INT136650

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Context Info
Confidence 0.51
First Reported 2001
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 18
Total Number 19
Disease Relevance 1.57
Pain Relevance 1.39

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

cytosol (Calm2) nucleoplasm (Calm2) cytoskeleton (Calm2)
cell cycle (Calm2) cellular_component (Calm2) biological_process (Calm2)
Anatomy Link Frequency
neurons 1
pituitary 1
Calm2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
analgesia 1 99.96 Very High Very High Very High
Kinase C 78 99.84 Very High Very High Very High
agonist 94 98.32 Very High Very High Very High
Dopamine 92 95.76 Very High Very High Very High
sodium channel 6 89.52 High High
addiction 98 87.00 High High
Peripheral nervous system 1 85.60 High High
Neurotransmitter 19 85.28 High High
antagonist 10 83.72 Quite High
Pyramidal cell 48 82.68 Quite High
Disease Link Frequency Relevance Heat
Status Epilepticus 114 99.20 Very High Very High Very High
Toxicity 2 95.16 Very High Very High Very High
Death 12 95.04 Very High Very High Very High
Ganglion Cysts 112 87.12 High High
Epilepsy 32 84.24 Quite High
Apoptosis 25 81.32 Quite High
Nociception 1 81.04 Quite High
INFLAMMATION 24 71.80 Quite High
Gliosis 8 71.24 Quite High
Convulsion 36 61.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The calmodulin (CaM) inhibitor trifluoperazine (TFP) can produce analgesia when given intrathecally to rats; however, the mechanism is not known.
Gene_expression (produce) of CaM associated with analgesia
1) Confidence 0.51 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16807347 Disease Relevance 0.08 Pain Relevance 0.43
Finally, the effect of CaM overexpression on Siah1a function was assessed.


Gene_expression (overexpression) of CaM
2) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.36 Pain Relevance 0.06
In this case, it must be assumed that under control conditions (cells heterologously expressing only the receptors), mGluRs associate with natively-expressed CaM.
Gene_expression (expressed) of CaM
3) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
CaM expression levels would presumably be much lower natively than in cells injected with CaM cDNA.
Gene_expression (expression) of CaM
4) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
It should also be noted that coexpression of CaM with mGluR5a in the absence of Siah1a yields no changes in calcium current modulation (data not shown).
Gene_expression (coexpression) of CaM
5) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
Next, when CaM was coexpressed with mGluR5b and Siah1a, calcium current modulation was significantly increased (over that in cells expressing mGluR5b and Siah1a) to 25 ± 5% (n = 12; figure 6).
Gene_expression (coexpressed) of CaM
6) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
Finally, coexpression of CaM reversed the effect of Siah1a on mGluR5b, indicating that the interaction of CaM and Siah1a in binding to group I mGluRs plays a novel and important role in mGluR function.


Gene_expression (coexpression) of CaM
7) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.07 Pain Relevance 0.03
Therefore, overexpression of CaM was tested for its ability to reverse the effect of Siah1a.
Gene_expression (overexpression) of CaM
8) Confidence 0.44 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
The reduced CaM expression in our study is also interesting since there is extensive evidence that CaM plays a critical role in the induction of cell death following Ca2+ overload, and inhibition of CaM function can protect neurons from death [48], [49].
Gene_expression (expression) of CaM in neurons associated with death
9) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2873964 Disease Relevance 0.73 Pain Relevance 0.10
The expression of calmodulin 1 (CaM1) and calmodulin 2 (CaM2) were down-regulated (?
Gene_expression (expression) of calmodulin 2
10) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2873964 Disease Relevance 0.32 Pain Relevance 0.10
To determine whether PKC or Ca2+/CaM were responsible for M1 mACh receptor-mediated MARCKS translocation the following protocol was used.
Gene_expression (/) of CaM associated with kinase c
11) Confidence 0.12 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.30
Finally, our new results about the end-stage effects of CDI, together with rapid advances concerning the early events underlying Ca2+/CaM modulation of CaV1/2 channels, set the stage for investigating the events that link these two realms.
Gene_expression (modulation) of CaM
12) Confidence 0.12 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2828906 Disease Relevance 0 Pain Relevance 0
Second, a single tethered CaM would be insufficient to trigger persistent activation of CaMKII, which has ?
Gene_expression (tethered) of CaM
13) Confidence 0.08 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
The millimolar peak levels of [Ca2+]i attained when channels are open will far exceed CaM's EC50 of 5–10 ?
Gene_expression (exceed) of CaM
14) Confidence 0.08 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
What features of CaM would allow it to play such a role?
Gene_expression (features) of CaM
15) Confidence 0.08 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
Second, a single tethered CaM would be insufficient to trigger persistent activation of CaMKII, which has ?
Gene_expression (single) of CaM
16) Confidence 0.08 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0
With stronger depolarization, unitary openings come in rapid succession, leaving less time for CaM dissociation, resulting in greater temporal summation and more CaMKII activation.
Gene_expression (dissociation) of CaM
17) Confidence 0.08 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2592819 Disease Relevance 0 Pain Relevance 0.08
Previous research demonstrated that CaM is expressed in the hypothalamus and the pituitary of goldfish and LY, but not SKF, decreased CaM mRNA levels in goldfish pituitary cells [46].
Gene_expression (expressed) of CaM in pituitary
18) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2924890 Disease Relevance 0 Pain Relevance 0.13
Calmodulin protein was decreased by LY, but not SKF, suggesting that in hypothalamic CaM expression is D2-, rather than D1-, receptor-regulated.
Gene_expression (expression) of CaM
19) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2924890 Disease Relevance 0 Pain Relevance 0.14

General Comments

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