Human Insulin R / CD220 (28-956) Protein
- Known as:
- Human Insulin R / CD220 (28-956) Protein
- Catalog number:
- INR-H5220
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Human Insulin / CD220 (28-956) Protein
Related genes to: Human Insulin R / CD220 (28-956) Protein
- Gene:
- INSR NIH gene
- Name:
- insulin receptor
- Previous symbol:
- -
- Synonyms:
- CD220
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-07
Related products to: Human Insulin R / CD220 (28-956) Protein
Related articles to: Human Insulin R / CD220 (28-956) Protein
- Circular RNAs (circRNAs) represent a class of covalently closed non-coding RNA molecules that exert vital regulatory effects on host-pathogen interplay. The H9N2 subtype of avian influenza virus (AIV) is a widespread pathogen on a global scale, inflicting considerable economic damage to the poultry sector and harboring potential risks of cross-species transmission to humans. Despite growing evidence suggesting that non-coding RNAs can modulate the replication of influenza viruses, the expression patterns and functions of avian-derived circRNAs during H9N2 AIV infection have been largely unclear. Here, we conducted a systematic investigation into the expression dynamics of circRNAs in DF1 cells infected with H9N2 AIV by high-throughput RNA sequencing technology. A total of 139 differentially expressed circRNAs were identified, with 58 exhibiting upregulation and 81 showing downregulation relative to non-infected control cells. Of note, a circRNA originating from exon 2 of the insulin receptor (INSR) gene displayed consistent upregulation during viral infection. Functional assays verified its contributing role in the replication of H9N2 AIV. Specifically, siRNA-mediated knockdown of circ-INSR significantly suppressed H9N2 AIV replication. This study is the first to identify circ-INSR as a host factor contributing to influenza virus replication. Our results provide a basis for developing circRNA-based strategies against H9N2 avian influenza virus. - Source: PubMed
Publication date: 2026/09/04
Liu ZhiyuanFan MengluZheng YiqingZeng YiranDeng LuluTian YusenSu JuanPing Jihui - Glyoxal exposure is associated with a spectrum of adverse health outcomes, including arterial injury. While existing evidence confirms that glyoxal targets oxidative stress and the mitogen-activated protein kinase pathway, the precise underlying mechanism of glyoxal-induced arterial damage remains elusive. In this study, we aimed to elucidate the molecular mechanism driving glyoxal-induced arterial injury through a combination of in vitro and in vivo experiments. In vitro, we treated human aortic endothelial cells with glyoxal, then performed cell viability assays, tandem mass tag (TMT)-based quantitative proteomics, parallel reaction monitoring (PRM), glutathione quantification for oxidative stress assessment, western blotting, and quantitative polymerase chain reaction (qPCR) analysis. In vivo, we administered glyoxal to C57BL/6 mice, after which we conducted biochemical, histological, and immunohistochemical assays to evaluate arterial pathological changes. In vitro, the proteomic profiling results were further validated via PRM and western blotting, which confirmed that glyoxal exposure induces energy metabolism dysfunction, aberrant vascular endothelial growth factor receptor (VEGF-R) expression, and signaling pathway inactivation. Consistent with the proteomic results, we detected reduced protein levels of VEGF-R (36.4% reduction), insulin-like growth factor receptor (IGF-R, 21.6% reduction ), and insulin receptor (INS-R, 16.4% reduction) relative to control after glyoxal treatment. Compared to the control group, the glyoxal-exposed group exhibited a 48.7% reduction in the phosphorylation levels of ErbB2 and ErbB4, while total protein levels of ErbB2 and ErbB4 (106.0% of the control level) were comparable between the two groups. In addition, the levels of Wnt signaling-related proteins-including β-catenin (52.5% of the control level) and Wnt ligands-were significantly decreased following glyoxal treatment, relative to the control. Consistent with our in vitro results, we observed that the protein levels of VEGF-R (47.7% reduction), β-catenin (25.7% reduction), and INS-R (66.0% reduction) were decreased relative to the control group after in vivo glyoxal treatment. Collectively, our findings outline a comprehensive molecular portrait of glyoxal-induced arterial injury, which provides a foundational framework that may advance the development of precision medicine strategies for glyoxal-related vascular disease. - Source: PubMed
Publication date: 2026/09/06
Xie Ming-ZhangYang XueWu Zhi-WeiZhou Lin-PingChu Hai-XiaZhang Qun-MeiZhang Yu-ChaoZhou Xiao-ChunZhao Meng-MengMo Qing-JiangWang Xiao-FangXv Wei-DongBian Wen-YanLi Ya-Nan - Alzheimer's disease (AD) features progressive cognitive decline, Aβ aggregation, neurofibrillary tangles, mitochondrial dysfunction and central insulin resistance, lacking effective disease-modifying treatments. Liuwei Dihuang Pills (LWDHP) exert neuroprotective effects, while its dual regulatory mechanisms targeting mitochondrial homeostasis and cerebral IRS/AKT/GSK3β insulin signaling remain unclear. - Source: PubMed
Publication date: 2026/08/20
Song JunyingYuan YongWang MaoLi JunlinDing RuiJia YaquanWang ZichuangXie ZhishenLi ZhonghuaZhang Zhenqiang - Aerobic exercise reduces cardiovascular disease risk, with atherosclerosis being a primary contributor. Although circulating extracellular vesicles (EVs) mediate intercellular communication, their role in this process remains unclear. This study aimed to investigate the role of aerobic exercise-derived circulating EVs in mitigating macrophage inflammation and lipid accumulation in an atherosclerotic model. Circulating EVs were isolated from the plasma of exercise-trained and sedentary mice. miRNA profiling of EVs was performed using miRNA arrays and quantitative real-time PCR. Aortic atherosclerosis was assessed by Oil Red O staining, immunofluorescence, and enzyme-linked immunosorbent assay. Functional validation of EV effects was performed through EV labeling, cell transfection, luciferase reporter assays, and flow cytometry. Aerobic exercise slowed the progression of atherosclerosis and altered the miRNA profile of circulating EVs, notably increasing miR-203a-3p and miR-133b-3p expression. EVs from exercise-trained mice inhibited macrophage-driven inflammation and lipid accumulation in vitro and in vivo. Treatment with miR-203a-3p and miR-133b-3p mimics reproduced the anti-atherosclerotic effects, whereas inhibitors of these miRNAs reversed the effects. Mechanistically, miR-203a-3p and miR-133b-3p reduced macrophage inflammation and lipid accumulation by targeting Tlr4 and Insr, respectively, thereby suppressing NF-κB/NLRP3 signaling. Notably, the increased expression of miR-203a-3p and miR-133b-3p was primarily derived from skeletal muscle. These findings highlight a novel mechanism linking aerobic exercise to atherosclerosis via EV-miRNAs, proposing potential therapeutic strategies for atherosclerosis based on exercise-induced circulating EVs miR-203a-3p and miR-133b-3p. - Source: PubMed
Publication date: 2026/09/02
Wang YingChu HoubinLiu YuxiangYang ChaoXu XinxinZhao ChuanrongWang GuixueSong Guohua - INSR-related insulin resistance is a form of monogenic diabetes caused by pathogenic variants in the INSR gene, resulting in impaired insulin receptor signalling and a spectrum of insulin resistance. Conventional diabetes management strategies relying on insulin sensitisation or augmentation are often less effective and evidence to guide treatment in those with heterozygous INSR mutations remains limited. - Source: PubMed
Publication date: 2026/09/01
Franklin DavidMahony JanPatel ChiragTriay Jessica