Recombinant Human IL2RB /CD122 Protein
- Known as:
- Recombinant Human IL2RB /CD122 Protein
- Catalog number:
- il-766
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human IL2RB /CD122 Protein
Related genes to: Recombinant Human IL2RB /CD122 Protein
- Gene:
- IL2RB NIH gene
- Name:
- interleukin 2 receptor subunit beta
- Previous symbol:
- IL15RB
- Synonyms:
- CD122
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-22
- Date modifiied:
- 2016-10-11
Related products to: Recombinant Human IL2RB /CD122 Protein
Related articles to: Recombinant Human IL2RB /CD122 Protein
- Edwardsiella piscicida is a potent intracellular pathogen that infects a wide variety of freshwater and marine fish, causing systemic hemorrhagic sepsis that results in lethality. Although vaccines against E. piscicida have been developed for many fish species, a direct comparison between innate and adaptive immunity in protecting fish from E. piscicida infection has not been performed. We established an il2rb mutant lacking natural killer (NK) cells, innate type lymphocytes, showing that NK cells are required for protection against E. piscicida infection in adult medaka. In addition, we elucidated the role of the TLR signaling pathway transmitted by Myd88 in resistance to E. piscicida infection in larvae and adults. These results indicate the requirement of innate immunity in resistance to this intracellular pathogen, providing insights into vaccination strategies for fish. - Source: PubMed
Publication date: 2026/05/22
Sakaguchi HiyoriMatsuda MasaruIwanami Norimasa - Abdominal aortic aneurysm (AAA) remains a life-threatening vascular disease with limited therapeutic options. The role of interleukin-2 receptor subunit beta (IL2RB) in AAA via mitochondrial dysfunction is unclear. In this study, integrated bioinformatics analyses identified IL2RB as a key gene. In a rat AAA model and angiotensin II-stimulated vascular smooth muscle cells (VSMCs), IL2RB was upregulated and associated with mitochondrial impairment. IL2RB knockdown attenuated aortic dilation, reduced elastic fiber degradation (decreased by 45%), restored adenosine triphosphate (ATP) production (increased by 126.9%), suppressed interleukin-6 (decreased by 49.3%) and tumor necrosis factor-alpha (decreased by 51.8%) release, and decreased malondialdehyde (reduced by 47.7%) and reactive oxygen species (reduced by 38.5%) production in the rat model. In VSMCs, silencing IL2RB rescued angiotensin II-induced ATP depletion, preserved mitochondrial membrane potential, and reduced apoptosis. Mechanistically, IL2RB knockdown downregulated dynamin-related protein 1, and upregulated mitofusin 1 and parkin RBR E3 ubiquitin protein ligase. IL2RB knockdown mitigates AAA progression by restoring mitochondrial homeostasis and suppressing inflammation, identifying IL2RB as a potential therapeutic target for AAA. - Source: PubMed
Li PangZhang HaoHuang JinfuGao Yijing - Coronary heart disease (CHD) and ischemic stroke (IS) frequently co-occur; however, their shared molecular drivers remain poorly understood, limiting the development of dual-indication therapies. This study aims to characterize the bidirectional genetic relationship between CHD and IS and to prioritize shared candidate proteins as potential therapeutic targets or biomarkers. - Source: PubMed
Publication date: 2026/04/16
Chen MiaoLiu ZongniLou Inmaculada XuWan HaitongZhou Huifen - There is a need for novel therapies for diabetic retinopathy (DR) because existing therapies treat only certain features of DR and do not work optimally for all patients. While proteomic studies provide insight into disease pathobiology, they are often limited to small sample sizes due to high costs, limiting their generalizability and reproducibility. Moreover, they often yield lists of tens to hundreds of proteins with differential expression, making it difficult to prioritize the most biologically relevant biomarkers beyond using arbitrary fold-change and false-detection rate cutoffs. Here, we applied a two-stage multimodal AI approach: first, we integrated EHR and proteomics data to rationally prioritize candidate protein biomarkers and, next, validated these biomarkers in an independent cohort. These protein biomarkers of DR are rooted in the EHR data and thereby more likely to be biological drivers of disease. - Source: PubMed
Publication date: 2026/02/24
Lin Jonathan BMataraso Samson JChadha MadhumeetaVelez GabrielMruthyunjaya PrithviAghaeepour NimaMahajan Vinit B - Exposure to immune stress or lipopolysaccharide (LPS) during critical developmental stages like puberty may lead to gut microbiome dysbiosis and epigenetic dysregulation in mammary glands, affecting gene expression and potentially elevating breast cancer susceptibility in adulthood. Although LPS's adverse impacts on intestinal and brain functions are well-documented, its effects on mammary glands remain underexplored. Using an immunocompetent BALB/c mouse model, we administered an acute LPS dose (1.5 mg/kg body weight) during puberty. The study evaluated the long-term consequences of LPS exposure alone and combined with AHCC (Lentinula edodes cultured extract, 2 g/kg body weight/day) on DNA methylation patterns, cytokine profiles, and microRNA expression in mammary glands at 9 weeks of age. Analyses included DNA methylation sequencing, multiplex immunoassays, quantitative PCR, and image processing. Pubertal LPS exposure produced persistent molecular dysregulation in mammary glands, including differential DNA methylation (> 5% change vs. control; FDR-adjusted p < 0.05), elevated inflammatory mediators, and altered microRNA expression. Differentially methylated regions were enriched in regulatory features, with decreased methylation at transcription start sites, promoters, and 5' UTRs of genes implicated in mammary development and oncogenic signaling (including Vav3, Pdgfa, Pdgfc, Jag2, Hras, Ksr1, Il2rb, Il17b, and Il17rb) in the LPS group, whereas the AHCC + LPS group exhibited a shift toward hypermethylation at these loci (approximately 5%-10% decrease). Inflammatory profiling showed increased IL-17A/F (∼2-fold vs. control; p < 0.05), while microRNA analyses indicated reduced let-7a/c (∼30% vs. control; p < 0.05). Notably, miR-130a and miR-34a increased ∼1.5-fold across all treatment groups relative to control. Pubertal LPS exposure induces enduring epigenetic and inflammatory changes in mammary glands that may heighten breast cancer risk. AHCC's mitigating role indicates potential for dietary interventions to counteract these effects. - Source: PubMed
Yasavoli-Sharahi HamedShahbazi RoghayehAlsadi NawalSahebi Nasim BondarCuenin CyrilleCahais VincentChung Felicia Fei-LeiHerceg ZdenkoMatar Chantal