ASGR1 Antibody - middle region (ARP33805_P050)
- Known as:
- ASGR1 Antibody - middle region (ARP33805_P050)
- Catalog number:
- arp33805_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ASGR1 Antibody - middle region (ARP33805_P050)
Related genes to: ASGR1 Antibody - middle region (ARP33805_P050)
- 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 - middle region (ARP33805_P050)
Related articles to: ASGR1 Antibody - middle region (ARP33805_P050)
- 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 - Advances in RNA interference technology have established it as a powerful therapeutic tool with important future potential. The design and the chemical modifications of the siRNA nucleotide backbone have greatly enhanced stability, durability, and pharmacokinetics while minimizing tolerability risks. The optimal combination of these modifications depends on the target gene, tissue, and RNA sequence, necessitating an iterative, experimental approach that currently relies heavily on animal models. To reduce the reliance and number of (humanized) animals required, we developed a human long-term liver 3D spheroid model designed for screening GalNAc-conjugated siRNAs which captures the process of uptake, potency, and durability for early in vitro screening. These liver spheroids remain viable in culture for at least 5 weeks while maintaining expression of the asialoglycoprotein receptor to facilitate GalNAc mediated uptake. siRNA was efficiently internalized by the spheroids without the need for transfection reagents, and its durable silencing efficiency was assessed by monitoring AHSA1 target gene expression over time. Target gene silencing in the spheroid model persisted up to 5 weeks post-treatment. Fluorescently labeled siRNA enabled visualization of uptake and distribution within the spheroid, revealing somewhat reduced siRNA accumulation in pericentral CYP3A4+ hepatocytes accompanied with somewhat reduced ASGR1 expression. No signs of hepatotoxicity were observed under the conditions used. By varying the number of phosphorothioate modifications in the siRNA backbone, distinct differences in silencing efficiency and durability were observed which were principally similar as obtained in vivo in mice. We propose that this long-term human liver spheroid model provides a valuable preclinical platform for evaluating siRNA-based therapeutics with respect to uptake, durability, and silencing efficiency, and could refine early in vitro screening and accelerate drug development. - Source: PubMed
Scholten Gijs-JanGrundmann ClaraNordling ÅsaCoskun CarolineEngelhardt VolkerSadhasivam LingheswarEinfalt TomažIngelman-Sundberg Magnusvan Riet Sander - Decabromodiphenyl ethane (DBDPE), a widely used novel brominated flame retardant, has been increasingly detected across environmental matrices and human samples. Owing to its marked persistence and bioaccumulation potential, DBDPE was designated as a Substance of Very High Concern (SVHC) by the European Chemicals Agency in 2025. However, evidence regarding its potential reproductive hazards remains limited. Here, we systematically investigated the molecular mechanisms underlying DBDPE-induced spermatogenic disorder using an integrated approach that combines network toxicology, machine learning, and in vivo validation. Intersecting 564 DBDPE-associated targets with 1,743 NOA-related differentially expressed genes identified 33 overlapping candidates that may mediate DBDPE-induced spermatogenic disorder. Enrichment analyses implicated the HIF-1 signaling and gap junction pathways in DBDPE-induced spermatogenic disorder. Machine learning prioritized five core genes, including PRKACG, WDR5, AURKC, PFKP, and ASGR1, all of which were downregulated in NOA patients. Molecular docking demonstrated stable binding between DBDPE and these core targets. In vivo, DBDPE exposure disrupted testicular structure, reduced sperm concentration and motility, and decreased expression of the five core proteins, confirming the predicted mechanisms. Additionally, we proposed an adverse outcome pathway (AOP) framework describing key events leading to DBDPE-induced spermatogenic impairment. Collectively, our findings revealed the reproductive toxicity of DBDPE and provided a mechanistic foundation for developing strategies to safeguard male fertility. - Source: PubMed
Publication date: 2026/03/27
Shi WeiSun YuantengLiu KejiaZhang YingLu LuZhou QianPu YuepuSun RongliYin Lihong - Sepsis remains a leading cause of childhood mortality worldwide. Most deaths occur within the first few days of presentation, underscoring the urgent need for early recognition and biologically informed treatment strategies. The heterogeneous etiology of sepsis involves complex, intertwined biological networks, explaining why single-biomarker approaches have proven inadequate for capturing this complexity. We used high-throughput proximity extension assay technology to comprehensively profile plasma proteins in critically ill pediatric sepsis patients, aiming to identify dysregulated biological pathways that could inform risk stratification and therapeutic development. - Source: PubMed
Publication date: 2026/03/27
Stranges VincenzoVan Nynatten Logan RTweddell DavidCela EnisMorello MariaDaley MarkO'Gorman David BCepinskas GediminasFraser Douglas D