INT111263

Context Info Confidence 0.75 First Reported 2000 Last Reported 2011 Negated 0 Speculated 0 Reported most in Body Documents 8 Total Number 10 Disease Relevance 8.51 Pain Relevance 3.00

signal transduction (Gnb5) plasma membrane (Gnb5) nucleus (Gnb5) signal transducer activity (Gnb5)

Anatomy Link Frequency brain 1 stem cells 1 central nervous system 1 neural 1 Gnb5 (Mus musculus)

Pain Link Frequency Relevance Heat Demyelination 21 100.00 Delta opioid receptors 2 99.76 Central nervous system 28 99.32 Inflammation 38 98.52 Morphine 18 98.28 Intracerebroventricular 3 96.24 Peripheral nervous system 10 93.76 tolerance 10 90.16 Analgesic 4 88.80 Potency 1 85.68

Disease Link Frequency Relevance Heat Syndrome 155 100.00 Demyelinating Disease 141 100.00 Increased Venous Pressure Under Development 14 99.44 Cancer 221 99.28 Muscle Weakness 6 98.96 Guillain-barre Syndrome 6 98.76 Glioblastoma 54 95.80 Neuropathy 16 95.44 Glioma 135 94.64 Autoimmune Disease 3 92.16

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Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

The expression of Gbeta5 and RGS9-2 proteins (member of the R7 subfamily of RGS) was reduced by blocking their mRNAs with antisense oligodeoxynucleotides (ODN).

Gene_expression (expression) of Gbeta5

1) Confidence 0.75 Published 2003 Journal Neuropharmacology Section Abstract Doc Link 12814661 Disease Relevance 0.09 Pain Relevance 0.76

Expression of neural RGS-R7 and Gbeta5 Proteins in Response to Acute and Chronic Morphine.

Gene_expression (Expression) of Gbeta5 in neural associated with morphine

2) Confidence 0.65 Published 2005 Journal Neuropsychopharmacology Section Title Doc Link 15199376 Disease Relevance 0.23 Pain Relevance 0.86

The R7 subfamily of regulators of G-protein signaling (RGS) proteins (RGS6, RGS7, RGS9-2, and RGS11), and its binding protein Gbeta5, are found in neural structures of mouse brain.

Gene_expression (found) of Gbeta5 in brain

3) Confidence 0.56 Published 2005 Journal Neuropsychopharmacology Section Abstract Doc Link 15199376 Disease Relevance 0 Pain Relevance 0.67

It is possible that the pathophysiologic process producing the acute peripheral demyelination of GBS may also affect central nervous system structures involved in the genesis of these symptoms, but there is a lack of evidence at present to support that hypothesis.

Gene_expression (producing) of GBS in central nervous system associated with demyelination, syndrome and central nervous system

4) Confidence 0.36 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2413194 Disease Relevance 0.81 Pain Relevance 0.24

Prognosis of GBS

Gene_expression (Prognosis) of GBS associated with syndrome

5) Confidence 0.09 Published 2010 Journal J Clin Immunol Section Body Doc Link PMC2883091 Disease Relevance 0.85 Pain Relevance 0

First, autoimmune antibodies were the cause of both GBS and isolated vasculitis of the CNS.

Gene_expression (cause) of GBS associated with syndrome, central nervous system and increased venous pressure under development

6) Confidence 0.07 Published 2000 Journal Crit Care Section Body Doc Link PMC29044 Disease Relevance 1.71 Pain Relevance 0.25

However recent studies, which also included additional sequencing of TP53, revealed that mutations are prevalent in primary GBs as well [13, 27].

Gene_expression (prevalent) of GBs

7) Confidence 0.06 Published 2011 Journal Journal of Oncology Section Body Doc Link PMC3010739 Disease Relevance 1.20 Pain Relevance 0

The model was created to mimic human secondary GBs characterized by combined PDGFRA overexpression/amplification and TP53 deletion/mutation, and results did prove that this combination is instrumental in generating GBs.

Gene_expression (overexpression) of GBs

8) Confidence 0.06 Published 2011 Journal Journal of Oncology Section Body Doc Link PMC3010739 Disease Relevance 0.80 Pain Relevance 0

GBs frequently overexpress genes typical of neural stem cells including Sox2 [106], Myc [27] and Oct4 [107].

Gene_expression (overexpress) of GBs in stem cells

9) Confidence 0.06 Published 2011 Journal Journal of Oncology Section Body Doc Link PMC3010739 Disease Relevance 1.05 Pain Relevance 0

Different subtypes producing the clinical picture of GBS have been described including acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor and sensory neuropathy (AMSAN), acute sensory neuronopathy, acute pandysautonomia and the Miller- Fisher syndrome [73].

Gene_expression (producing) of GBS associated with neuropathy, miller fisher syndrome, inflammation, syndrome and guillain-barre syndrome

10) Confidence 0.02 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923368 Disease Relevance 1.76 Pain Relevance 0.22

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