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APOB product is the main apolipoprotein of chylomicrons and low density lipoproteins. 再加上，我们可以发APOB 试剂盒 (135) 和 APOB 蛋白 (18)和数多这个蛋白质的别的产品。
Showing 10 out of 359 products:
Human Monoclonal APOB Primary Antibody for 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 for 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 Monoclonal APOB Primary Antibody for 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 for 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 for 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
Human Polyclonal APOB Primary Antibody for 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 for 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 Polyclonal APOB Primary Antibody for 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
Human Polyclonal APOB Primary Antibody for IP, ELISA - ABIN2477466
Davidson, Appel, Doster, Baker, Brown: Diseases and parasites of red foxes, gray foxes, and coyotes from commercial sources selling to fox-chasing enclosures. in Journal of wildlife diseases 1993
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that apos involved in TG metabolism such as apoC2 (显示 APOC2 抗体), C3, E, and A4 (micromolar concentration), and apoB48 and apoA5 (显示 APOA5 抗体) (single-digit nanomolar concentration) can be quantified from a single digestion mixture.
These findings indicate that maternal apo (显示 C9orf3 抗体) B levels are significantly associated with apo (显示 C9orf3 抗体) B levels in their pre-school age children, adjusted for confounding variables. Furthermore, the mother-child correlations in apo (显示 C9orf3 抗体) B levels were independent of mother-child adiposity. Measurement of apo (显示 C9orf3 抗体) B levels in mothers may identify both high-risk children and mothers who may benefit from intervention.
Individuals with apoB higher than predicted by non-HDL (显示 HSD11B1 抗体)-C had significantly higher levels of PAI-1 (显示 SERPINE1 抗体), which may contribute to the increased risk of future atherothrombotic events
analysis of five likely pathogenic heterozygous rare variants that include four novel nonsense mutations in APOB (p.Gln845*, p.Gln2571*, p.Cys2933* and p.Ser3718*) and a rare variant in PCSK9 (显示 PCSK9 抗体) (Minor Allele Frequency <0.1%).
The impact of smoking on the levels of apolipoprotein B (APOB) was evaluated by analyzing data from NHANES for the years 2007-2012 for US adolescents aged 12-19 years and adults aged greater than or eqult to 20 years. The study found that smoking did not influence the observed levels of APOB for either adolescents or adults.
Identify LDLR (显示 LDLR 抗体), APOB and PCSK9 (显示 PCSK9 抗体) novel mutations causing familial hypercholesterolemia in the central south region of China.
Rare variants of APOB or PCSK9 (显示 PCSK9 抗体) were identified in nine of the 22 study patients with extremely low LDL-C levels
Eicosapentaenoic acid has direct antioxidant benefits in various apoB-containing subfractions.
Association of plasma apoB with IR in obese subjects is dependent on gynoid WAT dysfunction
Serum ApoB was not significantly different between term SGA newborns and control term newborns.
enhanced VLDL TG secretion in the absence of hepatocyte ABCA1 (显示 ABCA1 抗体) 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 (显示 LDLR 抗体) and expressing only ApoB100 molecule (ApoB - LDLr (显示 LDLR 抗体)) 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 (显示 LDLR 抗体)(tm1Her) mice, expressing only ApoB100 and deficient in the low density lipoprotein receptor (显示 LDLR 抗体).
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 (显示 PCSK9 抗体) markedly increases intestinal triglyceride-rich apoB production through mechanisms mediated in part by transcriptional effects on apoB.
Mice that produce apoB100 in the RPE (显示 RPE 抗体) and liver secrete lipoproteins into Bruch's membrane, but not to the extent that distinct features of AMD (显示 AMD1 抗体) develop
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 (显示 GUSB 抗体) dysmotility.
Cardiac lipotoxicity may originate from direct inhibition of myocardial ApoB lipoprotein and subsequent decreased lipid export, caused by supraphysiological levels of catecholamines.
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 (显示 APOE 抗体), MTP (显示 MTTP 抗体), and LDLR (显示 LDLR 抗体), 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 (显示 MTTP 抗体)) and apolipoprotein E (显示 APOE 抗体) messenger RNA abundance were higher in the liver.
found association between genotypes for LDLR (显示 LDLR 抗体) 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