Relationship of inositol phospholipid metabolism to phospholipase A2.
The mechanism by which agonists stimulate phospholipase A2 of platelets is still much of a mystery. We have presented a discussion that suggests that neither Ca2+, protein kinase C or dissociation of the inhibitory GTP-binding protein Gi is solely responsible for activating this enzyme. We cannot exclude the possibility that there may be some contribution of each pathway for some agonists, and that the contribution may change with agonist concentration or potency. These possibilities await further clarification.
Lapetina
E G
EG
Molecular Biology Department, Burroughs Wellcome Co., Research Triangle Park, N.C. 27709.
Crouch
M F
MF
D001792:Blood Platelets / Q000378:metabolism*; D004075:Diglycerides / Q000097:blood; D019204:GTP-Binding Proteins / Q000097:blood; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000097:blood*; D010740:Phospholipases / Q000097:blood*; D010741:Phospholipases A / Q000097:blood*; D054467:Phospholipases A2; D013403:Sugar Phosphates / Q000097:blood*; D013917:Thrombin / Q000502:physiology; D010738:Type C Phospholipases / Q000097:blood*
D004075:Diglycerides; D007295:Inositol Phosphates; D013403:Sugar Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D010740:Phospholipases; D010741:Phospholipases A; D054467:Phospholipases A2; D010738:Type C Phospholipases; D013917:Thrombin; D019204:GTP-Binding Proteins