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Literature summary for 2.7.1.107 extracted from

  • Niizeki, T.; Takeishi, Y.; Kitahara, T.; Arimoto, T.; Koyama, Y.; Goto, K.; Mende, U.; Kubota, I.
    Diacylglycerol kinase zeta rescues G alpha q-induced heart failure in transgenic mice (2008), Circ. J., 72, 309-317.
    View publication on PubMed

Application

Application Comment Organism
medicine 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 Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information generation of double transgenic mice with cardiac-specific overexpression of both diacylglycerol kinase zeta and G-protein subunit alphaq. Diacylglycerol kinase zeta prevents cardiac dysfunction, determined by dilatation of left ventricular dimensions, reduction of left ventricular fractional shortening, and marked increases in left ventricular end-diastolic pressure in G-protein subunit alphaq transgenic mice. Translocation of protein kinase C isoforms, phosphorylation activity of c-jun N-terminal kinase and p38 mitogen-activated protein kinase in G-protein subunit alphaq transgenic mice are attenuated by diacylglycerol kinase zeta?. Diacylglycerol kinase zeta improves the survival rate of G-protein subunit alphaq transgenic mice Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus Q80UP3
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Source Tissue

Source Tissue Comment Organism Textmining