Disease relevance of Dgkz

• Selective translocation of diacylglycerol kinase zeta in hippocampal neurons under transient forebrain ischemia [1].
• CONCLUSIONS: These results demonstrated the first evidence that DGKzeta negatively regulated the hypertrophic signaling cascade and resultant cardiac hypertrophy in response to GPCR agonists without detectable adverse effects in in vivo hearts [2].
• Adenovirus-mediated overexpression of diacylglycerol kinase-zeta inhibits endothelin-1-induced cardiomyocyte hypertrophy [3].
• DGK I and DGK IV give different peptide maps after digestion with Staphylococcus aureus V8 protease or alpha-chymotrypsin [4].

High impact information on Dgkz

• However, DGK-IV was expressed primarily in the thymus and brain with relatively low expression in the eye and intestine [5].
• Furthermore, the primary structure of the DGK-IV included a nuclear targeting motif, and immunocytochemical analysis revealed DGK-IV to localize in the nucleus of COS-7 cells transfected with the epitope-tagged cDNA, suggesting an involvement of DGK-IV in intranuclear processes [5].
• A 104-kDa diacylglycerol kinase containing ankyrin-like repeats localizes in the cell nucleus [5].
• These enzymes both phosphorylate 1,2-dioleoyl glycerol at rates of 11.5 mumol/min/mg protein for DGK I and 5.2 mumol/min/mg protein for DGK IV [4].
• In addition, we have used deletion mutants to show that nuclear transport of DGK zeta depends on a cooperative interaction between the NLS and the C-terminal region including ankyrin repeats in a manner which suggests that the NLS is a cryptic site whose exposure is regulated by the C-terminal region [6].

Anatomical context of Dgkz

• DGKzeta protein in the LV myocardium translocated from the particulate to the cytosolic compartment in the aortic-banded rats [7].
• Intense expression signals for DGKzeta and -alpha were observed in the theca cells and moderate signals in the interstitium and corpora lutea of the ovary [8].
• DGKzeta signals were observed in all cellular components of the labyrinthine zone, including mesenchyme, trabecular trophoblasts, and cytotrophoblasts [8].
• In infarcted hearts, the expression of DGKzeta was enhanced in the peripheral zone of the necrotic area and at the border zone 3 and 7 days after MI, and to a lesser extent in the middle layer of the granulation tissue 21 days after MI [9].
• The enhanced DGKzeta expression in the infarcted and border areas could be attributed to granulocytes and macrophages [9].

Associations of Dgkz with chemical compounds

• Phenylephrine-induced increases in myocardial diacylglycerol levels were completely blocked in DGKzeta-TG mouse hearts, suggesting that DGKzeta regulated PKC activity by controlling cellular diacylglycerol levels [2].

Regulatory relationships of Dgkz

• ET-1-induced translocation of PKC-epsilon was blocked by Ad-DGKzeta (P<0.01) [3].

Other interactions of Dgkz

• METHODS AND RESULTS: Real-time reverse transcription-polymerase chain reaction demonstrated a significant increase of DGK-zeta mRNA by ET-1 in cardiomyocytes [3].
• At 28 days after surgery, the expression of DGKepsilon mRNA but not DGKzeta or PAP2b mRNA in the LV myocardium significantly decreased in the aortic-banded rats compared with the sham-operated rats [7].

Analytical, diagnostic and therapeutic context of Dgkz

• DGKzeta expression was evaluated by immunohistochemistry using affinity-purified anti-DGKzeta antibody [1].

References