INT114729

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Context Info
Confidence 0.82
First Reported 2001
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 110
Total Number 111
Disease Relevance 15.49
Pain Relevance 33.19

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

plasma membrane (Camk2a) kinase activity (Camk2a) cytoplasm (Camk2a)
Anatomy Link Frequency
brain 4
hippocampus 4
synapses 4
neurons 3
retina 2
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 461 100.00 Very High Very High Very High
Kinase C 450 100.00 Very High Very High Very High
opioid receptor 438 100.00 Very High Very High Very High
Calcium channel 29 100.00 Very High Very High Very High
Hippocampus 351 99.92 Very High Very High Very High
Opioid 81 99.84 Very High Very High Very High
central sensitization 80 99.84 Very High Very High Very High
Morphine 472 99.70 Very High Very High Very High
long-term potentiation 1018 99.66 Very High Very High Very High
Pain 416 99.60 Very High Very High Very High
Disease Link Frequency Relevance Heat
Injury 182 99.84 Very High Very High Very High
Morphine Dependence 27 99.56 Very High Very High Very High
INFLAMMATION 166 99.44 Very High Very High Very High
Pain 484 98.80 Very High Very High Very High
Neuropathic Pain 194 98.60 Very High Very High Very High
Targeted Disruption 1081 98.48 Very High Very High Very High
Urological Neuroanatomy 98 98.32 Very High Very High Very High
Repression 8 97.12 Very High Very High Very High
Nervous System Injury 66 96.32 Very High Very High Very High
Stress 97 96.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
While the autophosphorylation and dephosphorylation of CaMKII support the hypothesis that it can act as a "molecular switch" in plasticity and memory, recent studies favor a more sophisticated frequency-dependent biphasic modulation of CaMKII in learning-related synapses.
Phosphorylation (autophosphorylation) of CaMKII in synapses
1) Confidence 0.82 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.16 Pain Relevance 0.11
The ability of CaMKII to autophosphorylate, which prolongs activation in a CaM independent manner, supports an important role for CaMKII in synaptic plasticity [2].
Phosphorylation (autophosphorylate) of CaMKII
2) Confidence 0.82 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.15 Pain Relevance 0.09
The contribution of autophosphorylated alpha-calcium-calmodulin kinase II to injury-induced persistent pain.
Phosphorylation (autophosphorylated) of alpha-calcium-calmodulin kinase II associated with pain, nociceptor, lasting pain and injury
3) Confidence 0.82 Published 2004 Journal Neuroscience Section Title Doc Link 15464294 Disease Relevance 1.05 Pain Relevance 0.70
The ability of CaMKII to autophosphorylate, which prolongs activation in a CaM independent manner, supports an important role for CaMKII in synaptic plasticity [2].
Phosphorylation (autophosphorylate) of CaMKII
4) Confidence 0.81 Published 2006 Journal Mol Pain Section Body Doc Link PMC1513196 Disease Relevance 0.15 Pain Relevance 0.09
Thus, CaMKII autophosphorylation seems to augment the CaMKII activity soon after the [Ca2+]i increase, whereas the PDE1 inhibition pathway seems to attenuate the CaMKII inactivation later, presumably through suppressing the PP-1 activity.


Phosphorylation (autophosphorylation) of CaMKII
5) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
The rate (kcat) of CaMKII autophosphorylation predominantly determined the CaMKII activity.
Phosphorylation (autophosphorylation) of CaMKII
6) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Additionally, autophosphorylation of CaMKII at Thr286 in the ?
Phosphorylation (autophosphorylation) of CaMKII
7) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.09
To test whether sustained activation of CaMKII takes place in living Purkinje neurons, we stained active CaMKII autophosphorylated at Thr286 (in the ?
Phosphorylation (autophosphorylated) of CaMKII in neurons
8) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.08
The affinity of a type of PDE1 (PDE1B) to Ca2+/CaM is reduced to one sixth by CaMKII-mediated phosphorylation (Hashimoto et al, 1989).
Phosphorylation (phosphorylation) of CaMKII-mediated
9) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0.05 Pain Relevance 0.18
Experimental and simulation studies have suggested that autophosphorylation of CaMKII Thr286/287 works as a key positive-feedback loop for the long-term synaptic plasticity (Bhalla and Iyengar, 1999; Lisman et al, 2002; Hayer and Bhalla, 2005; Miller et al, 2005; Sanhueza et al, 2007; Urakubo et al, 2008).
Phosphorylation (autophosphorylation) of CaMKII
10) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Figure 5B shows the strength of CaMKII autophosphorylation and that of PDE1 phosphorylation required to maintain certain levels of CaMKII activity after the transient [Ca2+]i stimulation.
Phosphorylation (autophosphorylation) of CaMKII
11) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
Thus, the activity level of CaMKII seemed to mainly rely on the CaMKII autophosphorylation rather than PDE1 inhibition.
Phosphorylation (autophosphorylation) of CaMKII
12) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
When the kcat of CaMKII autophosphorylation was too high, CaMKII automatically shifted to a high-activity state with the basal [Ca2+]i (Figure 5C).
Phosphorylation (autophosphorylation) of CaMKII
13) Confidence 0.80 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
However, when the kcat of CaMKII autophosphorylation was too high, the CaMKII activity automatically shifted to a high state even in the basal condition (see Figure 5).
Phosphorylation (autophosphorylation) of CaMKII
14) Confidence 0.79 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
In the RP suppression, strong CaMKII autophosphorylation at Thr286/287 caused by the large [Ca2+]i increase seems to be counteracted by potent activation of PP-1 synergistically brought about by the calcineurin activity triggered by the [Ca2+]i increase and the GABABR-mediated downregulation of adenylyl cyclase activity.
Phosphorylation (autophosphorylation) of CaMKII
15) Confidence 0.79 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.03
M during the 10-s [Ca2+]i increase, the total CaMKII activity and GABAAR phosphorylation rapidly returned to the basal levels after the conditioning stimulation (Figure 2A and B, blue lines).
Phosphorylation (phosphorylation) of CaMKII
16) Confidence 0.79 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.05
The synergistic action of CaMKII autophosphorylation at Thr286/287 and PDE1 inhibition by CaMKII underlies the state switching of molecular networks regulating RP.
Phosphorylation (autophosphorylation) of CaMKII
17) Confidence 0.79 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.04
To further clarify the role of each positive-feedback loop, the effect of altering the strength of each phosphorylation on the CaMKII activity was examined.
Phosphorylation (phosphorylation) of CaMKII
18) Confidence 0.79 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
It seems that CaMKII phosphorylation of PhLPl stabilizes the PhLPl.Gbetagamma complex by promoting its binding to 14-3-3 proteins.
Phosphorylation (phosphorylation) of CaMKII
19) Confidence 0.77 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18006024 Disease Relevance 0 Pain Relevance 0.76
The levels of phosphorylated-CaMKII (p-CaMKII) in the limbic forebrain, but not in the frontal cortex and the lower midbrain, were significantly increased in morphine-conditioned mice, whereas the levels of CaMKII in three brain regions obtained from morphine-conditioned mice were not changed.
Phosphorylation (phosphorylated) of p-CaMKII in brain associated with urological neuroanatomy, midbrain and morphine
20) Confidence 0.71 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207359 Disease Relevance 0.10 Pain Relevance 1.04

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