|
Enter a Search String | Special character and space not allowed in the query term.
Search string should be at least 2 characters long. |
Molecule List for Accession CaMKII_2003 (Accession Number49) | Default ordering is done according to Pathway Number. Table headers can be used for changing the default ordering. arrow indicates that ordering is done according to ascending or descending order. The entries are grouped according to Pathway Number and are alternately color coded using and color. |
|
Name | Pathway Name / Pathway No. | Accession Type | Initial Conc. (uM) | Volume (fL) | Buffered | Sum Total Of | 1 | tot_CaM_CaMKII | CaMKII
Pathway No. 202 | Network | 0 | 1000 | No | CaMKII-CaM CaMKII-thr286*-C aM
| 2 | tot_autonomous_ CaMKII | CaMKII
Pathway No. 202 | Network | 0 | 1000 | No | CaMKII-thr286 CaMKII***
| 3 | PP2A | Shared_Object_ CaMKII_2003 Pathway No. 201Network | 0.12 | 1000 | No | - | 4 | PP1-I1* | PP1
Pathway No. 204 | Network | 0 | 1000 | No | - | 5 | PP1-I1 | PP1
Pathway No. 204 | Network | 0 | 1000 | No | - | 6 | PP1-active | Shared_Object_ CaMKII_2003 Pathway No. 201Network | 1.8 | 1000 | No | - | | | Cohen et al Meth Enz 159 390-408 is main source of info conc = 1.8 uM | 7 | PKC-active | Shared_Object_ CaMKII_2003 Pathway No. 201Network | 0.09 | 1000 | Yes | - | 8 | PKA-active | Shared_Object_ CaMKII_2003 Pathway No. 201Network | 0.015 | 1000 | Yes | - | 9 | neurogranin-CaM | CaM
Pathway No. 203 | Network | 0 | 1000 | No | - | 10 | neurogranin* | CaM
Pathway No. 203 | Network | 0 | 1000 | No | - | | The phosph form does not bind CaM (Huang et al ABB 305:2 570-580 1993) | 11 | neurogranin | CaM
Pathway No. 203 | Network | 10 | 1000 | No | - | | Also known as RC3 and p17 and BICKS. Conc in brain >> 2 uM from Martzen and Slemmon J neurosci 64 92-100 1995 but others say less without any #s. Conc in dend spines is much higher than overall, so it could be anywhere from 2 uM to 50. We will estimate 10 uM as a starting point. Gerendasy et al JBC 269:35 22420-22426 1994 have a skeleton model (no numbers) indicating CaM-Ca(n) binding .... | 12 | I1* | PP1
Pathway No. 204 | Network | 0.001 | 1000 | No | - | | Dephosph is mainly by PP2B | 13 | I1 | PP1
Pathway No. 204 | Network | 1.8 | 1000 | No | - | | I1 is a 'mixed' inhibitor, but at high enz concs it looks like a non-compet inhibitor (Foulkes et al Eur J Biochem 132 309-313 9183). We treat it as non-compet, so it just turns the enz off without interacting with the binding site. Cohen et al ann rev bioch refer to results where conc is 1.5 to 1.8 uM. In order to get complete inhib of PP1, which is at 1.8 uM, we need >= 1.8 uM. | 14 | CaNAB-Ca4 | Shared_Object_ CaMKII_2003 Pathway No. 201Network | 0 | 1000 | No | - | 15 | CaNAB-Ca2 | PP2B
Pathway No. 205 | Network | 0 | 1000 | No | - | 16 | CaNAB | PP2B
Pathway No. 205 | Network | 1 | 1000 | No | - | | We assume that the A and B subunits of PP2B are always bound under physiol conditions. Up to 1% of brain protein = 25 uM. I need to work out how it is distributed between cytosolic and particulate fractions. Tallant and Cheung '83 Biochem 22 3630-3635 have conc in many species, average for mammalian brain is around 1 uM. | 17 | CaMKII-thr286*-C aM | CaMKII
Pathway No. 202 | Network | 0 | 1000 | No | - | | From Hanson and Schulman, the thr286 is responsible for autonomous activation of CaMKII. | 18 | CaMKII-thr286 | CaMKII
Pathway No. 202 | Network | 0 | 1000 | No | - | | I am not sure if we need to endow this one with a lot of enzs. It is likely to be a short-lived intermediate, since it will be phosphorylated further as soon as the CAM falls off. | 19 | CaMKII-CaM | CaMKII
Pathway No. 202 | Network | 0 | 1000 | No | - | 20 | CaMKII*** | CaMKII
Pathway No. 202 | Network | 0 | 1000 | 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. | | | | |
| Database compilation and code copyright (C) 2022, Upinder S. Bhalla and NCBS/TIFR This Copyright is applied to ensure that the contents of this database remain freely available. Please see FAQ for details. |
|