"Apolipoprotein A-I" 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.
The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.
| Descriptor ID |
D016632
|
| MeSH Number(s) |
D10.532.091.200.100 D12.776.070.400.200.100 D12.776.521.120.200.100
|
| Concept/Terms |
Apolipoprotein A-I- Apolipoprotein A-I
- Apolipoprotein A I
- Apo A-I
- Apo A1
- Apolipoprotein AI
- ApoA-1
- ApoA-I
- Apolipoprotein A-1
- Apolipoprotein A 1
- Apolipoprotein A1
- Apo A-1
- Apo AI
Pro-Apolipoprotein A-I- Pro-Apolipoprotein A-I
- Pro Apolipoprotein A I
- Pro-Apo A-I
- Pro Apo A I
- Proapolipoprotein AI
- Apolipoprotein AI Propeptide
|
Below are MeSH descriptors whose meaning is more general than "Apolipoprotein A-I".
Below are MeSH descriptors whose meaning is more specific than "Apolipoprotein A-I".
This graph shows the total number of publications written about "Apolipoprotein A-I" by people in this website by year, and whether "Apolipoprotein A-I" 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 |
|---|
| 1996 | 1 | 1 | 2 |
| 1998 | 0 | 1 | 1 |
| 1999 | 1 | 0 | 1 |
| 2000 | 1 | 2 | 3 |
| 2001 | 2 | 2 | 4 |
| 2003 | 3 | 1 | 4 |
| 2004 | 2 | 1 | 3 |
| 2005 | 2 | 0 | 2 |
| 2008 | 4 | 1 | 5 |
| 2009 | 4 | 3 | 7 |
| 2010 | 2 | 3 | 5 |
| 2011 | 2 | 0 | 2 |
| 2012 | 3 | 1 | 4 |
| 2013 | 2 | 0 | 2 |
| 2014 | 4 | 1 | 5 |
| 2015 | 2 | 0 | 2 |
| 2016 | 1 | 0 | 1 |
| 2017 | 1 | 0 | 1 |
| 2018 | 1 | 1 | 2 |
| 2019 | 1 | 0 | 1 |
| 2022 | 0 | 1 | 1 |
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click here.
Below are the most recent publications written about "Apolipoprotein A-I" by people in Profiles.
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Adiponectin Stimulates Apolipoprotein A-1 Gene Expression in HepG2 Cells via AMPK, PPARa, and LXRs Signaling Mechanisms. Biochemistry (Mosc). 2022 Nov; 87(11):1252-1259.
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[Characterization of Distal and Proximal Alternative Promoters of the Human ApoA-I Gene]. Mol Biol (Mosk). 2019 May-Jun; 53(3):485-496.
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Interleukin-17 Drives Interstitial Entrapment of Tissue Lipoproteins in Experimental Psoriasis. Cell Metab. 2019 02 05; 29(2):475-487.e7.
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Tumor necrosis factor a stimulates endogenous apolipoprotein A-I expression and secretion by human monocytes and macrophages: role of MAP-kinases, NF-?B, and nuclear receptors PPARa and LXRs. Mol Cell Biochem. 2018 Nov; 448(1-2):211-223.
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Genetic control of apoprotein A-I and atheroprotection: some insights from inbred strains of mice. Curr Opin Lipidol. 2017 Oct; 28(5):403-407.
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Synthetic Amphipathic Helical Peptides Targeting CD36 Attenuate Lipopolysaccharide-Induced Inflammation and Acute Lung Injury. J Immunol. 2016 07 15; 197(2):611-9.
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PPAR? Represses Apolipoprotein A-I Gene but Impedes TNFa-Mediated ApoA-I Downregulation in HepG2 Cells. J Cell Biochem. 2016 09; 117(9):2010-22.
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Elucidation of the Aggregation Pathways of Helix-Turn-Helix Peptides: Stabilization at the Turn Region Is Critical for Fibril Formation. Biochemistry. 2015 Jul 07; 54(26):4050-62.
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Therapeutic ultrasound: Increased HDL-Cholesterol following infusions of acoustic microspheres and apolipoprotein A-I plasmids. Atherosclerosis. 2015 Jul; 241(1):92-9.
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Alginic acid cell entrapment: a novel method for measuring in vivo macrophage cholesterol homeostasis. J Lipid Res. 2015 Feb; 56(2):470-83.