Shared_Object_
CaMKII_noPKA_
model3
Pathway No. 257Network | 0 | 0.01 | No | - | 14 | CaM-PSD | CaM
Pathway No. 259 | Network | 26.3333 | 0.01 | No | - |
| There is a LOT of this in the cell: upto 1% of total protein mass. (Alberts et al) Say 25 uM. Meyer et al Science 256 1199-1202 1992 refer to studies saying it is comparable to CaMK levels. |
15 | CaM-TR2-Ca2 | Shared_Object_ CaMKII_noPKA_ model3 Pathway No. 257Network | 0 | 0.09 | No | - | |
| This is the intermediate where the TR2 end (the high-affinity end) has bound the Ca but the TR1 end has not. |
16 | CaM-TR2-Ca2-PSD | Shared_Object_ CaMKII_noPKA_ model3 Pathway No. 257Network | 0 | 0.01 | No | - | |
| This is the intermediate where the TR2 end (the high-affinity end) has bound the Ca but the TR1 end has not. |
17 | CaMK-thr305 | CaMKII
Pathway No. 258 | Network | 0 | 0.09 | No | - |
| This forms due to basal autophosphorylation, but I think it has to be considered as a pathway even if some CaM is floating around. In either case it will tend to block further binding of CaM, and will not display any enzyme activity. See Hanson and Schulman JBC 267:24 pp17216-17224 1992 |
18 | CaMKII | CaMKII
Pathway No. 258 | Network | 20 | 0.09 | No | - |
| Huge conc of CaMKII. In PSD it is 20-40% of protein, so we assume it is around 2.5% of protein in spine as a whole. This level is so high it is unlikely to matter much if we are off a bit. |
19 | CaMKII*** | CaMKII
Pathway No. 258 | Network | 0 | 0.09 | No | - |
| From Hanson and Schulman, the CaMKII does a lot of autophosphorylation just after the CaM is released. This prevents further CaM binding and renders the enzyme quite independent of Ca. |
20 | CaMKII***-PSD | Shared_Object_ CaMKII_noPKA_ model3 Pathway No. 257Network | 0 | 0.01 | No | - | |