INT198879

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Context Info
Confidence 0.39
First Reported 2006
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 0.58
Pain Relevance 1.10

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
cleavages 2
bile 2
Vldlr (Mus musculus)
Pain Link Frequency Relevance Heat
metalloproteinase 32 100.00 Very High Very High Very High
long-term potentiation 48 99.22 Very High Very High Very High
Bile 94 99.16 Very High Very High Very High
antagonist 4 86.36 High High
nMDA receptor 20 82.56 Quite High
glial activation 4 79.12 Quite High
cytokine 8 30.56 Quite Low
cINOD 4 5.00 Very Low Very Low Very Low
Inflammation 4 5.00 Very Low Very Low Very Low
isoflurane 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disorder Of Lipid Metabolism 25 97.44 Very High Very High Very High
Lipodystrophy 2 95.40 Very High Very High Very High
Targeted Disruption 37 90.60 High High
Obesity 5 84.60 Quite High
Cardiovascular Disease 5 70.92 Quite High
Hematological Disease 6 59.76 Quite High
Toxicity 8 36.72 Quite Low
Adhesions 24 27.36 Quite Low
Alzheimer's Dementia 36 25.48 Quite Low
Liver Disease 3 23.36 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Like LRP, ApoER2 and VLDLR undergo extracellular cleavages by metalloproteinases to release soluble receptors as well as C-terminal, cell-associated fragments, and these events are induced by Phorbol esters [148].
Localization (release) of VLDLR in cleavages associated with metalloproteinase
1) Confidence 0.39 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1635701 Disease Relevance 0 Pain Relevance 0.16
Thus, cleavages of ApoER2 and VLDLR are regulated in part by alternate splicing events.


Localization (cleavages) of VLDLR in cleavages
2) Confidence 0.39 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1635701 Disease Relevance 0 Pain Relevance 0.09
The release of soluble forms of ApoER2 and VLDLR is affected by the presence of splice variants.
Localization (release) of VLDLR
3) Confidence 0.39 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1635701 Disease Relevance 0 Pain Relevance 0.10
Moreover, Reelin application enhanced LTP induction, which was dependent on the presence of both ApoER2 and VLDLR [97].
Localization (presence) of VLDLR associated with long-term potentiation
4) Confidence 0.39 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1635701 Disease Relevance 0.17 Pain Relevance 0.47
To decipher the molecular basis of Kit-dependent steatosis, we determined the expression profiles of key genes involved in lipid hepatic metabolism: such as apoliproteins (Apoa1, ApoB), lipoprotein receptors (LdlR, VldlR, Scarb1, Lrp1), lipase (Lipc, LipH, Lpl) and others implicated in hepatic lipidogenesis (Scap, Srebf1, Srebf2), lipid secretion (Pltp, Mttp, Abca1), bile acid synthesis (Cyp8b1, Cyp7a1), lipid transport (Slc10a1, Abcb11, Abcb1a, Abcc2) and a lipodystrophy gene, Lipin 1 (Lpin1), encoding a phosphatidate phosphatase enzyme with transcription activity [26-28].
Localization (secretion) of VldlR in bile associated with bile and lipodystrophy
5) Confidence 0.28 Published 2007 Journal BMC Dev Biol Section Body Doc Link PMC1940254 Disease Relevance 0.16 Pain Relevance 0.05
Lin et al (1996a, 1996b) and Watanabe et al (2004) demonstrated that an increase in the intracellular bile acids concentration (in particular TCA) and decrease in hepatic bile acid synthesis inhibit the synthesis and secretion of VLDL-associated triglycerides from hepatocytes as well as the secretion of the apolipoprotein associated with transport of VLDL, namely apoB-100.
Localization (secretion) of VLDL-associated in bile associated with bile and disorder of lipid metabolism
6) Confidence 0.03 Published 2007 Journal Mol Syst Biol Section Body Doc Link PMC2673711 Disease Relevance 0.25 Pain Relevance 0.23

General Comments

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