INT167913

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Context Info
Confidence 0.75
First Reported 2010
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 3
Total Number 9
Disease Relevance 0.38
Pain Relevance 3.34

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

small molecule metabolic process (CACNA1C) plasma membrane (CACNA1C) transmembrane transport (CACNA1C)
cytoplasm (CACNA1C)
Anatomy Link Frequency
neural 2
myocardium 1
bone marrow 1
skeletal muscle 1
CACNA1C (Homo sapiens)
Pain Link Frequency Relevance Heat
tetrodotoxin 84 100.00 Very High Very High Very High
sodium channel 28 100.00 Very High Very High Very High
potassium channel 28 100.00 Very High Very High Very High
Calcium channel 22 100.00 Very High Very High Very High
Action potential 36 76.80 Quite High
addiction 7 75.20 Quite High
anesthesia 8 25.00 Low Low
fibrosis 2 8.48 Low Low
cytokine 7 5.00 Very Low Very Low Very Low
adenocard 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Malignant Hyperthermia 2 96.84 Very High Very High Very High
Hypertrophy 6 78.40 Quite High
Obesity 136 75.00 Quite High
Fibrosis 5 8.48 Low Low
Aging 11 5.00 Very Low Very Low Very Low
Heart Rate Under Development 9 5.00 Very Low Very Low Very Low
Disease 8 5.00 Very Low Very Low Very Low
Neurodegenerative Disease 7 5.00 Very Low Very Low Very Low
Injury 7 5.00 Very Low Very Low Very Low
Targeted Disruption 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the guinea pig, we have previously shown an age-dependent increase in SAN tissue lacking expression of Cx43 and Cav1.2 (major L-type Ca2+ channel isoform in working myocardium) [27,28].
Neg (lacking) Gene_expression (expression) of Cav1.2 in myocardium
1) Confidence 0.75 Published 2010 Journal Journal of Molecular and Cellular Cardiology Section Body Doc Link PMC2845824 Disease Relevance 0.08 Pain Relevance 0.16
The primary hADSCs expressed MaxiK (responsible for human large-conductance, voltage- and calcium-dependent K+ channel), Kv1.4 and Kv4.2 (human voltage-dependent K+ channel), Eag2 (human ether-รก-go-go K+ channel), SCN5A (TTX-insensitive Na+ channel), CACNA1C (human voltage-dependent L-type Ca2+ channel, alpha 1C subunit), and CACNA1G (human voltage-dependent T-type Ca2+ channel, alpha 1G subunit) constitutively.
Gene_expression (expressed) of CACNA1C associated with tetrodotoxin
2) Confidence 0.48 Published 2010 Journal BMC Cell Biol Section Body Doc Link PMC2867791 Disease Relevance 0 Pain Relevance 0.38
Following neural differentiation with bFGF and forskolin, the gene expression levels of MaxiK, Kv4.2, Eag2, SCN5A, CACNA1C, and CACNA1G in NI-hADSCs were significantly higher than in the primary hADSCs (Figure 4d, 4e).
Gene_expression (levels) of CACNA1C in neural
3) Confidence 0.48 Published 2010 Journal BMC Cell Biol Section Body Doc Link PMC2867791 Disease Relevance 0 Pain Relevance 0.18
Undifferentiated bone marrow-derived hMSCs are known to express the TTX-sensitive sodium channel gene (NE-Na), potassium channel genes (MaxiK, Kv1.4, Kv4.2, Kv4.3, and Eag1) and the calcium channel gene (CACNA1C) [56,57].
Gene_expression (express) of CACNA1C in bone marrow associated with tetrodotoxin, calcium channel, sodium channel and potassium channel
4) Confidence 0.48 Published 2010 Journal BMC Cell Biol Section Body Doc Link PMC2867791 Disease Relevance 0 Pain Relevance 0.62
Following neural differentiation with bFGF and forskolin, the gene expression levels of MaxiK, Kv4.2, Eag2, SCN5A, CACNA1C, and CACNA1G in NI-hADSCs were significantly higher than in the primary hADSCs (Figure 4d, 4e).
Gene_expression (expression) of CACNA1C in neural
5) Confidence 0.48 Published 2010 Journal BMC Cell Biol Section Body Doc Link PMC2867791 Disease Relevance 0 Pain Relevance 0.20
Further examination by RT-PCR showed that NI-hADSCs expressed high level of ionic channel genes for sodium (SCN5A), potassium (MaxiK, Kv4.2, and EAG2), and calcium channels (CACNA1C and CACNA1G), which were expressed constitutively in the primary hADSCs.
Gene_expression (expressed) of CACNA1C associated with calcium channel
6) Confidence 0.42 Published 2010 Journal BMC Cell Biol Section Abstract Doc Link PMC2867791 Disease Relevance 0.13 Pain Relevance 0.40
However, this study indicates that primary hADSCs also express ion channel mRNAs, including potassium channel genes (MaxiK, Kv1.4, Kv4.2, and Eag2), calcium channel genes (CACNA1C and CACN1G), and the TTX-insensitive sodium channel gene (SCN5A), but do not exhibit the TTX-sensitive sodium channel gene (NE-Na) and other voltage-dependent potassium channel genes (Kv4.3 and Eag1) (Figure 4d).
Gene_expression (express) of CACN1G associated with tetrodotoxin, calcium channel, sodium channel and potassium channel
7) Confidence 0.42 Published 2010 Journal BMC Cell Biol Section Body Doc Link PMC2867791 Disease Relevance 0 Pain Relevance 0.67
However, this study indicates that primary hADSCs also express ion channel mRNAs, including potassium channel genes (MaxiK, Kv1.4, Kv4.2, and Eag2), calcium channel genes (CACNA1C and CACN1G), and the TTX-insensitive sodium channel gene (SCN5A), but do not exhibit the TTX-sensitive sodium channel gene (NE-Na) and other voltage-dependent potassium channel genes (Kv4.3 and Eag1) (Figure 4d).
Gene_expression (express) of CACNA1C associated with tetrodotoxin, calcium channel, sodium channel and potassium channel
8) Confidence 0.42 Published 2010 Journal BMC Cell Biol Section Body Doc Link PMC2867791 Disease Relevance 0 Pain Relevance 0.67
PURPOSE: To report the identification of a novel mutation in the CACNA1S gene that encodes the alpha-1-subunit (Cav1.1) of the voltage-gated skeletal muscle L-type calcium channel in a patient with malignant hyperthermia.
Gene_expression (encodes) of alpha-1-subunit in skeletal muscle associated with calcium channel and malignant hyperthermia
9) Confidence 0.06 Published 2010 Journal Can J Anaesth Section Abstract Doc Link 20431982 Disease Relevance 0.17 Pain Relevance 0.05

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