INT95561

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Context Info
Confidence 0.53
First Reported 2001
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 9
Disease Relevance 2.59
Pain Relevance 0.84

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

transport (Vldlr) extracellular space (Vldlr) nucleus (Vldlr)
lipid metabolic process (Vldlr)
Anatomy Link Frequency
liver 2
juvenile 1
heart 1
Vldlr (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 5 97.28 Very High Very High Very High
Morphine 344 92.36 High High
Neuropeptide 2 72.08 Quite High
Glutamate receptor 2 69.20 Quite High
Analgesic 8 25.00 Low Low
Opioid 56 5.00 Very Low Very Low Very Low
Physical dependence 20 5.00 Very Low Very Low Very Low
withdrawal 18 5.00 Very Low Very Low Very Low
tolerance 16 5.00 Very Low Very Low Very Low
addiction 16 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Repression 4 100.00 Very High Very High Very High
Congenital Anomalies 23 99.44 Very High Very High Very High
Sprains And Strains 176 99.28 Very High Very High Very High
Heart Defects 3 98.04 Very High Very High Very High
Convulsion 4 97.60 Very High Very High Very High
Craniofacial Abnormalities 2 97.02 Very High Very High Very High
Disorder Of Lipid Metabolism 23 94.12 High High
Hyperlipidemia 13 92.28 High High
Syndrome 71 91.84 High High
Anaemia 20 77.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In such a way, Kit loss-of-function mimicked the downregulation of Lpin1, Lpl and Vldlr leading to juvenile steatosis and growth retardation.
Negative_regulation (downregulation) of Vldlr in juvenile
1) Confidence 0.53 Published 2007 Journal BMC Dev Biol Section Body Doc Link PMC1940254 Disease Relevance 0.37 Pain Relevance 0
Expression profiling for key genes participating to the metabolism, the transport, the modification, lipidogenesis and biliary acid synthesis in the liver revealed that only a few genes, namely Vldlr, Lpin1 and Lpl were downregulated in Kit mutants.
Negative_regulation (downregulated) of Vldlr in liver
2) Confidence 0.46 Published 2007 Journal BMC Dev Biol Section Body Doc Link PMC1940254 Disease Relevance 0.09 Pain Relevance 0
In addition to the Lpin1 downregulation, repression of Lpl and Vldlr would also contribute to the hepatic Kit-induced phenotype.
Negative_regulation (repression) of Vldlr associated with repression
3) Confidence 0.46 Published 2007 Journal BMC Dev Biol Section Body Doc Link PMC1940254 Disease Relevance 0.39 Pain Relevance 0
The hypocholesterolaemic effect of trans-dehydrocrotonin was more prominent at the dose of 50 mg kg(-1) with significant decreases in high-density lipoprotein, very-low-density lipoprotein and low-density lipoprotein cholesterol levels.
Negative_regulation (decreases) of very-low-density lipoprotein
4) Confidence 0.43 Published 2001 Journal J. Pharm. Pharmacol. Section Abstract Doc Link 11341371 Disease Relevance 0.18 Pain Relevance 0
Transcripts for very-low-density lipoprotein receptor (Vldlr) and sterol-C5-desaturase (Sc5d) were downregulated.
Negative_regulation (downregulated) of very-low-density lipoprotein receptor
5) Confidence 0.41 Published 2007 Journal Genome Biol Section Body Doc Link PMC2394777 Disease Relevance 0.44 Pain Relevance 0.40
Transcripts for very-low-density lipoprotein receptor (Vldlr) and sterol-C5-desaturase (Sc5d) were downregulated.
Negative_regulation (downregulated) of Vldlr
6) Confidence 0.41 Published 2007 Journal Genome Biol Section Body Doc Link PMC2394777 Disease Relevance 0.44 Pain Relevance 0.39
We found that, in addition to the classical phenotypes, mutations of Kit induced juvenile steatosis, associated with the downregulation of the three genes, VldlR, Lpin1 and Lpl, controlling lipid metabolism in the post-natal liver.
Negative_regulation (downregulation) of VldlR in liver
7) Confidence 0.39 Published 2007 Journal BMC Dev Biol Section Abstract Doc Link PMC1940254 Disease Relevance 0.07 Pain Relevance 0
These include skeletal and craniofacial abnormalities (Lpar1, Pitx2, Satb2, Tcof1, Trps1); heart defects (Adm, Cited2, Cxcl12, Gja1, Hey2, Pitx2, Mef2c); reduced body size (Ebf1, Lpar1, Hsd3b7, Mef2c); decreased adiposity (Cebpb, Ebf1, Lpar1, Npy, Vldlr); behavioral abnormalities (Avpr1a, Ctnnd2, Lpar1, Vldlr); seizures (Cdk5r1, Gabrb1, Gabrb2, Neto1, Nr4a3, Plcb1, S100b, Sv2b); and hearing deficits (Cldn11, Eya, Gjb2, Gjb6) [66], [92]–[124].
Negative_regulation (decreased) of Vldlr in heart associated with convulsion, congenital anomalies, heart defects and craniofacial abnormalities
8) Confidence 0.26 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2730539 Disease Relevance 0.60 Pain Relevance 0
Thus, inhibition of normal Reelin signaling through ApoER2 and VLDLR can acutely modulate other signaling mechanisms through changes in NMDA receptor activity and intracellular signaling pathways [84-89].
Negative_regulation (inhibition) of VLDLR associated with nmda receptor
9) Confidence 0.10 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1635701 Disease Relevance 0 Pain Relevance 0.05

General Comments

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