Apolipoprotein B (APOB), a large amphipathic glycoprotein, has hydrophobic lipid-binding and hydrophilic regions. It has a low-density lipoprotein (LDL)-receptor-binding domain. The APOB gene with 29 exons produces two forms, such as apoB-48 and apoB-100 in circulating lipoproteins. This gene is located on human chromosome 2p24.1.
면역원
Peptide with sequence C-TDLHLRYQKDKK from the internal region of the protein sequence according to NP_000375.2.
애플리케이션
Anti-APOB antibody produced in goat has been used in enzyme-linked immunosorbent assay (ELISA).[1]
생화학적/생리학적 작용
Apolipoprotein B (APOB) participates in human lipoprotein metabolism. APOB-48 plays an essential role in the synthesis of chylomicron. APOB-100 is required for the structural component of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and low-density lipoprotein (LDL). APOB is essential in the molecular diagnosis of familial hypercholesterolemia (FH). The hydrophobic lipid-binding and hydrophilic regions are capable of interacting with the aqueous plasma environment.
특징 및 장점
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물리적 형태
Supplied at 0.5 mg/mL in Tris saline with 0.02% sodium azide and 0.5% bovine serum albumin.
면책조항
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Plasma lipoproteins are important determinants of atherosclerosis. Apolipoprotein (apo) B is a large, amphipathic glycoprotein that plays a central role in human lipoprotein metabolism. Two forms of apoB are produced from the APOB gene by a unique posttranscriptional editing process:
Familial hypercholesterolemia (FH) is a monogenic dominant inherited disorder of lipid metabolism characterized by elevated low-density lipoprotein levels, and is mainly attributable to mutations in low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), and proportein convertase subtilisin/kexin type 9 (PCSK9) genes.
Patients with antiphospholipid syndrome have been identified to have higher incidence rates of atherosclerosis (AS) due to the elevated levels of anti‑β2‑glycoprotein I (β2GPI) antibody (Ab). Our previous studies revealed that the anti‑β2GPI Ab formed a stable oxidized low‑density lipoprotein (oxLDL)/β2GPI/anti‑β2GPI Ab complex
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