INT220506

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Context Info
Confidence 0.45
First Reported 2007
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 13
Total Number 14
Disease Relevance 5.46
Pain Relevance 0.38

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

endosome (Cav1) mitochondrion (Cav1) Golgi apparatus (Cav1)
endoplasmic reticulum (Cav1) intracellular (Cav1) protein complex (Cav1)
Anatomy Link Frequency
plasma 1
muscle 1
HeLa 1
fibroblasts 1
Cav1 (Mus musculus)
Pain Link Frequency Relevance Heat
potassium channel 14 92.04 High High
Inflammatory mediators 8 85.76 High High
anesthesia 9 84.04 Quite High
antagonist 12 81.72 Quite High
imagery 14 71.60 Quite High
cytokine 7 70.28 Quite High
agonist 23 66.12 Quite High
adenocard 2 65.60 Quite High
halothane 2 53.56 Quite High
Inflammation 18 38.48 Quite Low
Disease Link Frequency Relevance Heat
Stress 60 99.60 Very High Very High Very High
Lipodystrophy 24 98.84 Very High Very High Very High
Breast Cancer 124 98.64 Very High Very High Very High
Cancer 196 98.44 Very High Very High Very High
Obesity 22 96.56 Very High Very High Very High
Muscle Disease 16 96.04 Very High Very High Very High
Hypokalemic Periodic Paralysis 58 93.44 High High
Disease 64 89.44 High High
Targeted Disruption 25 88.24 High High
INFLAMMATION 36 85.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This gene was an attractive candidate because it had been shown to interact with caveolin-1 [16], whose mutations cause lipodystrophy [5] and with caveolin-3, whose mutations cause rippling muscle disease [17].
caveolin-1 Binding (interact) of in muscle associated with muscle disease and lipodystrophy
1) Confidence 0.45 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2837386 Disease Relevance 0.77 Pain Relevance 0
Absence of PTRF-CAVIN did not influence abundance of its binding partner caveolin-1 and caveolin-3.
caveolin-1 Binding (binding) of
2) Confidence 0.45 Published 2010 Journal PLoS Genetics Section Abstract Doc Link PMC2837386 Disease Relevance 1.16 Pain Relevance 0.04
A recent study investigating similar maxi-K channel mutants in HEK 293 cells found that single, double and triple substitutions of these aromatic amino acids fail to disrupt the interaction between the maxi-K channel and cav-1, but that complete deletion of the consensus site abolishes almost all (80-85%) interaction with cav-1 [8].
cav-1 Binding (interaction) of
3) Confidence 0.37 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0 Pain Relevance 0
In contrast, the Ltk- mouse fibroblasts used in our study expressed endogenous cav-1, thus providing a more physiological environment for the study of caveolin-maxi-K interactions.
caveolin-maxi-K Binding (interactions) of in fibroblasts
4) Confidence 0.32 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0.10 Pain Relevance 0
Several alternative loci have also been proposed, but so far, only the Cav1.1 ?
Cav1 Binding (only) of
5) Confidence 0.29 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.83 Pain Relevance 0.14
This is inconsistent with our demonstration that mutant Y1007A, F1012A, Y1015A was not present in caveolin-containing fractions, and that it neither immunoprecipitates with cav-1 or co-localizes with it at the plasma membrane.
cav-1 Binding (immunoprecipitates) of in plasma
6) Confidence 0.29 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0.06 Pain Relevance 0
A recent study investigating similar maxi-K channel mutants in HEK 293 cells found that single, double and triple substitutions of these aromatic amino acids fail to disrupt the interaction between the maxi-K channel and cav-1, but that complete deletion of the consensus site abolishes almost all (80-85%) interaction with cav-1 [8].
cav-1 Neg (fail) Binding (interaction) of
7) Confidence 0.29 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0 Pain Relevance 0
The maxi-K channel contains a consensus caveolin-binding motif (1007YNMLCFGIY1015) in its C-terminus [26], and mutation of phenylalanine within the caveolin-binding motif had previously been shown to disrupt the association between the ganglioside-specific sialidase Neu3 and cav-1 [27].
cav-1 Binding (association) of
8) Confidence 0.28 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0 Pain Relevance 0
Singh and colleagues [66] exploited the presence of a Cav1.3 CTM by functionally investigating the two human Cav1.3 ?
Cav1 Binding (investigating) of
9) Confidence 0.26 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0 Pain Relevance 0
Disruption of the maxi-K-caveolin-1 interaction alters current expression in human myometrial cells

Background

caveolin-1 Binding (interaction) of
10) Confidence 0.24 Published 2009 Journal Reprod Biol Endocrinol Section Title Doc Link PMC2785819 Disease Relevance 0 Pain Relevance 0.05
Caveolin-1, a 22 kDa protein, participates in caveolae formation and binds and inactivates cell surface protein kinases through its caveolar scaffolding domain (residues 82 to 101) [8].
Caveolin-1 Binding (binds) of
11) Confidence 0.16 Published 2007 Journal Breast Cancer Res Section Body Doc Link PMC2206732 Disease Relevance 1.01 Pain Relevance 0
binds to response elements in the caveolin-1 promoter and triggers caveolin-1 transcription [18,50].
caveolin-1 promoter Binding (binds) of
12) Confidence 0.12 Published 2007 Journal Breast Cancer Res Section Body Doc Link PMC2206732 Disease Relevance 0.85 Pain Relevance 0.07
However, it was shown that desmosterol in model membranes promotes the formation and stability of ordered domains somewhat less efficiently than cholesterol [53, 55], and recent data show that inhibition of 24-dehydrocholesterol reductase in HeLa cells increases the structural heterogeneity of caveolae due to a decreased affinity of caveolin-1 for sterol and a reduced stability of caveolin oligomers [19].
caveolin-1 Binding (affinity) of in HeLa
13) Confidence 0.12 Published 2008 Journal Neurochem Res Section Body Doc Link PMC2758381 Disease Relevance 0.11 Pain Relevance 0
To date, 3 caveolins (Cav-1, Cav-2, and Cav-3) with unique tissue distribution have been characterized.
Cav-1 Binding (characterized) of
14) Confidence 0.08 Published 2009 Journal Toxicological Sciences Section Body Doc Link PMC2769059 Disease Relevance 0.50 Pain Relevance 0.08

General Comments

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