Overexpression of Diacylglycerol Kinase η Enhances G α q -Coupled G Protein–Coupled Receptor Signaling
Molecular Pharmacology, ISSN: 0026-895X, Vol: 85, Issue: 5, Page: 800-810
2014
- 11Citations
- 29Captures
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Metrics Details
- Citations11
- Citation Indexes11
- CrossRef11
- Captures29
- Readers29
- 24
Article Description
Multiple genome-wide association studies have linked diacylglycerol kinase η (DGK η ) to bipolar disorder (BPD). Moreover, DGK η 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 DGK η in human embryonic kidney 293 cells to examine substrate specificity and signaling downstream of endogenous G protein–coupled receptors (GPCRs). We found that DGK η can phosphorylate diacylglycerol (DAG) with different acyl side chains (8:0, 12:0, 18:1). In addition, overexpression of DGK η enhanced calcium mobilization after stimulating muscarinic receptors with carbachol and after stimulating purinergic receptors with ATP. This effect required DGK η catalytic activity, as assessed using a kinase-dead (G389D) mutant and multiple truncation constructs. DGK η 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 DGK η. We found that acute activation of PKC with phorbol 12-myristate 13-acetate shortened carbachol-evoked calcium responses and occluded the effect of overexpressed DGK η. Moreover, inhibition of PKC activity with bisindolylmaleimide I (BIM I) produced the same enhancing effect on carbachol-evoked calcium mobilization as overexpressed DGK η, and overexpression of DGK η produced no additional effect on calcium mobilization in the presence of BIM I. Taken together, our data suggest that DGK η enhances GPCR signaling by reducing PKC activation.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0026895X24039221; http://dx.doi.org/10.1124/mol.113.091280; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84900454285&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/24608858; https://linkinghub.elsevier.com/retrieve/pii/S0026895X24039221; https://dx.doi.org/10.1124/mol.113.091280; https://molpharm.aspetjournals.org/content/85/5/800
Elsevier BV
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