| | Name | Initial Conc. (uM) | Volume (fL) | Buffered |
| 1 | AA | 0 | 1000 | No |
| | |
| 2 | BetaGamma | 0 | 1000 | No |
| | These exist in a nebulous sense in this model, basically only to balance the conservation equations. The details of their reassociation with G-GDP are not modeled Resting level =0.0094, stim level =.0236 from all42.g ish. |
| 3 | Ca | 0.08 | 1000 | Yes |
| | |
| 4 | CaM(Ca)n-CaNAB | 0 | 1000 | No |
| | |
| 5 | CaM-Ca3 | 0 | 1000 | No |
| | |
| 6 | CaM-Ca4 | 0 | 1000 | No |
| | |
| 7 | CaM-TR2-Ca2 | 0 | 1000 | No |
| | This is the intermediate where the TR2 end (the high-affinity end) has bound the Ca but the TR1 end has not. |
| 8 | cAMP | 0 | 1000 | No |
| | The conc of this has been a problem. Schaecter and Benowitz use 50 uM, but Shinomura et al have < 5. So I have altered the cAMP-dependent rates in the PKA model to reflect this. |
| 9 | CaNAB-Ca4 | 0 | 1000 | No |
| | |
| 10 | DAG | 0 | 1000 | No |
| | |
| 11 | G*GDP | 0 | 1000 | No |
| | |
| 12 | G*GTP | 0 | 1000 | No |
| | Activated G protein. Berstein et al indicate that about 20-40% of the total Gq alpha should bind GTP at steady stim. This sim gives more like 65%. |
| 13 | Glu | 0 | 1000 | Yes |
| | Varying the amount of (steady state) glu between .01 uM and up, the final amount of G*GTP complex does not change much. This means that the system should be reasonably robust wr to the amount of glu in the synaptic cleft. It would be nice to know how fast it is removed. |
| 14 | Gs-alpha | 0 | 1000 | No |
| | |
| 15 | IP3 | 0.73 | 1000 | No |
| | Peak IP3 is perhaps 15 uM, basal <= 0.2 uM. |
| 16 | MAPK* | 0 | 1000 | No |
| | |
| 17 | MKP-1 | 0.0024 | 1000 | No |
| | MKP-1 dephosphoryates and inactivates MAPK in vivo: Sun et al Cell 75 487-493 1993. Levels of MKP-1 are regulated, and rise in 1 hour. Kinetics from Charles et al PNAS 90:5292-5296 1993. They refer to Charles et al Oncogene 7 187-190 who show that half-life of MKP1/3CH134 is 40 min. 80% deph of MAPK in 20 min Sep 17 1997: CoInit now 0.4x to 0.0032. See parm searches from jun96 on. |
| 18 | PIP2 | 10 | 1000 | Yes |
| | |
| 19 | PKA-active | 0 | 1000 | No |
| | |
| 20 | PKC-active | 0.02 | 1000 | No |
| | |
| 21 | PP1-active | 1.8 | 1000 | No |
| | Cohen et al Meth Enz 159 390-408 is main source of info conc = 1.8 uM |
| 22 | PP2A | 0.12 | 1000 | No |
| | |
| 23 | PPhosphatase2A | 0.224 | 1000 | No |
| | Refs: Pato et al Biochem J 293:35-41(93); Takai&Mieskes Biochem J 275:233-239 k1=1.46e-4, k2=1000,k3=250. these use kcat values for calponin. Also, units of kcat may be in min! revert to Vmax base: k3=6, k2=25,k1=3.3e-6 or 6,6,1e-6 CoInit assumed 0.1 uM. See NOTES for MAPK_Ras50.g. CoInit now 0.08 Sep 17 1997: Raise CoInt 1.4x to 0.224, see parm searches from jun 96 on. |
| 24 | Shc*.Sos.Grb2 | 0 | 1000 | No |
| | |
| 25 | temp-PIP2 | 2.5 | 1000 | Yes |
| | This isn't explicitly present in the M&L model, but is obviously needed. I assume its conc is fixed at 1uM for now, which is a bit high. PLA2 is stim 7x by PIP2 @ 0.5 uM (Leslie and Channon BBA 1045:261(1990) Leslie and Channon say PIP2 is present at 0.1 - 0.2mol% range in membs, which comes to 50 nM. Ref is Majerus et al Cell 37 pp 701-703 1984 Lets use a lower level of 30 nM, same ref.... |
