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
- The biogenesis and transport of lipoproteins are essential for systemic homeostasis and cardiometabolic health, yet how the secretory pathway acquires specialization to support high-capacity lipoprotein export remains unclear. Here, we report SEC16B as a tissue-selective modulator of the COPII machinery, critical for the efficient secretion of APOB-containing lipoproteins. Integrative bioinformatic analyses identify that SEC16B co-emerges with core genes involved in lipoprotein biogenesis. Functional studies, coupled with AI-driven prediction, reveal that SEC16B acts as a molecular brake to fine-tune COPII condensation for lipoprotein export. Mining of UK biobank data links SEC16B to metabolic traits in humans and suggests HNF4A-dependent regulation of SEC16B expression. Hepatic deletion of SEC16B in mice markedly reduces circulating APOB, triglycerides and cholesterol, while conferring robust protection against atherosclerosis and cardiac dysfunction and maintaining liver health. Collectively, these findings position SEC16B as a specialized modulator of lipoprotein export via the general secretory (SEC) pathway in the liver, suggesting potential therapeutic avenues for combating cardiometabolic diseases. - Source: PubMed
Publication date: 2026/04/24
Wang XiaoHu YatingLiu LuHuang RunzeWang YaweiLiu BingZhao YifeiZhu YuangangLv JiaLiu LiangWang HuiminWu LingzhiXu XinxuanLi YaxinWang GuanlinChen Xiao-Wei - The liver plays a critical role in lipid homeostasis, where lipids are either secreted as very-low-density lipoproteins (VLDL) or stored in lipid droplets (LDs). However, the regulatory mechanisms governing these two interconnected processes remain poorly understood. Here, we demonstrate that SEC16B functions as a lipid-responsive regulator in the liver, promoting VLDL secretion and LD expansion to handle lipid flux and maintain lipid homeostasis. Genome-wide association studies have identified single-nucleotide polymorphisms in SEC16B to be highly associated with serum lipid levels in humans. Hepatic Sec16b deficiency decreases serum lipid levels by impairing VLDL secretion through mechanisms that are at least partially independent of microsomal triglyceride transfer protein (MTP)-mediated ApoB lipidation and COPII-mediated intracellular trafficking. SEC16B partially localizes at ER-LD contact sites and promotes LD expansion by facilitating the targeting of ER proteins to LDs. More importantly, suppression of Sec16b dramatically lowers serum lipid levels and reduces atherosclerotic lesion size in Ldlr null mice. These data reveal a mechanism that coordinates VLDL and LD metabolism and suggest SEC16B as a potential therapeutic target for atherosclerosis treatment. - Source: PubMed
Publication date: 2026/04/24
Lu WeiZhao ZhimingMolina DonaldFan HuaxunShi RuichengTian YeGopoju RajaYang TiantianZhang XinyuanZhang YanqiaoZhang KaiAmengual JaumeWang Bo - Cushing´s syndrome (CS) is associated with an unfavorable lipid profile. However, data on lipid alterations during early postoperative remission, a particularly cardiovascular vulnerable period, are lacking. - Source: PubMed
Publication date: 2026/04/24
Schrenk MoritzHaenelt MichaelOettle MatthiasKroiss MarkusZopp StephanieBraun Leah TRubinstein GermanRitzel KatrinStüfchen IsabelStifel UlrichSchilbach KatharinaBidlingmaier MartinTeupser DanielBeuschlein FelixReincke MartinVogel FrederickNowak Elisabeth - High plasma cholesterol levels substantially contribute to cardiovascular disease. Hepatic delivery of the microRNA-30c analog C2 decreased plasma cholesterol in apoB-containing lipoproteins in hypercholesterolemic C57BL/6 mice, in African green monkeys that spontaneously developed diabetes and hyperlipidemia and prevented diet-induced hypercholesterolemia in mice with humanized livers. Furthermore, C2 significantly reduced plasma cholesterol and atherosclerosis in LDL receptor knockout mice. C2 did not affect hepatic triglyceride and cholesterol, plasma ALT, AST, CK-MB, ALP, IL-6, TNF-α, and INF-ϒ, thus indicating an absence of tissue lipid accumulation and inflammatory response. In contrast, MTP inhibitor lomitapide significantly reduced plasma lipids and caused hepatic steatosis. Mechanistic studies revealed that C2 reduced hepatic microsomal triglyceride transfer protein expression, secretion of apolipoprotein B-containing lipoproteins and FA synthesis and increased hepatic FA oxidation, plasma bile acids and fecal cholesterol excretion. C2 is a first-in-class microRNA therapeutic that decreases plasma cholesterol and atherosclerosis, without causing hepatic injury and inflammatory response. - Source: PubMed
Publication date: 2026/04/24
Prakash BinuChang ZhihuaRajan SujithScarberry Shannon RGangula BhargaviHossain Md MusaPrakashmurthy ChandanaValmiki SwatiPulatov OtabekYadav Pradeep KumarCarsons Steven ETemel Ryan EKavanagh KylieSheng JiaHussain M Mahmood - Women with type 1 diabetes (T1D) experience a greater diabetes-related increase in cardiovascular disease (CVD) and mortality risk than men. This study aimed to examine early sex-related differences in CVD risk factors among youth with T1D. - Source: PubMed
Publication date: 2026/04/21
Schweiger Darja ŠmigocMlinarič ZalaMacedoni MaddalenaGiani ElisaPlesnik EmilHovnik TinkaKotnik PrimožDovč KlemenBratina NatašaBattelino TadejGrošelj Urh