INT141131

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Context Info
Confidence 0.61
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 18
Disease Relevance 16.60
Pain Relevance 1.36

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

Golgi apparatus (PRNP) endoplasmic reticulum (PRNP) nucleolus (PRNP)
plasma membrane (PRNP) nucleus (PRNP) cell cycle (PRNP)
Anatomy Link Frequency
brainstem 3
tube 2
adult brain 2
spinal cord 1
PRNP (Homo sapiens)
Pain Link Frequency Relevance Heat
cerebral cortex 6 99.96 Very High Very High Very High
medulla 12 99.68 Very High Very High Very High
Spinal cord 23 99.12 Very High Very High Very High
Demyelination 11 95.24 Very High Very High Very High
Central nervous system 28 94.40 High High
Substantia nigra 4 83.60 Quite High
aspirin 75 74.60 Quite High
Action potential 7 73.68 Quite High
Hippocampus 12 68.16 Quite High
Thalamus 8 67.56 Quite High
Disease Link Frequency Relevance Heat
Creutzfeldt Jakob Disease 669 100.00 Very High Very High Very High
Disease 596 100.00 Very High Very High Very High
Targeted Disruption 440 100.00 Very High Very High Very High
Alzheimer's Dementia 44 100.00 Very High Very High Very High
Prion Diseases 103 99.96 Very High Very High Very High
Sprains And Strains 536 99.28 Very High Very High Very High
Drug Induced Neurotoxicity 28 98.92 Very High Very High Very High
Neurologic Manifestations 4 97.80 Very High Very High Very High
Demyelinating Disease 21 95.24 Very High Very High Very High
Adhesions 115 93.56 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The vCJD prions transmit disease to wild-type mice far more efficiently than any other form of human prion disease [26,27,49,122] and in transgenic mice faithful propagation of the vCJD phenotype is dependent upon homozygous expression of human PrP 129 methionine [28,49,63,170,171] (Figure 2).
Positive_regulation (dependent) of Gene_expression (expression) of PrP associated with targeted disruption, creutzfeldt jakob disease and disease
1) Confidence 0.61 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 1.72 Pain Relevance 0.03
While PrP expression is absolutely required for prion propagation and neurotoxicity [124] knockout of PrPC in embryonic models [139,140] or in adult brain [141] has no overt phenotypic effect that influences lifespan or fertility.
Positive_regulation (required) of Gene_expression (expression) of PrP in adult brain associated with targeted disruption, drug induced neurotoxicity and lifespan
2) Confidence 0.50 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 0.60 Pain Relevance 0.09
The mechanisms underlying the neurologic symptoms and signs were unclear, but we speculate that, in addition to widespread involvement of the cerebral cortex, PrP deposition and microglial activation in the brainstem and spinal cord were responsible.
Positive_regulation (activation) of Gene_expression (deposition) of PrP in brainstem associated with medulla, cerebral cortex, neurologic manifestations and spinal cord
3) Confidence 0.47 Published 2006 Journal Neuropathology Section Abstract Doc Link 17203592 Disease Relevance 0.41 Pain Relevance 0.47
Two types of genetic modification can be used to generate human PrP-expressing mice, either transgenic expression of human PrP on a mouse PrP knockout background [62] or direct replacement of mouse PrP with human PrP using gene knock-in technology [61].


Positive_regulation (generate) of Gene_expression (expression) of PrP associated with targeted disruption
4) Confidence 0.47 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 1.49 Pain Relevance 0.03
Both transgenic and knock-in modelling of prion diseases provide complimentary results in most cases; however, over-expression of human PrP transgenes may be desirable.
Positive_regulation (over) of Gene_expression (expression) of PrP associated with targeted disruption and creutzfeldt jakob disease
5) Confidence 0.47 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 1.24 Pain Relevance 0
While spontaneous conversion of PrPC to PrPSc as a rare stochastic event, or somatic mutation of the PrP gene, resulting in expression of a pathogenic PrP mutant are plausible explanations for sporadic CJD [2,74,217,218], other causes for at least some cases, include environmental exposure to human prions [219–221] or exposure to animal prions.
Positive_regulation (resulting) of Gene_expression (expression) of PrP associated with creutzfeldt jakob disease
6) Confidence 0.47 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 1.43 Pain Relevance 0
This single tube was then centrifuged for 20 min at 205 × g resulting in the production of a PRP supernatant.
Positive_regulation (resulting) of Gene_expression (production) of PRP in tube
7) Confidence 0.45 Published 2009 Journal J Transl Med Section Body Doc Link PMC2699331 Disease Relevance 0.28 Pain Relevance 0.04
How pathogenic mutations in PRNP cause prion disease has yet to be resolved; however, in most cases the mutation is thought to lead to an increased tendency of PrPC to form PrPSc.
Positive_regulation (increased) of Gene_expression (form) of PrPC associated with creutzfeldt jakob disease
8) Confidence 0.44 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 0.68 Pain Relevance 0
Very recently it has been revealed that axonal PrPC expression is required for peripheral myelin maintenance [154] and this finding correlates strongly with earlier demonstrations of extensive demyelination in transgenic mice expressing PrP with deletion mutants in the central domain [155–157].
Positive_regulation (required) of Gene_expression (expression) of PrPC associated with targeted disruption and demyelination
9) Confidence 0.41 Published 2010 Journal Neuropathology and Applied Neurobiology Section Body Doc Link PMC3017745 Disease Relevance 1.13 Pain Relevance 0.08
The mechanisms underlying the neurologic symptoms and signs were unclear, but we speculate that, in addition to widespread involvement of the cerebral cortex, PrP deposition and microglial activation in the brainstem and spinal cord were responsible.
Positive_regulation (activation) of in spinal cord Gene_expression (deposition) of PrP in brainstem associated with medulla, cerebral cortex, neurologic manifestations and spinal cord
10) Confidence 0.16 Published 2006 Journal Neuropathology Section Abstract Doc Link 17203592 Disease Relevance 0.41 Pain Relevance 0.47
Spontaneous generation of PrPSc and infectivity was also described in an experiment in which a recombinant mouse PrP fragment (residues 89–230) assembled into amyloid fibrils was found to induce a TSE-like disease with PrPSc formation when injected in transgenic mice overexpressing the same PrP sequence [5].
Positive_regulation (generation) of Gene_expression (overexpressing) of PrP associated with targeted disruption, alzheimer's dementia and disease
11) Confidence 0.15 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2675078 Disease Relevance 0.94 Pain Relevance 0
Spontaneous generation of PrPSc and infectivity was also described in an experiment in which a recombinant mouse PrP fragment (residues 89–230) assembled into amyloid fibrils was found to induce a TSE-like disease with PrPSc formation when injected in transgenic mice overexpressing the same PrP sequence [5].
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of PrP associated with targeted disruption, alzheimer's dementia and disease
12) Confidence 0.15 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2675078 Disease Relevance 0.92 Pain Relevance 0
Spontaneous generation of PrPSc and infectivity was also described in an experiment in which a recombinant mouse PrP fragment (residues 89–230) assembled into amyloid fibrils was found to induce a TSE-like disease with PrPSc formation when injected in transgenic mice overexpressing the same PrP sequence [5].
Positive_regulation (generation) of Gene_expression (overexpressing) of PrP associated with targeted disruption, alzheimer's dementia and disease
13) Confidence 0.13 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2675078 Disease Relevance 0.94 Pain Relevance 0
Spontaneous generation of PrPSc and infectivity was also described in an experiment in which a recombinant mouse PrP fragment (residues 89–230) assembled into amyloid fibrils was found to induce a TSE-like disease with PrPSc formation when injected in transgenic mice overexpressing the same PrP sequence [5].
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of PrP associated with targeted disruption, alzheimer's dementia and disease
14) Confidence 0.13 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2675078 Disease Relevance 0.85 Pain Relevance 0
Enhanced expression of AQP4 in Creutzfeldt-Jakob disease (CJD) was first reported by Iwasaki’s laboratory [37].
Positive_regulation (Enhanced) of Gene_expression (expression) of CJD associated with creutzfeldt jakob disease and disease
15) Confidence 0.09 Published 2010 Journal Current Neuropharmacology Section Body Doc Link PMC2923365 Disease Relevance 1.54 Pain Relevance 0.07
Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are caused by the conversion of the host-encoded prion protein (PrP) or normal cellular prion protein (PrPc) into a misfolded abnormal form of the protein.
Positive_regulation (conversion) of Gene_expression (conversion) of host-encoded prion protein associated with prion diseases
16) Confidence 0.07 Published 2008 Journal Mamm Genome Section Body Doc Link PMC2323435 Disease Relevance 0.71 Pain Relevance 0
Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are caused by the conversion of the host-encoded prion protein (PrP) or normal cellular prion protein (PrPc) into a misfolded abnormal form of the protein.
Positive_regulation (conversion) of Gene_expression (conversion) of PrPc associated with prion diseases
17) Confidence 0.07 Published 2008 Journal Mamm Genome Section Body Doc Link PMC2323435 Disease Relevance 0.71 Pain Relevance 0
Here, we report that prion infectivity was generated in Syrian hamsters after inoculating full-length rPrP that had been converted into the cross-?
Positive_regulation (generated) of Gene_expression (infectivity) of prion
18) Confidence 0.07 Published 2010 Journal Acta Neuropathol Section Abstract Doc Link PMC2808531 Disease Relevance 0.59 Pain Relevance 0.07

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