INT170719

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Context Info
Confidence 0.01
First Reported 2001
Last Reported 2001
Negated 1
Speculated 0
Reported most in Body
Documents 1
Total Number 9
Disease Relevance 1.10
Pain Relevance 0.28

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

cytoplasm (Grm5, Siah1a) cell differentiation (Siah1a) ligase activity (Siah1a)
signal transducer activity (Grm5) cytosol (Siah1a) plasma membrane (Grm5)
Anatomy Link Frequency
tail 1
SCG 1
Grm5 (Rattus norvegicus)
Siah1a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate 108 92.00 High High
Glutamate receptor 36 65.28 Quite High
addiction 9 19.60 Low Low
Neuronal excitability 9 9.48 Low Low
imagery 18 5.00 Very Low Very Low Very Low
tetrodotoxin 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 9 97.76 Very High Very High Very High
Cancer 9 97.12 Very High Very High Very High
Ganglion Cysts 54 96.60 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, Siah1a had no detectable effect on mGluR2-mediated calcium current inhibition, consistent with reports demonstrating that Siah1a does not bind to group II mGluRs [36].
mGluRs Neg (not) Binding (bind) of Siah1a
1) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0.15
Association of Siah1a with group I mGluRs can also prevent the interaction of CaM and the receptor [36].
mGluRs Binding (Association) of Siah1a
2) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0.06
By analogy to group III mGluRs, the ability of Siah1a to compete with CaM for binding to group I mGluRs was considered a potential mechanism for the actions of Siah1a on group I mGluR-mediated calcium current inhibition.
mGluRs Binding (binding) of Siah1a
3) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
Further studies will be needed to determine if group I mGluRs and Siah1a interact physiologically, and whether this interaction has functional consequences.
mGluRs Binding (interact) of Siah1a
4) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0 Pain Relevance 0
More recently, an interaction between Siah1a and the C-terminal tail of group I mGluRs was demonstrated [36].
mGluRs Binding (interaction) of Siah1a in tail
5) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.30 Pain Relevance 0
To assess the role of Siah1a binding, specific group I mGluRs were heterologously expressed in sympathetic neurons from the rat superior cervical ganglion (SCG), which do not natively express mGluRs [37,38].
mGluRs Binding (binding) of Siah1a in SCG associated with ganglion cysts
6) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.34 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.


mGluRs Binding (interaction) of Siah1a
7) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.07 Pain Relevance 0.03
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.


mGluRs Binding (binding) of Siah1a
8) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.07 Pain Relevance 0.03
To date the functional consequences of Siah1a association with group I mGluRs are unknown.
mGluRs Binding (association) of Siah1a
9) Confidence 0.01 Published 2001 Journal BMC Neurosci Section Body Doc Link PMC58838 Disease Relevance 0.33 Pain Relevance 0

General Comments

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