INT134786

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Context Info
Confidence 0.68
First Reported 2005
Last Reported 2011
Negated 1
Speculated 0
Reported most in Body
Documents 17
Total Number 17
Disease Relevance 7.61
Pain Relevance 3.29

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

peptidase activity (Adam10) nucleocytoplasmic transport (Adam10) Golgi apparatus (Adam10)
nucleus (Adam10) cytoplasm (Adam10)
Anatomy Link Frequency
Notch 1
neuronal 1
brains 1
astrocytes 1
Adam10 (Mus musculus)
Pain Link Frequency Relevance Heat
metalloproteinase 126 100.00 Very High Very High Very High
substance P 15 99.40 Very High Very High Very High
Inflammation 182 99.24 Very High Very High Very High
long-term potentiation 12 98.36 Very High Very High Very High
Inflammatory mediators 14 89.56 High High
qutenza 15 84.44 Quite High
cINOD 148 81.68 Quite High
COX-2 inhibitor 3 69.84 Quite High
cytokine 41 62.64 Quite High
glial activation 7 54.76 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 301 99.64 Very High Very High Very High
INFLAMMATION 221 99.24 Very High Very High Very High
Cognitive Disorder 160 98.92 Very High Very High Very High
Apoptosis 19 98.56 Very High Very High Very High
Amyloid Plaque 103 98.04 Very High Very High Very High
Cancer 38 94.32 High High
Disease 615 92.88 High High
Necrosis 16 92.00 High High
Infection 41 91.60 High High
Toxicity 19 76.72 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Interestingly, low levels of cholesterol leads to high expression of Adam10, coding for a protease also known as Kuzbanian, which is essential for Notch activation [55].
Gene_expression (expression) of Adam10 in Notch
1) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2699037 Disease Relevance 0 Pain Relevance 0
Moreover, when Adam10 is not expressed Dll1 is overexpressed [56].
Neg (not) Gene_expression (expressed) of Adam10
2) Confidence 0.68 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2699037 Disease Relevance 0 Pain Relevance 0
In light of the latter observation, it is perhaps of little surprise that it has more recently been shown that ADAM10 and not ADAM17 or 9 is the physiologically relevant basal ?
Gene_expression (relevant) of ADAM10
3) Confidence 0.51 Published 2011 Journal Biochemistry Research International Section Body Doc Link PMC2989646 Disease Relevance 0.43 Pain Relevance 0.09
Like other ADAM family members, ADAM10 has a modular ectodomain structure and is synthesized as an inactive zymogen being activated only after enzymatic removal of its prodomain [35].
Gene_expression (synthesized) of ADAM10
4) Confidence 0.46 Published 2011 Journal Biochemistry Research International Section Body Doc Link PMC2989646 Disease Relevance 0.07 Pain Relevance 0.03
A moderate neuronal over-expression of ADAM10 in mice transgenic for human APP([V717I]) showed increased secretion of the neurotrophic soluble ?
Gene_expression (expression) of ADAM10 in neuronal associated with targeted disruption
5) Confidence 0.45 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2442055 Disease Relevance 0.90 Pain Relevance 0.65
production than when either enzyme was transfected into cells expressing only endogenous ADAM10 [35] suggesting that it was the removal specifically of the ADAM10 prodomain and subsequent activation of the enzyme that correlated with the level of ?
Gene_expression (expressing) of ADAM10
6) Confidence 0.40 Published 2011 Journal Biochemistry Research International Section Body Doc Link PMC2989646 Disease Relevance 0.20 Pain Relevance 0.09
-secretase is involved in inflammation is supported by the observation that ADAM-10 is expressed constitutively by astrocytes in the normal and inflamed human CNS [64].
Gene_expression (expressed) of ADAM-10 in astrocytes associated with inflammation
7) Confidence 0.40 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2442055 Disease Relevance 0.46 Pain Relevance 0.23
Specifically ADAM-10 produces the same growth-inhibitory products from Substance P (i.e., SP (1-7)) that Neprilysin does, so that loss of ADAM-10 expression actually results in loss of production of growth inhibitory peptides from Substance P.
Gene_expression (expression) of ADAM-10 associated with substance p
8) Confidence 0.39 Published 2006 Journal Breast Cancer Res. Treat. Section Abstract Doc Link 16583263 Disease Relevance 0.49 Pain Relevance 0.36
Specifically ADAM-10 produces the same growth-inhibitory products from Substance P (i.e., SP (1-7)) that Neprilysin does, so that loss of ADAM-10 expression actually results in loss of production of growth inhibitory peptides from Substance P.
Gene_expression (produces) of ADAM-10 associated with substance p
9) Confidence 0.39 Published 2006 Journal Breast Cancer Res. Treat. Section Abstract Doc Link 16583263 Disease Relevance 0.55 Pain Relevance 0.41
Expression of mutant catalytically inactive ADAM10 led to an enhancement of the number and size of amyloid plaques in the brains of double-transgenic mice.
Gene_expression (Expression) of ADAM10 in brains associated with targeted disruption and amyloid plaque
10) Confidence 0.39 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2442055 Disease Relevance 0.94 Pain Relevance 0.38
(amphiregulin, Adam10) [61] were differentially expressed in any group of mice.
Gene_expression (expressed) of Adam10
11) Confidence 0.37 Published 2009 Journal Mol Cancer Section Body Doc Link PMC2667483 Disease Relevance 0.52 Pain Relevance 0.07
Overexpression of ADAM10 increases ?
Gene_expression (Overexpression) of ADAM10
12) Confidence 0.36 Published 2011 Journal Mol Brain Section Body Doc Link PMC3022812 Disease Relevance 0.25 Pain Relevance 0.05
At first glance, loss of ADAM-10 expression would be expected to result in decreased invasive capability, due to loss of matrix metalloprotease activity.
Gene_expression (expression) of ADAM-10
13) Confidence 0.30 Published 2006 Journal Breast Cancer Res. Treat. Section Abstract Doc Link 16583263 Disease Relevance 0.73 Pain Relevance 0.41
In contrast, the expression of an inactive mutant of ADAM10 worsened the pathology [243].


Gene_expression (expression) of ADAM10
14) Confidence 0.29 Published 2007 Journal Acta Neuropathol Section Body Doc Link PMC2100431 Disease Relevance 0.65 Pain Relevance 0.07
Transgenic mice that have an overexpression of disintegrin and metalloprotease-10 (ADAM-10), which activates ?
Gene_expression (overexpression) of metalloprotease-10 associated with targeted disruption
15) Confidence 0.29 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2536544 Disease Relevance 0.71 Pain Relevance 0.19
Transgenic mice that have an overexpression of disintegrin and metalloprotease-10 (ADAM-10), which activates ?
Gene_expression (overexpression) of ADAM-10 associated with targeted disruption
16) Confidence 0.29 Published 2008 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2536544 Disease Relevance 0.71 Pain Relevance 0.19
Ultimately, the integral cell-surface metalloproteinases ADAM-10 and ADAM-17/TACE were found to underlie ?
Gene_expression (found) of metalloproteinases ADAM-10 associated with metalloproteinase
17) Confidence 0.09 Published 2005 Journal PLoS Medicine Section Body Doc Link PMC543463 Disease Relevance 0 Pain Relevance 0.05

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