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
- Aerobic exercise reduces cardiovascular disease risk, with atherosclerosis being a primary contributor. While 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 ELISA. Functional validation of EV effects was carried out through EVs 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, while 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 - Gestational diabetes mellitus (GDM) is linked to poor infant metabolic outcomes, potentially via altered human milk (HM) hormones and microRNAs. Since their specific roles remain unclear, this study synthesizes current evidence on HM adipose tissue-derived hormones (particularly adiponectin, leptin, and resistin) and microRNA modifications during gestational diabetes. Firstly, a systematic review following PRISMA 2020 guidelines was conducted (PROSPERO: CRD42024612813). Searches in major databases identified studies comparing HM adiponectin, leptin, or resistin concentrations and/or miRNA profiles between GDM and normoglycemic mothers. Secondly, bioinformatics analysis using miRWalk 3.0, functional enrichment, and network topology mapping examined miRNA interactions with , and genes. Twelve studies were included. Adiponectin showed the most consistent GDM-associated reductions, though findings were context-dependent. Leptin was primarily associated with maternal adiposity rather than GDM status. Resistin evidence was insufficient. Three miRNA studies revealed stage-dependent dysregulation in GDM, with , and linked to infant growth outcomes during the first 6 months. Bioinformatics identified and as targeting all three adipokine genes, with enrichment in glucose homeostasis and insulin resistance pathways. Network analysis highlighted , and as central nodes. GDM is associated with selective alterations in HM adipokines and miRNAs, with adiponectin and specific miRNAs showing the strongest signals. These findings support a conceptual model where GDM shapes HM's molecular composition through interacting endocrine and posttranscriptional mechanisms, potentially influencing infant metabolic programming. Larger longitudinal studies are needed to validate these observations and determine clinical relevance. - Source: PubMed
Publication date: 2026/08/31
Zhang ZhijunDavoudi MaryamGhafourian AmirrezaDehghan ParmidaAhmadi MojdeAyyoubzadeh Seyed MohammadMiao XiaoleiChoobineh HamidAfrisham Reza - This research aimed to develop a next-generation ultra-long-acting insulin analog with dual long-chain fatty acid conjugation, addressing unmet needs of frequent injections and hypoglycemia risk in diabetes therapy. - Source: PubMed
Publication date: 2026/08/31
Tou YiweiLuo JihongSun JiuyiLiu PaiHuang QishenZhang Yun-Hong - Astragalus species have long been recognized for their pharmacological relevance, yet the antidiabetic properties of Link (Ac) remain poorly explored. This study aimed to investigate the antidiabetic potential of Link and to elucidate possible underlying mechanisms. The ethanolic extract of Ac (AcEE) was prepared and analyzed for phenolic and flavonoid content. Antioxidant activity was assessed through a series of in vitro assays. The in vitro inhibition of α-amylase and α-glucosidase was assessed, followed by molecular docking to probe ligand-enzyme interactions. LC-ESI-MS analysis revealed a polyphenol-rich profile, with rutin (953.54 µg/g extract) and quinic acid (797.18 µg/g of extract) identified as main compounds. The AcEE showed significant inhibitory activity against both α-amylase and α-glucosidase (IC = 239.30 ± 7.40 and 192.60 ± 15.51 μg/mL, respectively). Moreover, low cytotoxic effects were observed in hepatic cell lines. Computational analysis revealed stable interactions between rutin and both enzymes (-12.935 and -8.073 Kcal/mol, respectively). Network pharmacology revealed that AcEE may modulate key targets, including IL-6, TNF-α, IL-1β, Akt-1, STAT3, EGFR, and INSR as well as pathways related to insulin resistance, AGE-RAGE, and inflammation. These findings suggest that AcEE exerts significant antidiabetic effects through multitarget modulation, highlighting its potential as a natural therapeutic agent for T2DM. - Source: PubMed
Publication date: 2026/08/13
Bellebcir LeilaDerardja ImeneRebai RedouaneJasmin LucBoudah Abdennacer