INT208551

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Context Info
Confidence 0.48
First Reported 2007
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 10
Disease Relevance 6.28
Pain Relevance 0.12

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

mitochondrion (Mutyh) hydrolase activity, acting on glycosyl bonds (Mutyh) nucleus (Mutyh)
Anatomy Link Frequency
plasma 1
spleen 1
Mutyh (Mus musculus)
Pain Link Frequency Relevance Heat
Calcium channel 24 91.76 High High
adenocard 5 68.40 Quite High
Pyramidal cell 9 47.12 Quite Low
imagery 25 5.00 Very Low Very Low Very Low
Bile 20 5.00 Very Low Very Low Very Low
Central nervous system 16 5.00 Very Low Very Low Very Low
abdominal pain 15 5.00 Very Low Very Low Very Low
COX-2 inhibitor 10 5.00 Very Low Very Low Very Low
depression 9 5.00 Very Low Very Low Very Low
Glutamate 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Familial Adenomatous Polyposis 1200 100.00 Very High Very High Very High
Colon Cancer 165 100.00 Very High Very High Very High
Disease 155 99.42 Very High Very High Very High
Spinocerebellar Ataxia Type 2 47 99.26 Very High Very High Very High
Polyps 340 97.44 Very High Very High Very High
Hereditary Nonpolyposis Colorectal Neoplasms 20 97.20 Very High Very High Very High
Hyperplasia 15 97.16 Very High Very High Very High
Carcinoma 20 96.92 Very High Very High Very High
Adenoma 290 96.48 Very High Very High Very High
Cancer 330 95.48 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Normal MUTYH structure and functions in humans
Gene_expression (structure) of MUTYH
1) Confidence 0.48 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2772987 Disease Relevance 0.36 Pain Relevance 0.03
MUTYH associated polyposis is a frequent inherited CRC predisposition, which can be mostly in a recessive form of inheritance (bi-allelic or compound mutations) but also as a dominant component, and therefore DNA screening of the MUTYH gene should look for both heterozygous and homozygous mutations [46].
Gene_expression (predisposition) of MUTYH associated with colon cancer
2) Confidence 0.48 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2772987 Disease Relevance 1.30 Pain Relevance 0
MUTYH-genotype/phenotype correlations to "FAP" features
Gene_expression (features) of MUTYH associated with familial adenomatous polyposis
3) Confidence 0.48 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2772987 Disease Relevance 1.65 Pain Relevance 0
Tests for MUTYH
Gene_expression (Tests) of MUTYH
4) Confidence 0.48 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2772987 Disease Relevance 1.47 Pain Relevance 0
What to test for first: APC or MUTYH mutation?
Gene_expression (mutation) of MUTYH associated with familial adenomatous polyposis
5) Confidence 0.48 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2772987 Disease Relevance 0.66 Pain Relevance 0
Full-length protein was detected in spleen samples with Western blots (Figure 3), confirming that the alternatively spliced mRNA species is capable of producing Cav1.4 channel proteins with a molecular mass of ?
Gene_expression (detected) of Full-length protein in spleen
6) Confidence 0.07 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0.04
Because of their highly repetitive sequence, transposable elements have previously been shown to undergo alternative splicing; this allows for full-length protein to be produced, albeit at reduced levels relative to those in WT controls [26], [27].
Gene_expression (produced) of full-length protein
7) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0.05
While we did not map the exact residues in this 20 amino acid region necessary for this interaction, these data suggest that the CSNB2-like phenotype of the Cacna1fnob2 mouse may result not only from lower Cav1.4-mediated calcium-current densities, due to the diminished production of full-length protein, but also to a failure of targeting of the mutant protein to the plasma membrane, due to its inability to interact with filamin.
Gene_expression (production) of full-length protein in plasma
8) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0
We have found two mRNA species in the Cacna1fnob2 mouse, one of which encodes an in-frame stop codon, and another in which the stop codon is missing as a result of splicing within the ETn; as a result, full-length protein was detectable by Western blotting using an antibody raised against the C-terminus of the ?
Gene_expression (detectable) of full-length protein
9) Confidence 0.06 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0
Here, we show the beneficial effects of chronic lithium treatment on multiple measures in an SCA1 disease model—Sca1154Q/2Q mice—that express the full-length mutant protein in the endogenous spatiotemporal pattern and reproduce most features of human SCA1.
Gene_expression (express) of full-length mutant protein associated with spinocerebellar ataxia type 2 and disease
10) Confidence 0.05 Published 2007 Journal PLoS Medicine Section Body Doc Link PMC1880853 Disease Relevance 0.85 Pain Relevance 0

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