INT28817

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Context Info
Confidence 0.39
First Reported 1989
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 18
Disease Relevance 3.92
Pain Relevance 2.59

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

cell death (TRPV4) plasma membrane (TRPV4) transmembrane transport (TRPV4)
Anatomy Link Frequency
lobe 2
sensory neurons 1
tails 1
motor neuron 1
TRPV4 (Homo sapiens)
Pain Link Frequency Relevance Heat
TRP channel 57 100.00 Very High Very High Very High
Hyperalgesia 14 99.36 Very High Very High Very High
Pain 20 99.04 Very High Very High Very High
Hypoesthesia 1 95.24 Very High Very High Very High
Mechanotransduction 2 91.28 High High
antagonist 27 88.00 High High
vincristine 4 87.20 High High
peripheral neuropathy 2 85.36 High High
Inflammation 7 83.52 Quite High
intrathecal 2 82.00 Quite High
Disease Link Frequency Relevance Heat
Neuropathic Pain 11 100.00 Very High Very High Very High
Hyperalgesia 19 99.36 Very High Very High Very High
Motor Neuron Diseases 3 99.12 Very High Very High Very High
Pain 18 99.04 Very High Very High Very High
Hereditary Spastic Paraplegia 1 98.04 Very High Very High Very High
Hypesthesia 1 95.24 Very High Very High Very High
Foot Deformities 10 94.28 High High
Fasciculation 1 93.84 High High
Targeted Disruption 10 89.16 High High
Diabetes Mellitus 4 87.72 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
All data provide strong evidence for an interaction in TRPV4 between an N-terminal domain represented by the P2 peptide and a site in the C terminus, P5, that also binds to CaM.
TRPV4 Binding (interaction) of
1) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0
The C-terminal CaM binding site in TRPV4 binds to the CaM C lobe
TRPV4 Binding (binds) of in lobe
2) Confidence 0.39 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.06
In the present study, we examined the common requirement for TRPV4 in mechanical hyperalgesia associated with diverse pain models and investigated whether the very close association observed between TRPV4 and mechanical hyperalgesia, regardless of etiology, reflects a close functional connection of TRPV4 with other molecules implicated in mechanical transduction.
TRPV4 Binding (association) of associated with pain and hyperalgesia
3) Confidence 0.37 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18234883 Disease Relevance 1.10 Pain Relevance 0.83
Furthermore, we establish a direct interaction between TRPV4, alpha2 integrin, and the Src tyrosine kinase Lyn in sensory neurons.
TRPV4 Binding (interaction) of in sensory neurons
4) Confidence 0.37 Published 2008 Journal J. Neurosci. Section Abstract Doc Link 18234883 Disease Relevance 1.14 Pain Relevance 0.90
Indeed, previous studies [42] demonstrated that strong binding between the N-terminal tails exists in TRPV4.
TRPV4 Binding (binding) of in tails
5) Confidence 0.34 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0
We conclude that there is significant interaction between two molecules of the full-length TRPV4 N terminus that is dependent on the integrity of the domain formed by the P2 peptide.
TRPV4 Binding (interaction) of
6) Confidence 0.34 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0
This suggests that, in spite of its lower affinity to the C-terminal CaM binding site in TRPV4, the CaM N lobe contributes functionally to TRPV4 potentiation by a mechanism which remains unclear.
TRPV4 Binding (affinity) of in lobe
7) Confidence 0.30 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.08
In contrast, current increases were significantly smaller with the mutant CaM12 that binds to TRPV4.
TRPV4 Binding (binds) of
8) Confidence 0.30 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.03
Very high Ca2+ concentrations above 100 ┬ÁM, however, inhibited binding of the fragments, a process that is probably secondary to unspecific Ca2+ binding and has been observed for other protein interactions including CaM binding to TRPV4 [11].
TRPV4 Binding (interactions) of
9) Confidence 0.29 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.04
Using protein interaction experiments and functional assays, we show that the molecular correlate of Ca2+-dependent current potentiation is disruption of an interdomain interaction within TRPV4 resulting from CaM binding to a C-terminal site.
TRPV4 Binding (interaction) of
10) Confidence 0.29 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.07
Using protein interaction experiments and functional assays, we show that the molecular correlate of Ca2+-dependent current potentiation is disruption of an interdomain interaction within TRPV4 resulting from CaM binding to a C-terminal site.
TRPV4 Binding (binding) of
11) Confidence 0.29 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.07
Surprisingly, instead of CaM-dependent complex formation, a strong constitutive interaction between the N- and C-terminal TRPV4 fragments was observed in the absence of CaM (Fig. 3A).
TRPV4 Binding (interaction) of
12) Confidence 0.29 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0.03
Inhibition of the interaction between N and C termini renders TRPV4 permanently potentiated
TRPV4 Binding (potentiated) of
13) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0
-PMA were similar to those for wild type TRPV4 after potentiation by Ca2+.
TRPV4 Binding (potentiation) of
14) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0
The association of HMSN-I with MND has not been previously described in literature.
HMSN-I Binding (association) of
15) Confidence 0.26 Published 1989 Journal Acta Neurol (Napoli) Section Abstract Doc Link 2801256 Disease Relevance 0.52 Pain Relevance 0.10
This is in agreement with a recent study [42] that showed high FRET efficiency in TRPV4 for both homologous N-terminal and N-terminal to C-terminal interactions.
TRPV4 Binding (interactions) of
16) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2867956 Disease Relevance 0 Pain Relevance 0
Chemical ligands are known to interact within the transmembrane domains 2 to 4 region for the other well studied TRP channels such as TRPV1 [23-25], TRPM8 [26]and TRPV4 [27], but critical residues for heat activation are still unknown.
TRPV4 Binding (interact) of associated with trp channel
17) Confidence 0.16 Published 2007 Journal Mol Pain Section Body Doc Link PMC2222611 Disease Relevance 0 Pain Relevance 0.38
Several of these genes are also associated with HMSN subtypes, hereditary motor neuron diseases, and hereditary spastic paraplegias, indicating an overlapping clinical spectrum.
HMSN Binding (associated) of in motor neuron associated with neuropathic pain, hereditary spastic paraplegia and motor neuron diseases
18) Confidence 0.00 Published 2009 Journal Neurogenetics Section Body Doc Link PMC2758216 Disease Relevance 1.15 Pain Relevance 0

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