INT112089

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Context Info
Confidence 0.75
First Reported 2003
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 73
Total Number 74
Disease Relevance 23.80
Pain Relevance 1.97

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
brain 4
fibroblasts 4
plasma 2
retina 2
sinoatrial node 2
Cav1 (Mus musculus)
Pain Link Frequency Relevance Heat
metalloproteinase 19 99.56 Very High Very High Very High
amygdala 27 97.60 Very High Very High Very High
long-term potentiation 57 96.96 Very High Very High Very High
nMDA receptor 24 96.76 Very High Very High Very High
fibrosis 56 95.76 Very High Very High Very High
Calcium channel 43 95.68 Very High Very High Very High
Hippocampus 28 95.16 Very High Very High Very High
antagonist 56 94.24 High High
cINOD 54 92.72 High High
Action potential 86 90.48 High High
Disease Link Frequency Relevance Heat
Channelopathies 459 100.00 Very High Very High Very High
Disease 515 99.92 Very High Very High Very High
Hypokalemic Periodic Paralysis 783 99.76 Very High Very High Very High
Anxiety Disorder 54 99.44 Very High Very High Very High
Cancer 1121 99.40 Very High Very High Very High
Adenocarcinoma 10 98.40 Very High Very High Very High
Breast Cancer 612 98.36 Very High Very High Very High
Metastasis 51 96.84 Very High Very High Very High
Dystonia 270 96.36 Very High Very High Very High
Death 113 96.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Taken together these data indicate that following loss of CaV1.3 alpha 1 subunit expression there is sufficient residual activity of other Ca2+ channel subtypes to support NMDA receptor-independent long-term potentiation and some forms of sensory behavior/function.
Gene_expression (expression) of CaV1 associated with nmda receptor and long-term potentiation
1) Confidence 0.75 Published 2003 Journal Neuroscience Section Abstract Doc Link 12890513 Disease Relevance 0.19 Pain Relevance 0.34
On the one hand, the loss of synapses in the OPL and the sprouting of dendrites into the ONL point to significant defects in the synthesis of Cav1.4 protein, and consequently of transmitter release, in the vast majority of photoreceptor cells; this suggests that nearly all Cacna1fnob2 photoreceptor cells are making insufficient amounts of functional channel protein.
Gene_expression (synthesis) of Cav1 in dendrites
2) Confidence 0.69 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0.06 Pain Relevance 0
While full-length Cav1.4 protein is produced (albeit at presumably reduced levels) in the Cacna1fnob2 mouse, the encoded amino acid sequence differs from that in the wild type by approximately 20 residues in the N-terminus of the protein (Figure 2C).
Gene_expression (produced) of Cav1
3) Confidence 0.69 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0
PTRF-CAVIN protein was completely absent from fibroblasts and skeletal muscle, whereas the caveolin-1 and caveolin-3 abundance was unchanged (Figure 4D and 4G).
Gene_expression (abundance) of caveolin-1 in skeletal muscle
4) Confidence 0.63 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2837386 Disease Relevance 0.26 Pain Relevance 0
The discovery of single missense CACNA1S mutations in humans with HPP-1 which still allow expression of a full-length Cav1.1 ?
Gene_expression (expression) of Cav1 associated with hypokalemic periodic paralysis
5) Confidence 0.61 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 1.06 Pain Relevance 0
Cav1.3 is expressed together with Cav1.2 in many tissues, such as the sinoatrial node and heart atria, neurons, chromaffin cells, and pancreatic islets.
Gene_expression (expressed) of Cav1 in sinoatrial node
6) Confidence 0.61 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.16 Pain Relevance 0
Cav1.3 is expressed together with Cav1.2 in many tissues, such as the sinoatrial node and heart atria, neurons, chromaffin cells, and pancreatic islets.
Gene_expression (expressed) of Cav1 in sinoatrial node
7) Confidence 0.61 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.16 Pain Relevance 0
We attempted to detect Cav1.4 channel protein in sections of mouse retina; however our antibody is directed against the C-terminus of the human protein, which shares only ?
Gene_expression (detect) of Cav1 in retina
8) Confidence 0.60 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0.03
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.
Gene_expression (expressed) of cav-1 in fibroblasts
9) Confidence 0.60 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0.09 Pain Relevance 0
To establish whether interactions between maxi-K channels and caveolin affect the endogenous myometrial total outward K+ current, we used a siRNA to inhibit cav-1 gene expression in hMSMCs.
Gene_expression (expression) of cav-1 gene
10) Confidence 0.60 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0 Pain Relevance 0
As caveolin-1 was present in patient fibroblasts in normal quantities (Figure 4D) lack of PTRF-CAVIN seems to disable recruitment of caveolin-1 into the caveolar microdomains of the outer cell membrane.
Gene_expression (present) of caveolin-1 in fibroblasts
11) Confidence 0.57 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2837386 Disease Relevance 0.34 Pain Relevance 0
The blots were probed with anti-caveolin-1, anti-caveolin-3 and anti-PTRF as primary antibodies and corresponding peroxidase-labeled secondary antibodies.
Gene_expression (probed) of anti-caveolin-1
12) Confidence 0.55 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2837386 Disease Relevance 0 Pain Relevance 0
Cells were labeled with anti-caveolin-1 and anti-PTRF antibodies and subsequently with appropriate secondary fluorescent antibodies.
Gene_expression (labeled) of anti-caveolin-1
13) Confidence 0.55 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2837386 Disease Relevance 0.17 Pain Relevance 0
We hypothesized that the difference in phenotypes of the two mouse models was the result of alternative splicing of the ETn element, which would allow some transcription and synthesis of Cav1.4 protein.
Gene_expression (synthesis) of Cav1
14) Confidence 0.54 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0
These results indicated that a full-length Cav1.4 channel (corresponding to the mRNA sequence from the smaller Mr, less intense band in Figure 1B) could be present in the Cacna1fnob2 mouse.
Gene_expression (present) of Cav1 in band
15) Confidence 0.54 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0.09 Pain Relevance 0.05
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 (producing) of Cav1 in spleen
16) Confidence 0.54 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2432030 Disease Relevance 0 Pain Relevance 0.03
So far, no human diseases resulting from mutations in the CACNA1D gene encoding the Cav1.3 ?
Gene_expression (encoding) of Cav1 associated with disease
17) Confidence 0.53 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.55 Pain Relevance 0
Cav1.1-deficient skeletal muscle myotubes were successfully used to demonstrate that the Cav1.1 ?
Gene_expression (demonstrate) of Cav1 in myotubes
18) Confidence 0.53 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0 Pain Relevance 0
Since K+-channels are not mutated in HPP-1 or HPP-2, the only possibility is that mutations observed in the pore-forming subunits of Cav1.1 ?
Gene_expression (forming) of Cav1 in pore associated with hypokalemic periodic paralysis
19) Confidence 0.53 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.53 Pain Relevance 0
Like other VGCCs (such as Cav1.2 and Cav1.3) Cav1.4 channels are capable of undergoing robust CDI in a CaM-dependent manner [67] when this inhibitory domain is removed.
Gene_expression (channels) of Cav1
20) Confidence 0.53 Published 2010 Journal Pflugers Arch Section Body Doc Link PMC2883925 Disease Relevance 0.20 Pain Relevance 0.03

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