Ask about this productRelated genes to: ApoB antibody
- Gene:
- APOB NIH gene
- Name:
- apolipoprotein B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: ApoB antibody
Related articles to: ApoB antibody
- A diffuse-type tenosynovial giant cell tumor (D-TGCT) is a rare, locally invasive tumor that mainly involves large weight-bearing joints, such as the knees, hips, and ankles. Herein, we report a rare case of D-TGCT of the hip joint in a 14-year-old girl. The patient presented with pain and limited movement without a history of trauma. Owing to the continuous progression of hip synovitis, whole exome sequencing was performed, which identified pathogenic variations in the frizzled class receptor 4 (NM_012193.3:c.379C>T(p.Arg127Cys)) and apolipoprotein B (NM_000384.2:c.10579C>T(p.Arg3527Trp)) genes. APOB mutations are associated with hypercholesterolemia. Magnetic resonance imaging of the right hip joint showed thickening of the synovial membrane with irregular edges, low signal intensity on T1-weighted images, and high signal intensity on PDWI+FS images. Small nodules with low signal intensity and clear boundaries were also observed on both types of images. An arthroscopic examination revealed numerous white synovial, chondromate-like tissues under the articular capsule, and D-TGCT was diagnosed based on the histopathological results. One year after the surgery, the patient had good functional recovery and no tumor recurrence. - Source: PubMed
Publication date: 2026/05/15
Wang YujiaZhang ShaohuaGe ShuqiongZheng HongruiXin Hanlong - Reducing atherogenic lipoproteins to lower cardiovascular risk is a key objective in obesity treatment. Accurate lipoprotein measurements are essential for determining the need for therapy and guiding its management. To identify the best equation for estimating LDL cholesterol, LDL measured directly (LDL-D) is compared to LDL calculated using equations developed by Friedewald (LDL-F), Martin (LDL-M) and Sampson/NIH (LDL-S). This study also examines the change of LDL and apolipoprotein B levels during a multidisciplinary obesity treatment programme. - Source: PubMed
Oswald JohannesBregulla IrisBröder MonikaReiter RaphaelEberhardt JulianGomahr JulianSchaffler-Schaden Dagmar - High-density lipoprotein cholesterol (HDL-C) has been inversely associated with atherosclerotic cardiovascular disease (ASCVD) risk. This relationship is the foundation of the "HDL hypothesis," which states that increasing plasma HDL-C levels would result in a decrease in cardiovascular events. The recent surge in clinical testing of cholesteryl ester transfer protein (CETP) inhibitors provides valuable data for this hypothesis. The CETP inhibitors increase plasma HDL-C along with variable effects on low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apoB). The clinical outcomes of randomized controlled trials were heterogeneous, with several studies showing either neutral or adverse clinical outcomes despite robust increases in HDL-C values. These observations along with Mendelian randomization studies suggest that low HDL-C is a risk marker, not a causal mediator of ASCVD. New evidence points to HDL functionality, specifically cholesterol efflux potential and particle composition, instead of HDL-C concentration as a more relevant determinant of ASCVD risk. The favorable clinical outcomes observed with certain CETP inhibitors are more consistently explained by reductions in apoB-containing lipoproteins (including LDL-C and non-HDL-C), rather than increases in HDL-C itself. This distinction reframes the HDL hypothesis where HDL-C is merely a biomarker of ASCVD while apoB-containing lipoproteins are the more plausible causal treatment pathway. These findings have shifted the focus of the HDL hypothesis from the "quantity" to the "quality" of HDL. - Source: PubMed
Publication date: 2026/05/16
Chehade Michael JHaas Michael JMooradian Arshag D - Dyslipidemia comprises interacting disturbances in lipids and lipoproteins that track with metabolic status, vascular biology, and inflammation. Ocular imaging offers scalable, quantifiable phenotypes to interrogate lipid-related pathways and to develop oculomics. We conducted a scoping review to map evidence linking dyslipidemia and lipid-related biomarkers with ocular phenotypes across the ocular surface, lens, macula, retinal microvasculature, and vascular occlusive disease, and to consider implications for AI-based risk modeling. We searched PubMed, Embase, Scopus, and Web of Science, supplemented by reference screening, and charted lipid exposures such as LDL-C, non-HDL-C, apoB/apoA-I, and the triglyceride-glucose index. The biologically grounded patterns were observed in macular disease, where cholesterol- and apolipoprotein-related material within the RPE-Bruch's membrane complex and drusen-related phenotypes support lipid-handling and innate immune pathways in age-related macular degeneration. Retinal vascular phenotypes showed generally consistent signals compatible with endothelial stress and microvascular remodeling. Epidemiologic associations were apparent in metabolically co-traveling conditions such as meibomian gland dysfunction and diabetic retinopathy, in which triglyceride-rich dyslipidemia and insulin resistance markers were often more informative than LDL-C alone and associations were often non-linear or interaction-dependent. By contrast, findings for glaucoma and cataract were modest and inconsistent, while vascular occlusive phenotypes clustered with broader atherosclerotic risk. Statin associations varied by outcome and were vulnerable to confounding. Predicting individual lipid analytes from retinal images appears limited, whereas integrated ocular signatures may support cardiovascular risk stratification. Future studies should refine phenotype definitions, model non-linearity, account for lipid-lowering therapy, and prospectively validate multimodal oculomics and AI across devices and populations. - Source: PubMed
Publication date: 2026/05/16
Kim HeesukJoe Byung-HyunNam DongjinYoo Tae Keun - Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors have become an important therapeutic option for patients with dyslipidemia. Evolocumab and alirocumab are monoclonal antibodies targeting circulating PCSK9, whereas inclisiran is a small interfering RNA (siRNA) agent that suppresses hepatic PCSK9 synthesis and requires only twice-yearly dosing. Although these agents are proven effective in clinical trials, direct real-world comparative evidence on lipid-lowering efficacy, apolipoprotein B (apoB) reduction, safety, and adherence remains limited. - Source: PubMed
Publication date: 2026/05/16
Yao JiafangSun QiyinLiu DanLin JunlingWang WenJuan