"Mice, Knockout, ApoE" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
Strains of mice that contain genetic disruptions (knockout) of APOLIPOPROTEINS E genes. They are used as models for ATHEROSCLEROSIS research.
Descriptor ID |
D000074085
|
MeSH Number(s) |
B01.050.050.136.500.500.500 B01.050.150.900.649.313.992.635.505.500.550.455.500 B01.050.150.900.649.313.992.635.505.500.800.500.512
|
Concept/Terms |
Mice, Knockout, ApoE- Mice, Knockout, ApoE
- Apo E Knockout Mice
- ApoE Knockout Mice
- Knockout Mice, ApoE
- Mice, ApoE Knockout
|
Below are MeSH descriptors whose meaning is more general than "Mice, Knockout, ApoE".
- Organisms [B]
- Eukaryota [B01]
- Animals [B01.050]
- Animal Population Groups [B01.050.050]
- Animals, Genetically Modified [B01.050.050.136]
- Mice, Transgenic [B01.050.050.136.500]
- Mice, Knockout [B01.050.050.136.500.500]
- Mice, Knockout, ApoE [B01.050.050.136.500.500.500]
- Chordata [B01.050.150]
- Vertebrates [B01.050.150.900]
- Mammals [B01.050.150.900.649]
- Eutheria [B01.050.150.900.649.313]
- Rodentia [B01.050.150.900.649.313.992]
- Muridae [B01.050.150.900.649.313.992.635]
- Murinae [B01.050.150.900.649.313.992.635.505]
- Mice [B01.050.150.900.649.313.992.635.505.500]
- Mice, Mutant Strains [B01.050.150.900.649.313.992.635.505.500.550]
- Mice, Knockout [B01.050.150.900.649.313.992.635.505.500.550.455]
- Mice, Knockout, ApoE [B01.050.150.900.649.313.992.635.505.500.550.455.500]
- Mice, Transgenic [B01.050.150.900.649.313.992.635.505.500.800]
- Mice, Knockout [B01.050.150.900.649.313.992.635.505.500.800.500]
- Mice, Knockout, ApoE [B01.050.150.900.649.313.992.635.505.500.800.500.512]
Below are MeSH descriptors whose meaning is more specific than "Mice, Knockout, ApoE".
This graph shows the total number of publications written about "Mice, Knockout, ApoE" by people in this website by year, and whether "Mice, Knockout, ApoE" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
Year | Major Topic | Minor Topic | Total |
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2016 | 0 | 1 | 1 |
2017 | 0 | 2 | 2 |
2018 | 0 | 6 | 6 |
2019 | 0 | 4 | 4 |
2020 | 0 | 1 | 1 |
To return to the timeline, click here.
Below are the most recent publications written about "Mice, Knockout, ApoE" by people in Profiles.
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Direct reprogramming induces vascular regeneration post muscle ischemic injury. Mol Ther. 2021 10 06; 29(10):3042-3058.
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Single systemic transfer of a human gene associated with exceptional longevity halts the progression of atherosclerosis and inflammation in ApoE knockout mice through a CXCR4-mediated mechanism. Eur Heart J. 2020 07 07; 41(26):2487-2497.
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Platelet-Derived Exosomal MicroRNA-25-3p Inhibits Coronary Vascular Endothelial Cell Inflammation Through Adam10 via the NF-?B Signaling Pathway in ApoE-/- Mice. Front Immunol. 2019; 10:2205.
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Amorphous nano-selenium quantum dots improve endothelial dysfunction in rats and prevent atherosclerosis in mice through Na+/H+ exchanger 1 inhibition. Vascul Pharmacol. 2019 04; 115:26-32.
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Deficiency of Monoacylglycerol Lipase Enhances IgM Plasma Levels and Limits Atherogenesis in a CB2-Dependent Manner. Thromb Haemost. 2019 Feb; 119(2):348-351.
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Cystathionine ? Lyase Sulfhydrates the RNA Binding Protein Human Antigen R to Preserve Endothelial Cell Function and Delay Atherogenesis. Circulation. 2019 01 02; 139(1):101-114.
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6-Gingerol Ameliorates Behavioral Changes and Atherosclerotic Lesions in ApoE-/- Mice Exposed to Chronic Mild Stress. Cardiovasc Toxicol. 2018 10; 18(5):420-430.
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Canagliflozin attenuates the progression of atherosclerosis and inflammation process in APOE knockout mice. Cardiovasc Diabetol. 2018 07 26; 17(1):106.
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Mindin deficiency in macrophages protects against foam cell formation and atherosclerosis by targeting LXR-ß. Clin Sci (Lond). 2018 06 15; 132(11):1199-1213.
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SGK1 induces vascular smooth muscle cell calcification through NF-?B signaling. J Clin Invest. 2018 07 02; 128(7):3024-3040.