E-Conference: Defining Calcium Entry Signals
Calcium entry at low agonist concentrations
17 June 2004
I would be interested in hearing your opinion on the following questions:
1. How general (ubiquitous) do you think ARC is in comparison to SOC? Do you envisage these two mechanisms to always act as a tandem (ying-yanging at different agonist concentrations)? Is ARC regulated (i.e. do you see larger/ smaller ARC in say preactivated cells)?
2. How do you see the signaling cascades for typical PLC-coupled agonists (considering that in RBL and Jurkats both PLCbeta and PLCgamma converge on the same SOC)? Does every PLC-coupled receptor produce both AA and IP3? And how would that be transduced?
3. What about the Ca2+ dependence of ARC? You say it's inactivated by Ca2+ (via calcineurin). But CRAC is also very strongly inhibited by Ca2+ entry, so much so that we can't detect it when we leave the cytosol unbuffered. Wouldn't ARC actually limit CRAC if it preceded it rather than CRAC inhibiting ARC?
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