INT22142

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Context Info
Confidence 0.58
First Reported 1990
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 9
Total Number 11
Disease Relevance 1.84
Pain Relevance 2.93

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

cytosol (Calb1) nucleus (Calb1) intracellular (Calb1)
cytoplasm (Calb1)
Anatomy Link Frequency
putamen 2
lateral region 2
Purkinje cells 2
brain 1
SCN 1
Calb1 (Mus musculus)
Calb1 - D28K (5)
Pain Link Frequency Relevance Heat
Glutamate 34 100.00 Very High Very High Very High
gABA 3 100.00 Very High Very High Very High
Ventral tegmentum 21 99.98 Very High Very High Very High
midbrain 78 98.80 Very High Very High Very High
substance P 4 94.64 High High
Enkephalin 9 94.52 High High
Neuropeptide 4 94.24 High High
5HT 1 92.40 High High
Dorsal column 2 91.08 High High
medulla 17 86.36 High High
Disease Link Frequency Relevance Heat
Parkinson's Disease 126 93.40 High High
Vibrio Infection 1 89.24 High High
Depression 38 77.56 Quite High
Freckles 4 75.00 Quite High
Stress 35 68.92 Quite High
Congenital Anomalies 10 67.68 Quite High
Dystonia 4 64.00 Quite High
Dysphagia 2 57.20 Quite High
Deafness 2 56.36 Quite High
Peripheral Neuropathy 2 55.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Neurons of the SCN core synthesize GABA, CALB, VIP, calretinin (CALR), gastrin releasing peptide (GRP), and neurotensin (NT), and receive input from the retina and from fibers that contain neuropeptide Y (NPY) and 5-hydroxytryptamine (5HT).
Gene_expression (synthesize) of CALB in SCN associated with gaba, 5ht and neuropeptide
1) Confidence 0.58 Published 2001 Journal Brain Res. Section Abstract Doc Link 11597605 Disease Relevance 0.09 Pain Relevance 0.28
Putative Renshaw cells labeled with the virus usually formed small clusters at the most ventral edge of the MN pool (Fig. 6A–C), had cell bodies 10–20 µm in diameter and expressed the calcium binding protein calbindin-D28K (Fig. 6B; [29]).
Gene_expression (expressed) of calbindin-D28K (D28K) in edge
2) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909228 Disease Relevance 0 Pain Relevance 0.10
In P21 mice, degeneration of Purkinje cells is well underway, but the surviving Purkinje cells continue to express the mRNAs for both glutamate decarboxylase and calbindin D28K, two proteins whose expression is characteristic of normal Purkinje neurons.
Gene_expression (express) of D28K (D28K) in Purkinje cells associated with glutamate
3) Confidence 0.06 Published 1990 Journal J. Neurosci. Res. Section Abstract Doc Link 2254957 Disease Relevance 0 Pain Relevance 0.05
In P21 mice, degeneration of Purkinje cells is well underway, but the surviving Purkinje cells continue to express the mRNAs for both glutamate decarboxylase and calbindin D28K, two proteins whose expression is characteristic of normal Purkinje neurons.
Gene_expression (expression) of D28K (D28K) in Purkinje cells associated with glutamate
4) Confidence 0.06 Published 1990 Journal J. Neurosci. Res. Section Abstract Doc Link 2254957 Disease Relevance 0 Pain Relevance 0.05
Furthermore, interneurons that co-express various calcium binding proteins such calbindin-D28k and parvalbumin [29] and parvalbumin and calretinin [48] were also found in this region known to be populated with last order premotor interneurons [49].
Gene_expression (express) of calbindin-D28k in interneurons
5) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2909228 Disease Relevance 0 Pain Relevance 0.03
Reinforcing the role Ca2+ homeostasis in the differential vulnerability of midbrain DA-cells, DA-cells in the dorsomedial region of SN and VTA express calbindin-D28k(Gerfen et al., 1987; McRitchie and Halliday, 1995; Liang et al., 1996; McRitchie et al., 1996).
Gene_expression (express) of calbindin-D28k in midbrain associated with ventral tegmentum and midbrain
6) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.22 Pain Relevance 0.22
Furthermore, DA-cells in the lateral region of the SN which express calbindin-D28k are more sensitive to the neurotoxic effect of 6-OHDA than other SN DA-cells which do not express calbindin-D28k (Rodriguez et al., 2001).


Neg (not) Gene_expression (express) of calbindin-D28k in lateral region
7) Confidence 0.04 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.15 Pain Relevance 0.18
Furthermore, DA-cells in the lateral region of the SN which express calbindin-D28k are more sensitive to the neurotoxic effect of 6-OHDA than other SN DA-cells which do not express calbindin-D28k (Rodriguez et al., 2001).


Gene_expression (express) of calbindin-D28k in lateral region
8) Confidence 0.03 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.16 Pain Relevance 0.21
The large cell neurons in the putamen were preferentially reduced, the immunoreactivity for tyrosine hydroxylase reflecting the dopaminergic afferent and efferent pathways was severely affected, and the expression of 3 calcium binding proteins (i.e. parvalbumin, calbindin-D28K, and calretinin) was disturbed in various ways.
Gene_expression (expression) of calbindin-D28K (D28K) in putamen
9) Confidence 0.03 Published 2004 Journal J. Neuropathol. Exp. Neurol. Section Abstract Doc Link 15535132 Disease Relevance 0.50 Pain Relevance 0.83
The large cell neurons in the putamen were preferentially reduced, the immunoreactivity for tyrosine hydroxylase reflecting the dopaminergic afferent and efferent pathways was severely affected, and the expression of 3 calcium binding proteins (i.e. parvalbumin, calbindin-D28K, and calretinin) was disturbed in various ways.
Gene_expression (expression) of calbindin-D28K (D28K) in putamen
10) Confidence 0.03 Published 2004 Journal J. Neuropathol. Exp. Neurol. Section Abstract Doc Link 15535132 Disease Relevance 0.50 Pain Relevance 0.83
In most brain areas, pharmacological experiments using blocker of eCB synthesis suggest that eCB-mediated synaptic plasticity involves 2-AG rather that anandamide [1], [39], [40], [49]–[55].
Gene_expression (synthesis) of eCB in brain
11) Confidence 0.02 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1933592 Disease Relevance 0.22 Pain Relevance 0.15

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