(Its official name is apolipoprotein B.) Find out in this article. ApoB (the bad protein) and Cholesterol. We all know about the bad cholesterol – LDL. But science is. Cholesterol-rich, apolipoprotein B (apoB)-containing lipoproteins are now widely accepted as the most important causal agents of. The APOB gene provides instructions for making two versions of the apolipoprotein B protein, a short version called apolipoprotein B and a longer version.
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Macrophage scavenger receptor class A: It is true that apo B measurement is less precise than total serum cholesterol. Paradoxical association of enhanced cholesterol efflux with increased incident cardiovascular risks. Hence hepatic and intestinal apo B are termed apo B and apo B 48respectively. There are also some indications that this loop region is formed between the mooring sequence and the 3′ regulatory region of the ApoB mRNA.
On the other hand, high-density lipoprotein HDL is seen as anti-atherogenic because of its role in cellular cholesterol extraction and reverse cholesterol transport.
APOB – Apolipoprotein B precursor – Homo sapiens (Human) – APOB gene & protein
Apolipoprotein B is the primary apolipoprotein of chylomicronsVLDLIDLand LDL particles LDL – known commonly by the misnomer “bad cholesterol ” when in reference to both heart disease and vascular disease in generalwhich is responsible for carrying fat molecules lipidsincluding cholesterolaround the body within the water outside cells to all cells within all tissues.
In animal models, atherosclerosis will not occur in the absence of greatly elevated levels of plasma cholesterol. Arterioscler Thromb Vasc Biol. Ensembl intermediate-density lipoprotein particle Source: TreeFam database of animal gene trees More ApoB is an important component of many of the most atherogenic lipoprotein particles.
JAMA ; Intensive versus moderate lipid lowering with statins after acute coronary syndromes. Cholesterol crystals cause mechanical damage to biological membranes: This has brought in renewed energy for the discovery of novel cholesterol-lowering strategies.
Open in a separate window. Unlike the LDLR, scavenger receptors are not subject to feedback regulation by cellular cholesterol levels; thus, arterial macrophages can internalize unregulated quantities of cholesterol ester and eventually transform into foam cells 15 Mutations in PCSK9 cause autosomal dominant hypercholesterolemia.
Manual assertion inferred from combination of experimental and apolipoproteunas evidence i. ProtoNet; Automatic hierarchical classification of proteins More Animal experiments involving transplantation of atherosclerotic aortic segments into normolipidemic hosts demonstrate decreases in the macrophage content of the transplanted aorta After most of the lipids in the chylomicron have been absorbed, ApoB48 returns to the liver as part of the chylomicron remnant, where it is endocytosed and degraded.
The referees who approved this article are: Evolving Vascular Biology and Clinical Implications”.
It is useful for tracking sequence updates. It lists the nodes as they apolipoproteinss top-down apolipoproteinaas the taxonomic tree, with the more general grouping listed first. The referees who approved the final version are listed with their names and affiliations but without their reports on earlier versions any comments will already have been addressed in the published version.
Intestinal proteins containing ApoB48 are metabolised to chylomicron remnant particles which are taken up by remnant receptors.
Apolipoprotein B (apoB) | ApoB and risk for heart disease
The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Accepted Feb Any medical or genetic information present in this entry is provided for research, educational and informational purposes only. National Center for Biotechnology InformationU.
These bridging molecules work together in sync with other proatherogenic modifications of the extracellular matrix and LDL, culminating in enhanced retention of atherogenic lipoproteins In the future, it may be possible to develop apo B apolipoproteiinas that are even more informative about coronary heart disease risk by, for example, designing them to be particularly sensitive to epitopes displayed in small, dense LDL or oxidatively modified LDL.
Reactome endosome lumen Source: Interestingly, triglyceride-rich apoB-containing lipoproteins that is, remnants do not require oxidative modification to be recognized and massively taken up by arterial macrophages. HDL consists of particles that vary in size, composition, and function As discussed thus far, apoB-containing lipoproteins are intrinsically linked to the initiation, development, and propagation of atherosclerosis.
Apolipoprotein B (apoB)
These local coronary hemodynamic factors and flow characteristics are intrinsically linked to endothelial function, inflammation, and the subsequent development of atherosclerosis 5. The network of endoplasmic reticulum-resident chaperones ERp72, GRP94, calreticulin, and BiP interacts with apolipoprotein b regardless of its lipidation state”. The immune system in atherosclerosis. HPA neuronal cell body Source: Hence, using that fact, one can quantify the number of lipoprotein particles by noting the total ApoB concentration in the circulation.
This occurs as a result of modified-LDL’s toxic effect on vascular endothelium as well its ability both to recruit immune effector cells and to promote platelet activation. Modulation by fasting and refeeding a high carbohydrate diet”. These atherogenic lipoproteins comprise chylomicron remnants, very-low-density lipoprotein VLDLintermediate-density lipoprotein, LDL, and lipoprotein a.
Select item s and click on “Add to basket” to create your own collection here entries max. Please consider upgrading your browser. The algorithm is described in the ISO standard. Z clinical events, such as myocardial infarction are uncommon among individuals with lifelong very low plasma cholesterol levels.
From Wikipedia, the free encyclopedia. However, mounting evidence demonstrates that most apoB-containing lipoproteins up to about 70 nm in diameterexcept for fully formed chylomicrons and large VLDL, are capable of promoting plaque formation 4. Rather, these hemodynamic factors induce specific coronary segments and their gene expression profile to differentially interact with systemic factors, resulting in susceptibility to atherosclerosis at specific locations 7.