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anti-Human APOB Antikörper:
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Human Polyclonal APOB Primary Antibody für ELISA, IHC - ABIN5596981
Sołtysik, Ohsaki, Tatematsu, Cheng, Fujimoto: Nuclear lipid droplets derive from a lipoprotein precursor and regulate phosphatidylcholine synthesis. in Nature communications 2019
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Human Polyclonal APOB Primary Antibody für RID, WB - ABIN152417
Tsai, Hsu, Hsu, Lai, Chen, Shen, Huang, Chen, Lee, Tsai, Hsu, Wu, Huang, Shiao, Hsiao, Tsou: MicroRNA-122 plays a critical role in liver homeostasis and hepatocarcinogenesis. in The Journal of clinical investigation 2012
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Human Monoclonal APOB Primary Antibody für ICC, FACS - ABIN968961
Peterson, Mack, Hall, Alsup, Alexander, Sully, Sawires, Cheung, Otto, Gresham: Apolipoprotein B Is an innate barrier against invasive Staphylococcus aureus infection. in Cell host & microbe 2008
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Guinea Pig Polyclonal APOB Primary Antibody für ID - ABIN2477467
Hazell, Arnold, Flowers, Waeg, Malle, Stocker: Presence of hypochlorite-modified proteins in human atherosclerotic lesions. in The Journal of clinical investigation 1996
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Human Polyclonal APOB Primary Antibody für ELISA, WB - ABIN449695
Benn, Nordestgaard, Jensen, Tybjaerg-Hansen: Polymorphisms in apolipoprotein B and risk of ischemic stroke. in The Journal of clinical endocrinology and metabolism 2007
Human Polyclonal APOB Primary Antibody für IHC (p), IP - ABIN267960
Bakillah, Tedla, Ayoub, John, Norin, Hussain, Brown: Plasma Nitration of High-Density and Low-Density Lipoproteins in Chronic Kidney Disease Patients Receiving Kidney Transplants. in Mediators of inflammation 2015
Human Monoclonal APOB Primary Antibody für RIA, ELISA - ABIN535615
Lin, Gordon, Wetterau: Microsomal triglyceride transfer protein (MTP) regulation in HepG2 cells: insulin negatively regulates MTP gene expression. in Journal of lipid research 1995
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Human Monoclonal APOB Primary Antibody für FACS, IF - ABIN965573
Benn: Apolipoprotein B levels, APOB alleles, and risk of ischemic cardiovascular disease in the general population, a review. in Atherosclerosis 2009
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Human Polyclonal APOB Primary Antibody für IF (p), IHC (p) - ABIN872950
Choi, de Poot, Lee, Kim, Han, Kim, Finley, Lee: Open-gate mutants of the mammalian proteasome show enhanced ubiquitin-conjugate degradation. in Nature communications 2016
Elevated Apo-B level was related to the % necrotic core in target coronary artery lesions in stable coronary artery disease patients, suggesting a role of Apo-B as a biomarker of unstable plaque in this population.
Report familial hypercholesterolaemia in Portugese patients with novel APOB mutations.
Higher apoB/apoA-I ratio is significantly associated with faster hemodynamic progression of aortic stenosis in the younger patients.
Major histocompatibility complex class II molecule-restricted peptide epitopes of ApoB function as Treg epitopes.
The rs670, rs5070 of APOA1 and rs693 of APOB polymorphisms are not genetic susceptibility factors for ACS in Mexican population and had no effect on their apolipoprotein concentrations.
ABCA1-mediated cholesterol efflux and apoB-lipoprotein secretion in the retinal pigment epithelium
PCSK9 association with intestinal secretion and plasma overaccumulation of TRL apoB-48 in men with IR
Pathogenic mutations in LDLR, APOB, PCSK9 and LDLRAP1 genes were found in 17 of 225 patients with familial hypercholesterolemia leading to premature myocardial infarction.
Circulating IgG for ApoB100-derived peptide antigens may be a useful biomarker of Acute coronary syndrome (ACS), although anti-ApoB IgG levels were not associated with the coronary artery plaque burden characterized by the coronary Gensini score.
APOB inactivation is associated with poor prognosis in hepatocellular carcinoma.
In Singapore, 4.2% (n=4) familial hypercholesterolemia had APOB mutations.
These results indicate the potential of liquid chromatography-multiple-reaction-monitoring mass spectrometry to become of clinical importance in the future for intrauterine growth restriction risk assessment based on maternal apolipoprotein B100 serum levels.
Significant prognostic risk factors for the mentioned comorbid pathologies were lipid metabolism parameters HDL-Ch, LDL-Ch, VLDL-Ch and carrier state of the +83T allele of the ApoA1 gene and Del allele of the ApoB gene.
We confirmed the association between the apolipoprotein B rs151009667 polymorphism and Familial Hypercholesterolemia in a Saudi population. The Val2095Glu novel variant did not appear in either patients with Familial Hypercholesterolemia or controls.
ApoA-I, apoB and the apoB/apoA-I ratio showed strong association with ultrasound indicators of carotid atherosclerosis in ischemic stroke patients.
Mutation spectrum and genotype-phenotype correlation was analyzed in patients with familial hypercholesterolemia in Chinese population.
Serum ApoA-1, ApoB, and ApoB/ApoA-1 ratio may not have significant advantage over conventional lipoproteins in evaluating the presence of systemic inflammation, MS, and risk of atherosclerosis in obese adolescents.
The objective of this study was to evaluate whether apolipoprotein gene polymorphisms confer susceptibility to osteonecrosis of the femoral head.
Authors performed an analysis of public databases and literature for every variant published associated with FH, in the genes LDLR, APOB, and PCSK9.
An increased apo B/apo A1 ratio was independently associated with all-cause mortality and cardiovascular events in peritoneal dialysis patients.
Type 2 diabetic, hyperlipidemic LDLr(-/-)ApoB(100/100) mice show increased calcific aortic valve disease.
This study demonstrates that prevention of renal apoB accumulation is a mechanism by which TGF-beta inhibition is nephroprotective.
Atorvastatin therapy did not show cholesterol-independent effects on inflammation in atherosclerotic lesions in Ldlr(-/-)Apob(100/100) mice, whereas a cholesterol-lowering diet intervention was effective.
A peptide fragment of apoB-100 altered the immune-dominant epitope of CD8+ T cells and reduced atherosclerosis.
BI-1-mediated enhancement of ApoB secretion regulates hepatic lipid accumulation.
enhanced VLDL TG secretion in the absence of hepatocyte ABCA1 is due to altered intracellular trafficking of apolipoprotein B (apoB), resulting in augmented TG addition to nascent VLDL.
We carried out our experiment in mice deficient in the low density lipoprotein (LDL) receptor and expressing only ApoB100 molecule (ApoB - LDLr) where the development of atherosclerosis is known to closely mimic human atherosclerosis
The effect of hypercholesterolemia induced immune response and inflammation on progression of atherosclerosis in ApoB(tm25gy) LDLr(tm1Her) mice, expressing only ApoB100 and deficient in the low density lipoprotein receptor.
ApoB-containing lipoproteins contribute to augmentation of AngII-induced abdominal aortic aneurysms in male mice.
Immunization with human apolipoprotein B100 (ApoB) resulted in four-fold increased accumulation of effector T cells in ApoB-containing matrigel
PCSK9 markedly increases intestinal triglyceride-rich apoB production through mechanisms mediated in part by transcriptional effects on apoB.
Mice that produce apoB100 in the RPE and liver secrete lipoproteins into Bruch's membrane, but not to the extent that distinct features of AMD develop
Its overexpression induce memory and cognitive decline in older animals, which indicates the importance of balanced lipid metabolism.
The aim of this study was to characterize the ocular morphology of low-density lipoprotein receptor-deficient apolipoprotein B-100-only mice, with IGF-II overexpression.
Our data establish the role of APOB gene in severe gut dysmotility.
Cardiac lipotoxicity may originate from direct inhibition of myocardial ApoB lipoprotein and subsequent decreased lipid export, caused by supraphysiological levels of catecholamines.
ApoB-100 transgenic animals present i) elevated serum and cerebral levels of triglycerides and ApoB-100, ii) increased cerebral tau phosphorylation at phosphosites Ser(199), Ser(199/202), Ser(396) and Ser(404).
model in which increased hepatic sortilin binds intracellular APOB-containing particles in the Golgi apparatus as well as extracellular LDL at the plasma membrane and traffics them to the lysosome for degradation
propose a new role for PCSK9 that involves shuttling between apoB and low-density lipoprotein receptor
Study concludes that APOB-associated cholesterol deficiency represents most likely an incomplete dominant inherited metabolic disease with incomplete penetrance in heterozygotes.
The clinicopathological phenotype of affected Holstein cattle homozygous for the causative apolipoprotein B gene (APOB) mutation associated with cholesterol deficiency is described.
Beyond malabsorption of dietary lipids, deleterious effects of apolipoprotein B deficiency on hepatic lipid metabolism, steroid biosynthesis, and cell membrane function can be expected, which may result in unspecific symptoms of reduced fertility, growth, and health.
Cholesterol deficiency results from a 1.3kbp insertion of an endogenous retrovirus (ERV2-1-LTR_BT) into exon 5 of the APOB gene at BTA11:77,959kb. The insertion is flanked by 6bp target site duplications as described for insertions mediated by retroviral integrases.
A transposable element insertion in APOB causes cholesterol deficiency in Holstein cattle
Nonesterified fatty acids significantly inhibit the expression of ApoB100, ApoE, MTP, and LDLR, thereby decreasing the synthesis and assembly of VLDL and inducing TG accumulation in bovine hepatocytes.
after calving the apolipoprotein B(100) mRNA synthesis was lower, whereas microsomal triglyceride transfer protein (MTP) and apolipoprotein E messenger RNA abundance were higher in the liver.
found association between genotypes for LDLR and APOB polymorphisms and serum lipid levels, but none of them seem to be the causal mutation but probably represent closely linked polymorphisms
This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. It occurs in plasma as two main isoforms, apoB-48 and apoB-100: the former is synthesized exclusively in the gut and the latter in the liver. The intestinal and the hepatic forms of apoB are encoded by a single gene from a single, very long mRNA. The two isoforms share a common N-terminal sequence. The shorter apoB-48 protein is produced after RNA editing of the apoB-100 transcript at residue 2180 (CAA->UAA), resulting in the creation of a stop codon, and early translation termination. Mutations in this gene or its regulatory region cause hypobetalipoproteinemia, normotriglyceridemic hypobetalipoproteinemia, and hypercholesterolemia due to ligand-defective apoB, diseases affecting plasma cholesterol and apoB levels.
, apolipoprotein B (including Ag(x) antigen)
, apolipoprotein B-100
, apolipoprotein B48
, mutant Apo B 100
, apolipoprotein B PI
, apolipoprotein B-48
, apolipoprotein B