INT119529

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Context Info
Confidence 0.60
First Reported 2001
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 16
Total Number 18
Disease Relevance 1.49
Pain Relevance 8.94

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
hypothalamus 2
cardiac myocytes 2
retina 2
neurons 2
Camk2a (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 88 100.00 Very High Very High Very High
midbrain 5 100.00 Very High Very High Very High
Morphine 104 99.84 Very High Very High Very High
Opioid 22 99.84 Very High Very High Very High
tolerance 36 99.56 Very High Very High Very High
long-term potentiation 346 99.38 Very High Very High Very High
addiction 7 99.00 Very High Very High Very High
Antinociceptive 6 98.52 Very High Very High Very High
Intracerebroventricular 5 98.44 Very High Very High Very High
Spinal cord 124 98.04 Very High Very High Very High
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 20 100.00 Very High Very High Very High
Ganglion Cysts 6 83.60 Quite High
Hypertrophy 12 81.52 Quite High
Nociception 38 77.08 Quite High
Inflammatory Pain 9 74.80 Quite High
Coronary Heart Disease 39 74.24 Quite High
Neuropathic Pain 16 72.72 Quite High
Pain 39 63.72 Quite High
Body Weight 17 62.88 Quite High
Natriuresis 15 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, enhanced phosphorylation by CaMKII may be involved in the altered levels of NMDA-receptor subunits observed here, but this remains to be tested.
Positive_regulation (enhanced) of Phosphorylation (phosphorylation) of CaMKII
1) Confidence 0.60 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC32198 Disease Relevance 0.15 Pain Relevance 0.18
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.


Positive_regulation (augment) of Phosphorylation (autophosphorylation) of CaMKII
2) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0
To test whether sustained activation of CaMKII takes place in living Purkinje neurons, we stained active CaMKII autophosphorylated at Thr286 (in the ?
Positive_regulation (active) of Phosphorylation (autophosphorylated) of CaMKII in neurons
3) Confidence 0.49 Published 2009 Journal Mol Syst Biol Section Body Doc Link PMC2710870 Disease Relevance 0 Pain Relevance 0.08
It seems that CaMKII phosphorylation of PhLPl stabilizes the PhLPl.Gbetagamma complex by promoting its binding to 14-3-3 proteins.
Positive_regulation (stabilizes) of Phosphorylation (phosphorylation) of CaMKII
4) Confidence 0.47 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.
Positive_regulation (increased) of Phosphorylation (phosphorylated) of p-CaMKII in brain associated with urological neuroanatomy, midbrain and morphine
5) Confidence 0.44 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207359 Disease Relevance 0.10 Pain Relevance 1.07
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.
Positive_regulation (increased) of Phosphorylation (phosphorylated) of phosphorylated-CaMKII in brain associated with urological neuroanatomy, midbrain and morphine
6) Confidence 0.44 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207359 Disease Relevance 0.10 Pain Relevance 1.07
To determine if GluR1 phosphorylation by CaMKII in vivo is altered in the rdta retina, the SPM proteins of the rdta retina and their littermate controls are back phosphorylated by endogenous CaMKII in the presence of Ca2+/CaM (1 mM CaCl2 and 0.02 mg/ml calmodulin).
Positive_regulation (presence) of Phosphorylation (phosphorylated) of CaMKII in retina
7) Confidence 0.43 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC32198 Disease Relevance 0 Pain Relevance 0
Phosphorylation of neurogranin, protein kinase C, and Ca2+/calmodulin dependent protein kinase II in opioid tolerance and dependence.
Positive_regulation (dependent) of Phosphorylation (Phosphorylation) of calmodulin dependent protein kinase II associated with addiction, kinase c, tolerance and opioid
8) Confidence 0.43 Published 2006 Journal Neurosci. Lett. Section Title Doc Link 16824682 Disease Relevance 0 Pain Relevance 1.37
Note that the transient, peak phosphorylation of both CaMKII and ERK occured within 5–10 min of HFS, while phosphorylation of CREB reached its peak approximately 2–3 h after HFS.
Positive_regulation (occured) of Phosphorylation (phosphorylation) of CaMKII
9) Confidence 0.42 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0.06 Pain Relevance 0.75
We further examined the effects of EphB2-Fc application and targeted mutation of the EphB1 receptor on HFS-induced phosphorylation of CaMKII, ERK and CREB proteins and c-Fos expression.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of CaMKII
10) Confidence 0.42 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0 Pain Relevance 0.34
This study presents the first description of the time course of HFS-induced phosphorylation of CaMKII, ERK and CREB and altered expression of c-Fos in the SC of mice and rats.
Positive_regulation (induced) of Phosphorylation (phosphorylation) of CaMKII associated with spinal cord
11) Confidence 0.42 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0.06 Pain Relevance 0.75
Targeted mutation of the EphB1 gene successfully prevented development of LTP and suppressed the associated activation (phosphorylation) of CaMKII, ERK, and CREB as well as increased c-Fos expression.
Positive_regulation (activation) of Phosphorylation (phosphorylation) of CaMKII associated with long-term potentiation
12) Confidence 0.39 Published 2009 Journal Mol Pain Section Body Doc Link PMC2704201 Disease Relevance 0 Pain Relevance 0.39
Indeed, these changes are associated with the activating Thr286 autophosphorylation of CaMKII.
Positive_regulation (activating) of Phosphorylation (autophosphorylation) of CaMKII
13) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0 Pain Relevance 1.19
In control mice chronic Ang II or ISO treatment significantly increased cardiac CaMKII autophosphorylation.
Positive_regulation (increased) of Phosphorylation (autophosphorylation) of CaMKII
14) Confidence 0.34 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.28 Pain Relevance 0
In contrast, ISO treatment did not further increase pCaMKII levels in hearts of CM GC-A KO mice (Fig. 6b).Fig. 6Effect of chronic Ang II (a) or ISO infusion (b) on the cardiac expression and autophosphorylation of CaMKII.
Neg (not) Positive_regulation (increase) of Phosphorylation (autophosphorylation) of CaMKII in hearts
15) Confidence 0.34 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.26 Pain Relevance 0
Bottom levels of phosphorylated CaMKII were normalized to the total levels of CaMKII and calculated as X-fold respective vehicle-treated control mice; (n = 8; *P < 0.05 when compared with vehicle; #P < 0.05 compared with controls)

TRPC3/C6 channels are involved in the calcium responses of adult cardiac myocytes to Ang II, but not to ISO

Positive_regulation (calculated) of Phosphorylation (phosphorylated) of CaMKII in cardiac myocytes
16) Confidence 0.34 Published 2010 Journal Basic Res Cardiol Section Body Doc Link PMC2916114 Disease Relevance 0.12 Pain Relevance 0
In the immunoblot assay, the increases of phosphorylated extracellular signal-regulated protein kinase (pERK) as well as phosphorylated calcium/calmodulin-dependent protein kinase IIalpha (pCaMK-IIalpha) expression induced by noxious stimuli were attenuated by intracerebroventricular (i.c.v.) beta-endorphin pretreatment in the hypothalamus, but not by i.c.v. morphine pretreatment.
Positive_regulation (induced) of Phosphorylation (phosphorylated) of pCaMK-IIalpha in hypothalamus associated with intracerebroventricular and morphine
17) Confidence 0.34 Published 2008 Journal Neuropeptides Section Abstract Doc Link 18359081 Disease Relevance 0.07 Pain Relevance 0.48
CaMKII may indirectly mediate the phosphorylation of GluR1 at the Serine845 site through adenylate cyclase and PKA, since the Ca2+-calmodulin complex can stimulate adenylate cyclase, and subsequently activate more cAMP production and PKA activity.
Positive_regulation (through) of Phosphorylation (phosphorylation) of CaMKII
18) Confidence 0.29 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.29 Pain Relevance 0.50

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