ApoB antibody
- Known as:
- ApoB (anti-)
- Catalog number:
- 10-1840
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- ApoB antibody
Related 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
- Females with a normal body mass index (BMI) and high body fat percent (i.e., normal-weight obesity or NWO) are at increased risk for cardiometabolic diseases compared to normal-weight lean (NWL) counterparts. However, underlying mechanisms remain unclear. Here, we examined postprandial lipids, gut permeability biomarkers, and arterial stiffness outcomes as potential factors implicated in cardiometabolic disease development. Females (N=33) with a normal BMI were grouped as NWO (body fat percent ≥33.0%; n=18) or NWL (body fat percent <33.0; n=15). Following IV insertion and baseline blood collection, a high-fat meal was consumed. Additional blood samples were collected at 1-, 2-, 3-, and 4-hours post-meal for determination of lipids (triglycerides, HDL-C, apolipoprotein [apo] B) and intestinal permeability biomarkers (lipopolysaccharide binding protein [LBP], soluble cluster differentiation 14 [sCD14], LBP:sCD14). Pulse wave analysis and pulse wave velocity were measured as indicators of arterial stiffness at 0, 2, and 4 hours. Across both groups, the high-fat meal impacted triglycerides (increased), HDL-C (decreased), apolipoprotein-B (decreased; ≤0.001). The frequency of adverse postprandial triglyceride responses was higher in NWO compared to NWL females (p<0.05). Further, non-significant (≤0.08), medium effect sizes (ηp2≥0.12) were observed for triglycerides and apoB, consistent with NWO>NWL, regardless of time point. LBP and LBP:sCD14 increased, while sCD14 decreased, following the high-fat meal (≤0.05). Additionally, NWO had higher LBP regardless of time point compared to NWL (<0.05). All arterial stiffness measures decreased post-meal (≤0.05). In conclusion, this work provides early of evidence of postprandial dyslipidemia and basalintestinal hyperpermeability in females with NWO. - Source: PubMed
Publication date: 2026/09/10
Quirk Alexis RSchifferer Jenna KCline Brooklyn RWolf Emily RPathangi Dhanya OBowling Quinn EMallick AmnaWiersma Lydia RKeirns Natalie GKeirns Bryant H - Calculated low-density lipoprotein cholesterol (LDL-C) is widely reported, but formula-dependent estimation differences may alter classification near decision thresholds. We assessed formula-dependent LDL-C classification relative to direct LDL-C in UK Biobank and examined cardiovascular outcomes descriptively. - Source: PubMed
Publication date: 2026/09/11
Xue BohaoMa TengShen ChengPan XinLing YichenChu LiangyuYan WentingWang NingjianLi JinXu Dachun - Remnant cholesterol (RC) has been associated with adverse cardiovascular outcomes; however, the relationship between cumulative RC exposure and clinical outcomes after percutaneous coronary intervention (PCI) in patients with ST-segment elevation myocardial infarction (STEMI) remains unclear. This study aimed to evaluate the association between cumulative remnant cholesterol (cumRC) and major adverse cardiovascular and cerebrovascular events (MACCEs) after PCI. - Source: PubMed
Publication date: 2026/08/26
Sun YazhaoShao FeilongXu XinxinLiu YayunMa Ya - Low-density lipoprotein cholesterol (LDL-C) goal attainment is central to primary atherosclerotic cardiovascular disease (ASCVD) prevention, but LDL-C may not fully reflect the burden of apolipoprotein B (ApoB)-containing atherogenic particles. The prevalence and clinical correlates of residual ApoB elevation among adults who have attained PREVENT risk-stratified LDL-C goals remain unclear. - Source: PubMed
Publication date: 2026/09/09
Shi YanpingTang YuanWang MengtingZhu XuZhang Haifeng - The limited benefits of high-density lipoprotein (HDL)-targeted therapies have shifted the research focus to HDL quality; some HDL subtypes may be pro-atherogenic and may counteract the potential benefits of HDL therapies. This study investigated the pathological mechanism of H5, a highly electronegative and compositionally abnormal HDL subfraction characterized by impaired cholesterol efflux. We used anion-exchange chromatography to separate HDL into five subfractions (H1-H5) from blood from 131 asymptomatic individuals (95 with metabolic syndrome and 36 without [controls]). Plasma H5 levels were significantly elevated in individuals with cardiovascular disease risk compared to controls (4.0 ± 3.5% vs. 2.7 ± 1.0%, p = 0.024). Clinically, elevated H5 levels were independently associated with structural markers of subclinical carotid atherosclerosis, including increased intima-media thickness (IMT) and plaque burden, in an imaging cohort of 118 participants. Mechanistically, the triglyceride-rich H5 showed a distinct lipoproteome, enriched with apolipoproteins including Apo(a), ApoB, and ApoC3. H5 induced endothelial dysfunction through pathways associated with reactive oxygen species (ROS) accumulation, DNA damage, and cellular senescence in vitro and in vivo. The p53-p21 signaling axis was the central mediator of this H5-induced dysfunction. In mice, H5-induced dysfunction promoted a pro-atherogenic phenotype, mediated centrally by the p53-p21 signaling axis. Our study suggests that elevated Apo(a)-rich H5 levels are associated with atherosclerotic cardiovascular disease (ASCVD) risk and validates targeting HDL quality-specifically the H5 subfraction-as a novel therapeutic strategy. - Source: PubMed
Publication date: 2026/09/09
Hsu Wen-LiChung Chi-PeiChung ClaireWei Wei-YenChen Tzu-YinAkyol OmerChiang Huan-HsingChou Mei-ChuanKraler SimonLüscher ThomasTsai Ming-HsienChen Chu-Huang