CD220 / INSR pThr1375 antibody Ab
- Known as:
- CD220 / INSR pThr1375 (anti-) Antibody
- Catalog number:
- 1488139
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CD220 / INSR pThr1375 antibody
Related genes to: CD220 / INSR pThr1375 antibody Ab
- 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: CD220 / INSR pThr1375 antibody Ab
Related articles to: CD220 / INSR pThr1375 antibody Ab
- Lupus nephritis (LN) is a severe complication of systemic lupus erythematosus (SLE), leading to progressive renal fibrosis and functional decline. Understanding the interplay between immune cells and stromal cells is needed to develop effective therapeutic strategies. In this study, we investigated the landscape of macrophage-fibroblast interactions in human LN and validated these findings in mouse models. - Source: PubMed
Publication date: 2026/08/13
Raparia ChiragHoover PaulAi JuntingClark MarcusShah Sujal Diamond BettyHacohen NirArazi ArnonDavidson Anne - Cystic echinococcosis, caused by the larval stage of Echinococcus granulosus, predominantly affects the liver. Components of hydatid cyst fluid (HCF), including extracellular vesicles (EVs), have been suggested to participate in host-parasite communication. The present study investigated whether HCF and EVs derived from it can influence insulin-related genes in hepatocyte cells. EVs were isolated from the HCF obtained from the liver of an infected sheep using differential centrifugation and were characterized by western blotting, scanning electron microscopy (SEM), dynamic light scattering (DLS), and zeta potential analysis. HepG2 cells were treated with EVs and HCF for 24 and 48 h. The expression of insulin-related genes, including INSR, AKT, IDE, and INSIG2, was then evaluated by quantitative real-time PCR. EV significantly up-regulated AKT (1.98 ± 0.17, p < 0.0001), INSR (2.09 ± 0.34, P = 0.0008), IDE (1.40 ± 0.17, P = 0.0031), and INSIG2 (1.67 ± 0.17, P = 0.0005) at 24 h; however, at 48 h, AKT (-2.68 ± 0.4), INSR (-3.75 ± 0.4), and IDE (-3.6 ± 0.93) were significantly down-regulated (all P < 0.0001), while INSIG2 remained up-regulated (3.81 ± 0.85, P = 0.0006). In contrast, HCF exposure predominantly caused gene down-regulation, with significant decreases in AKT (-1.41 ± 0.4), INSR (-1.9 ± 0.72), and IDE (-1.6 ± 0.34) at 24 h (all P ≤ 0.0002) and a more pronounced downregulation of all genes at 48 h, including AKT (-6.67 ± 1.56), INSR (-5.89 ± 0.76), IDE (-6.8 ± 1.2), and INSIG2 (-1.16 ± 0.06) (all P < 0.0001). Our findings showed that exposure to EVs was associated with reduced expression of INSR and AKT and increased expression of IDE and INSIG2. This metabolic reprogramming appears to be a coordinated strategy to divert host energetic resources to favor parasite survival. - Source: PubMed
Publication date: 2026/08/10
Zanjirani Farahani LeyliRouhani SoheilaNiyyati MaryamEslami NasimFasihi Harandi MajidMirjalali Hamed - Diabetic retinopathy (DR) requires robust biomarkers. To overcome the limitations of bulk sequencing, we integrated single-cell eQTL mapping with Mendelian randomization to identify causal cell populations and genes. CD8 Teff cells were expanded in peripheral blood, showing elevation in non-DR diabetes and reaching maximal levels in DR. Mendelian randomization analysis implicated IL2RB as a putative causal marker, with the lead eQTL SNP rs3184504 demonstrating strong association ( = 8.5467 × 10). Colocalization analysis with DR GWAS and validation in bulk data reinforced this signal. In tissues, CellChat predicted more interactions for IL2RB compared to IL2RB CD8 Teff cells, including IL16-CD4 with macrophages and NAMPT interactions with both ITGA5+ITGB1 and INSR on endothelial cells, implicating immune-vascular regulation. Together, these findings nominate IL2RB as a biomarker and therapeutic target while clarifying mechanisms underlying DR. - Source: PubMed
Publication date: 2026/08/05
Cao LizhiWang ZumingCai XiaoweiZhou YongkangYan Yu - Linn. contains abundant free phenolic (PEFP) and bound phenolic (PEBP), both of which have demonstrated potential antidiabetic activities. However, their comparative hypoglycemic effects and underlying mechanisms remain unclear. This study investigated the effects of PEFP and PEBP using insulin-resistant HepG2 (IR-HepG2) cells and a high-fat diet/streptozotocin (HFD/STZ)-induced type 2 diabetes mellitus (T2DM) mouse model. PEFP and PEBP showed no cytotoxicity toward HepG2 cells and significantly enhanced glucose consumption, glycogen synthesis, and hexokinase and pyruvate kinase activities in IR-HepG2 cells. Treatment with 160 μg mL PEFP and PEBP increased glucose consumption in IR-HepG2 cells to 7.13 ± 0.30 and 6.73 ± 0.37 mmol L, respectively, restoring levels comparable to control cells (7.23 ± 0.69 mmol L). In HFD/STZ-induced T2DM mice, PEFP and PEBP significantly improved glucose homeostasis, insulin sensitivity, dyslipidemia, oxidative stress, and inflammatory responses after 10 weeks of intervention. High-dose PEFP and PEBP reduced fasting blood glucose from 13.02 ± 1.19 mmol L in diabetic mice to 7.47 ± 1.18 and 9.87 ± 0.93 mmol L, respectively. At the molecular level, both treatments were associated with upregulation of insulin signaling-related genes (, , , , and ) and suppression of gluconeogenic genes (, , and ) in the liver. Notably, distinct functional patterns were observed. PEFP, particularly at high doses, showed stronger associations with restoration of insulin signaling and inhibition of gluconeogenesis, whereas PEBP was more closely associated with glucose utilization and glycogen storage. In addition, PEFP and PEBP inhibited jejunal α-glucosidase and α-amylase activities and altered gut microbiota composition. These findings demonstrate that PEFP and PEBP exert multifaceted antidiabetic effects, which were closely associated with the modulation of hepatic insulin signaling-related gene expression, intestinal carbohydrate digestion, and gut microbiota composition, highlighting their potential as functional food ingredients for T2DM management. - Source: PubMed
Publication date: 2026/08/03
Xing MingxiaShen TingtingXie FanWu HaomingWang GuangqiangXia YongjunSong XinFu QiangqiangSheng YiAi Lianzhong - This cross-sectional case-control study aimed to investigate the association between germline and sporadic variations in the gene, risk factors, and the differential expression of circulating miRNA-21 and miRNA-146a in the onset of Type 2 diabetes mellitus (T2DM). - Source: PubMed
Publication date: 2026/07/22
Gul HiraMasood Nosheen