Ask about this productRelated genes to: ASGR1 antibody
- Gene:
- ASGR1 NIH gene
- Name:
- asialoglycoprotein receptor 1
- Previous symbol:
- -
- Synonyms:
- CLEC4H1
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-24
- Date modifiied:
- 2016-10-05
Related products to: ASGR1 antibody
Related articles to: ASGR1 antibody
- Base editing enables the precise, permanent modulation of gene expression, offering a promising therapeutic avenue for targeting lipid-regulating genes. Recently, asialoglycoprotein receptor 1 (ASGR1), a liver-specific receptor, has emerged as a potential therapeutic target for the control of circulating lipid levels. Here we employed adeno-associated virus serotype 8 (AAV8) to deliver an all-in-one adenine base editor (ABE) to target Asgr1 in mice. Systemic administration of Asgr1-targeting ABE achieved 54.7 ± 2.2% editing efficiency, leading to a marked depletion of hepatic ASGR1 and significant reductions in serum and hepatic total cholesterol (TC) and triglyceride (TG). These effects were mediated, in part, by the modulation of biliary cholesterol excretion pathways. No overt liver injury was observed following in vivo base editing of Asgr1. Moreover, combined treatment with Asgr1 base editing and the lipid-lowering drug ezetimibe produced an additive reduction in TC levels. Finally, lipid nanoparticles (LNPs)-delivered base editing of ASGR1 in human HepG2 cells achieved >91% editing, near-complete protein knockout, which significantly lowered cellular cholesterol. Collectively, our results demonstrate that ASGR1 base editing represents a promising strategy for blood lipid control. - Source: PubMed
Publication date: 2026/05/26
Agrahari GauravThi Kieu Nguyen NuongLi MengzhenZhang ChenXu JieZhang JifengChen Y EugeneHan Renzhi - Accurately quantifying protein-protein binding at the single-molecule level is essential for understanding the mechanisms of viral infection and therapeutic targeting. Here, we use solid-state nanopores (SSNs) to detect complex formation between the SARS-CoV-2 Spike receptor-binding domain (Spike RBD) and the alternative host receptors KREMEN1 and Asialoglycoprotein Preceptor 1 (ASGR1). Single-molecule translocation events were analyzed using unsupervised Gaussian mixture modeling and a control-anchored semisupervised classification framework to resolve overlapping free-protein and complex populations. This approach enabled direct identification of receptor-Spike RBD complexes and calculation of apparent dissociation constants under experimental conditions. The inferred affinities were 261.1 nM for ASGR1 and 56.6 nM for KREMEN1, in good agreement with reported literature values and can be used as rough estimates on Spike and its receptor affinities. A negative control using human serum transferrin and Spike RBD showed no emergent high-Δ population, supporting the specificity of the observed interactions. These results establish SSNs as a scalable and quantitative platform for single-molecule affinity measurements. - Source: PubMed
Publication date: 2026/05/17
O'Donohue MatthewThyashan NavodKim Min Jun - Asialoglycoprotein receptor 1 (ASGR1) is associated with lipid metabolism and coronary artery disease (CAD) risk, but its expression patterns, diagnostic performance, and prognostic significance in hypertensive patients with CAD remain unelucidated. This single-center study enrolled 345 hypertensive patients between 2022 and 2025 (59 with hypertension alone, 286 with hypertension and CAD). Plasma ASGR1 levels were measured by enzyme-linked immunosorbent assay. Receiver operating characteristic (ROC) curves, Spearman correlation, and Cox proportional hazards modeling were performed to assess the diagnostic efficacy of ASGR1 in CAD and its prognostic value for all-cause rehospitalization. Plasma ASGR1 levels were significantly higher in hypertensive patients with CAD than in those with hypertension alone (p < 0.001) and higher ASGR1 expression is accompanied by more severe coronary lesions and adverse clinical phenotypes. Inflammatory markers, liver injury biomarkers and cardiac injury biomarkers were positively correlated with ASGR1, whereas high-density lipoprotein cholesterol (HDL-C) was negatively correlated. ASGR1 showed excellent diagnostic ability for CAD in hypertensive patients with area under the curve of 0.937 (95% CI: 0.906-0.960). Multivariate analysis showed that each 1-unit increase in ASGR1 was associated with a 37% higher risk of CAD (odds ratio 1.37, 95% CI: 1.24-1.52, p < 0.001). Longitudinally, elevated baseline ASGR1 was independently associated with an increased risk of all-cause rehospitalization (adjusted hazard ratio 1.97, 95% CI: 1.16-3.35, p = 0.012). These findings support ASGR1 may serve as a diagnostic biomarker and prognostic indicator for hypertensive patients with CAD. - Source: PubMed
Liu YingZhou XinyuHao PengGuo YingWang NingLi KuibaoChi HongjieLi HongYang XiaoyanLi JingZhong JiuchangZhao LinDong Ying - Cardiac dysfunction is a crucial culprit for the high mortality of sepsis in intensive care units. The underlying targets and mechanisms of sepsis-induced myocardial dysfunction (SIMD) in sepsis are awaiting profound exploration. The present study investigates the contribution and mechanism of ASGR1 to the progression of SIMD. Herein, we show that ASGR1 in heart tissue is highly related to SIMD. Anti-Ly6G and GSK484 deplete neutrophils and neutrophil extracellular traps (NETs), alleviating myocardial injury and cardiac dysfunction, and promoting survival of LPS-challenged mice. Neutrophils and NETs are observably declined in ASGR1 knockout mice and conditional knockout neutrophils, respectively. In ASGR1 deficiency mice, LPS challenge results in elevated neutrophils and NETs using FACS and confocal microscopy, respectively, leading to reduced myocardial dysfunction and mortality. ASGR1 promotes neutrophil activation and NET accumulation via SLC7A11-dependent ferroptosis. ASGR1 acts as a bridge to transfer the attached ubiquitin to SLC7A11 and facilitates K48-linked ubiquitination degradation of SLC7A11 by SOCS2. Our findings suggest that ASGR1 is a principal indicator of SIMD by inducing NET formation. In addition, the regulation of NET formation could be a potential treatment for SIMD. - Source: PubMed
Publication date: 2026/04/21
Shi RuiWang FangLi ChaozhongXiao ChuangBai ChunyunChen Alex FYang Weimin - Metabolic-associated steatotic liver disease (MASLD) is a prevalent chronic liver disorder driven by a complex interplay of lipid accumulation, oxidative stress, and inflammation, for which effective targeted therapies remain limited. To address this multifactorial pathology, we developed an integrated nano-therapeutic platform, termed CMEPA, that unites three complementary components: a copper-based nanozyme with dual superoxide dismutase (SOD)- and catalase (CAT)-like activities, human umbilical cord mesenchymal stem cell-derived exosomes (UC-MSC-Exos) enriched in regulatory microRNAs, and a hepatocyte-targeting antibody against ASGR1. In vitro, CMEPA efficiently scavenged reactive oxygen species (ROS), significantly reduced lipid droplet accumulation, and suppressed apoptosis in palmitic acid-challenged hepatocytes. In vivo, CMEPA exhibited preferential hepatic accumulation and an excellent biosafety profile, with no observable systemic toxicity. Therapeutic evaluation in a diet-induced murine MASLD model revealed that CMEPA administration significantly improved serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride, and cholesterol levels, alleviated hepatic steatosis as confirmed by histopathology, enhanced endogenous SOD and CAT activities, and attenuated inflammatory and lipogenic signaling pathways, as revealed by transcriptomic analysis. Collectively, these results establish CMEPA as a robust, multi-modal nano-therapeutic strategy that integrates catalytic antioxidation, exosome-mediated gene regulation, and active hepatocyte targeting, offering a promising translational approach for MASLD treatment. - Source: PubMed
Publication date: 2026/04/12
Yu KunLi XinweiLiu YingyingZhang HaonanLiu GuojieJi TuoGao YuzhiWang LinBian YuweiChen GuohuaZhao ZhiwenWang FengYu XiaomingHe JiachenGao Xuzhu