generation of transgenic tobacco plants constitutively expressing rice diacylglycerol kinase. Overexpression results in enhanced resistance against infection by tobacco mosaic virus and Phytophthora parasitica var. nicotianae
generation of a soluble mutant selection assay based on a library of random diacylglycerol kinase delta1 mutants of sterile alpha-motif and murine dihydrofolate reductase as the selectable marker
comparison of transgenic mice with cardiac-specific overexpression of diacylglycerol kinase zeta and wild-type mice in streptozotocin-induced diabetic and non-diabetic conditions. After 8 weeks, decreases in heart weight and heart weight/body weight ratio in diabetic wild-type mice are inhibited in transgenic mice. Decreases in left ventricular end-diastolic diameter and fractional shortening observed in wild-type mice are attenuated in transgenic mice. Thinning of the interventricular septum and the posterior wall in diabetic wild-type hearts are blocked in transgenic mice. Reduction of transverse diameter of cardiomyocytes isolated from the left ventricle in diabetic wild-type mice is attenuated in transgenic mice. Cardiac fibrosis was much less in diabetic transgenic than in diabetic wild-type mice
creation of thoracic transverse aortic constriction in transgenic mice with cardiac-specific overexpression of diacylglycerol kinase zeta and wild-type mice. Increases in heart weight at 4 weeks after thoracic transverse aortic constriction are attenuated in diacylglycerol kinase zeta transgenic mice compared with wild-type mice. Increases in interventricular septal thickness, dilatation of the left ventricular cavity, and decreases in left ventricular systolic function in wild-type mice are observed at 4 weeks after surgery and are attenuated in diacylglycerol kinase zetatransgenic mice. Contrary to wild-type, cardiac fibrosis and gene induction of type I and type III collagens, but not transforming growth factor are blocked in diacylglycerol kinase zeta transgenic mice
deficiency for diacylglycerol kinase zeta results in impaired interleukin 12 and tumor necrosis factor alpha production following toll-like receptor stimulation in vitro and in vivo, increased resistance to endotoxin shock, and enhanced susceptibility to Toxoplasma gondii infection
diacylglycerol kinase zeta blocks cardiac dysfunction and progression to lethal heart failure by activated G-protein subunit alphaq protein without detectable adverse effects in the in-vivo heart
in a female patient with a de novo balanced translocation, 46,X,t(X,2)(p11.2,q37)dn, who exhibits seizures, capillary abnormality, developmental delay, infantile hypotonia, and obesity, diacylglycerol kinase delta is disrupted at 2q37.Diacylglycerol kinase delta is involved in the etiology of seizures
overexpression of wild-type diacylglycerol kinase alpha, but not of its kinase-dead mutant, markedly suppresses tumor necrosis factor alpha-induced apoptosis of AKI human melanoma cells and enhances the tumor necrosis factor alpha-stimulated transcriptional activity of transcription factor NF-kappaB. siRNA-mediated knock-down of diacylglycerol kinase alpha enhances the apoptosis. Overexpression of isoforms beta and gamma has no detectable effect on apoptosis
patients with certain forms of systematic vasculitis, such as Wegeners granulomatosis, have circulating antineutrophil cytoplasmic antibodies. Diacylglycerol kinase is selectively activated by circulating antineutrophil cytoplasmic antibodies and the generated phosphatidic acid is responsible for promoting neutrophil adhesion, in part through integrin activation
study on genetic basis of bipolar disorder. Of 37 single nucleotide polymorphisms selected for individual genotyping, the strongest association signal is detected at a marker within the diacylglycerol kinase eta. Several genes, each of modest effect, reproducibly influence disease risk. Bipolar disorder may be a polygenic disease
transgenic mice with cardiac-specific overexpression of diacylglycerol kinase zeta. Left ventricular chamber dilatation, reduction of left ventricular systolic function and increases in left ventricular weight and lung weight at 4 weeks after myocardial infarction are attenuated in transgenic mice compared with wild-type mice. In the noninfarct area, fibrosis fraction and upregulation of profibrotic genes, such as transforming growth factor-1, collagen type I, and collagen type III, are blocked in transgenic mice. Survival rate at 4 weeks after myocardial infarction is higher in transgenic mice than in wild-type
diaclyglycerol kinase activity is reduced by oxidative stress in glomerular mesangial cells cultured under high glucose conditions. Antioxidants, including D-alpha-tocopherol and probucol may improve hyperglycemia-induced diacylglycerol-protein kinase C activation by enhancing diacylglycerol kinase activity