Tumor promoters and diacylglycerol activate the Na+/H+ antiporter of sea urchin eggs.
Various tumor promoters (TPA, lyngbyatoxin and aplysiatoxin) and diacylglycerol induced cytoplasmic alkalinization of sea urchin eggs independently of intracellular Ca2+ release. This response stimulated protein synthesis and was blocked by amiloride or a lack of extracellular Na+, procedures which inhibit the Na+/H+ antiporter. These results suggest that the antiporter which is responsible for cytoplasmic alkalinization in sea urchin eggs is activated directly or indirectly by protein kinase C in a Ca2+-independent manner.
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002273:Carcinogens / Q000494:pharmacology*; D002352:Carrier Proteins / Q000378:metabolism*; D004075:Diglycerides / Q000494:pharmacology*; D005989:Glycerides / Q000494:pharmacology*; D006863:Hydrogen-Ion Concentration; D008235:Lyngbya Toxins / Q000494:pharmacology; D010063:Ovum / Q000378:metabolism*; D014176:Protein Biosynthesis; D011493:Protein Kinase C / Q000378:metabolism; D012617:Sea Urchins; D017923:Sodium-Hydrogen Exchangers; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D002273:Carcinogens; D002352:Carrier Proteins; D004075:Diglycerides; D005989:Glycerides; D008235:Lyngbya Toxins; D017923:Sodium-Hydrogen Exchangers; C006610:aplysiatoxin; D000584:Amiloride; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate; C019457:lyngbyatoxin A