INT148562

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Context Info
Confidence 0.16
First Reported 2005
Last Reported 2009
Negated 1
Speculated 0
Reported most in Body
Documents 13
Total Number 13
Disease Relevance 5.31
Pain Relevance 1.32

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

small molecule metabolic process (GNAS) intracellular (GNAS) GTPase activity (GNAS)
transmembrane transport (GNAS) cytoplasm (GNAS) signal transducer activity (GNAS)
Anatomy Link Frequency
nucleus accumbens 1
thalamus 1
GNAS (Homo sapiens)
Pain Link Frequency Relevance Heat
Nucleus accumbens 1 99.04 Very High Very High Very High
Thalamus 8 97.00 Very High Very High Very High
amygdala 16 91.04 High High
Migraine 89 87.68 High High
Hyperalgesia 2 86.28 High High
Nerve growth factor 12 83.80 Quite High
withdrawal 1 81.60 Quite High
induced neuropathy 2 75.00 Quite High
Kinase C 1 75.00 Quite High
peripheral neuropathy 1 73.44 Quite High
Disease Link Frequency Relevance Heat
Cadasil 25 99.74 Very High Very High Very High
Disease 70 99.52 Very High Very High Very High
Spinal Muscular Atrophy 16 99.24 Very High Very High Very High
Cleidocranial Dysplasia 27 99.10 Very High Very High Very High
Urological Neuroanatomy 8 96.48 Very High Very High Very High
Hyperalgesia 5 93.80 High High
Supranuclear Palsy 30 93.72 High High
Parkinson's Disease 6 90.72 High High
Frontotemporal Dementia 6 90.00 High High
Congenital Anomalies 11 89.64 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Fibrous dysplasia is a genetic disease caused by postzygotic, activating mutations of the GNAS gene, which impair the GTPase activity of Gs-alpha thus resulting in excess intracellular cAMP.
Positive_regulation (activating) of GNAS gene associated with cleidocranial dysplasia and disease
1) Confidence 0.16 Published 2008 Journal Cases J Section Body Doc Link PMC2611982 Disease Relevance 1.58 Pain Relevance 0
In silico and RT-PCR analyses showed that alternative splicing from the antiBDNF pre-mRNA produces more than 300 transcripts, but exon 1 of antiBDNF is always used as the most 5?
Positive_regulation (used) of exon
2) Confidence 0.07 Published 2007 Journal Genomics Section Body Doc Link PMC2568880 Disease Relevance 0 Pain Relevance 0
Human BDNF exon VIIIh, which is not linked to a separate promoter, is also not present in rodent BDNF.
Positive_regulation (Human) of exon
3) Confidence 0.07 Published 2007 Journal Genomics Section Body Doc Link PMC2568880 Disease Relevance 0 Pain Relevance 0
exon usage, two separate polyadenylation signals in exon IX can be utilized in BDNF transcripts.
Positive_regulation (utilized) of exon
4) Confidence 0.07 Published 2007 Journal Genomics Section Body Doc Link PMC2568880 Disease Relevance 0 Pain Relevance 0
We show that in human the rarely used exon VIII of BDNF is exclusively spliced to exon V.
Positive_regulation (used) of exon VIII
5) Confidence 0.07 Published 2007 Journal Genomics Section Body Doc Link PMC2568880 Disease Relevance 0 Pain Relevance 0
Fourth, in contrast to the rodent BDNF genes we found that exon VIII of the human BDNF is not used as a 5?
Neg (not) Positive_regulation (used) of exon VIII
6) Confidence 0.07 Published 2007 Journal Genomics Section Body Doc Link PMC2568880 Disease Relevance 0 Pain Relevance 0
Expression of behavioral sensitization in RHA-I rats activated secretogranin and PSD-95 mRNA in the nucleus accumbens core.
Positive_regulation (activated) of secretogranin in nucleus accumbens associated with nucleus accumbens
7) Confidence 0.06 Published 2008 Journal Neuroscience Section Abstract Doc Link 18093743 Disease Relevance 0.07 Pain Relevance 0.18
Increased exon 7 insertion into SMN2 mRNA has been suggested as a potentially effective approach for SMA treatment [88].
Positive_regulation (Increased) of exon associated with spinal muscular atrophy
8) Confidence 0.01 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2604894 Disease Relevance 0.70 Pain Relevance 0.09
A group of these mutations alters splicing of exon 10, resulting in an increase in exon 10 inclusion into tau mRNA.
Positive_regulation (increase) of exon
9) Confidence 0.01 Published 2008 Journal BMC Neurosci Section Abstract Doc Link PMC2604894 Disease Relevance 0.84 Pain Relevance 0
The results taken together with other findings that confirm the existence and/or induction of the canonical exon 1 [5,11,15] point to the usage of two alternative promoters.


Positive_regulation (induction) of exon
10) Confidence 0.01 Published 2007 Journal BMC Genomics Section Body Doc Link PMC2228316 Disease Relevance 0 Pain Relevance 0
Exon 8 of the p62/SQSTM1 gene was amplified by PCR (I-Cycler; Bio-Rad Laboratories, Milan, Italy) using a couple of primers located in the flanking intron: 5'-CAGTGTGGCCTGTGAGGAC-3'/5'-CAGTGAGCCTTGGGTCTCG-3'.
Positive_regulation (amplified) of Exon
11) Confidence 0.01 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1297578 Disease Relevance 0.26 Pain Relevance 0
The authors suggested that on the basis of this spectrum the suggested protocol for genetic diagnostic testing for CADASIL would be to screen exon 4 and proceed to mutational screening of exons 3, 5, and 6 where indicated [28].
Positive_regulation (screen) of exon associated with cadasil
12) Confidence 0.01 Published 2008 Journal The Open Neurology Journal Section Body Doc Link PMC2577928 Disease Relevance 1.00 Pain Relevance 0.48
Concurrently, oxaliplatin chronic treatment induced a specific upregulation of gamma isoforms of PKC and increased phosphorylation of gamma/epsilon PKC isoforms within thalamus and PAG.
Positive_regulation (upregulation) of isoforms in thalamus associated with urological neuroanatomy and thalamus
13) Confidence 0.00 Published 2009 Journal Pain Section Abstract Doc Link 19683395 Disease Relevance 0.84 Pain Relevance 0.57

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