1 ated death, presumably through activation of P2Z receptors.

2 otides; 3) oxidized ATP, an inhibitor of the P2z receptor, abolished the response.

3 d cytotoxic agents that act independently of P2Z receptor activation is also presented.

4 eby modulating macrophage cell death through P2Z receptor activation.

5 KN-04) potently inhibit the human lymphocyte P2Z receptor, an ATP-gated cation channel.

6 ed by benzoylbenzoic ATP (a known agonist of P2Z receptors) and blocked by oxidized ATP, DIDS, surami

7                                ATP acted via P2Z receptors because these effects were mimicked by ben

8 s and their respective regulation by P2U and P2Z receptors can be used to co-ordinate membrane transp

9 d to 0.1 mM Mg(2+), where surface-associated P2Z receptors could not be activated, were not susceptib

10 rgely NHE1-like activity, and stimulation of P2Z receptors expressed in the LM activated largely NHE2

11 ugh the molecular identity of the lymphocyte P2Z receptor has not been established, it shares many fu

12  that duct and possibly acinar cells express P2z receptors in the luminal and P2u receptors in the ba

13 s been cloned and emphasized as a prototypic P2Z receptor involved in neurotransmission in the centra

14                                              P2z receptors mediated these effects because: 1) reducti

15                         It is suggested that P2Z receptor-mediated signaling could be involved in the

16 e better agonists than ATP in activating the P2Z receptors or may act through the activation of addit

17 s macrophage-or mast cell surface-associated P2Z receptors promote their cell death in the presence o

18 s with purified Ndk/ATPase and hyperproduced P2Z receptor protein will demonstrate whether these enzy

19 acteria to sequester ATP from the macrophage P2Z receptors, thereby preventing phagosome-lysosome fus

20  activation of macrophage surface-associated P2Z receptors, whose activation has been postulated to a