suggest that DGKη enhances GPCR signaling by reducing PKC activation.
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Registered trials
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