IL2R Antibody
- Known as:
- IL2R Antibody
- Catalog number:
- 29047
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- IL2R Antibody
Related genes to: IL2R Antibody
- Gene:
- IL2RA NIH gene
- Name:
- interleukin 2 receptor subunit alpha
- Previous symbol:
- IL2R, IDDM10
- Synonyms:
- CD25
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-01-22
- Date modifiied:
- 2019-04-23
Related products to: IL2R Antibody
Related articles to: IL2R Antibody
- Beyond conventional transcriptome profiling, RNA-sequencing (RNA-Seq) enables the discovery of variants within expressed genes linked to complex traits such as mastitis resistance or susceptibility. In this study, RNA-Seq was performed on milk somatic cells from uninfected Holstein cows with no history of mastitis (Neg, n = 9) or with subclinical intramammary infections (sIMI) caused by Prototheca spp. (P+ , n = 11) or Streptococcus agalactiae (Sa+ , n = 11). The objective was to identify transcriptome-derived sequence variants detectable under specific microbiological conditions that may contribute to the modulation of host transcriptional responses. By integrating these transcript-derived variants with quantitative trait locus (QTL) annotations and enrichment analyses, we aimed to highlight genomic regions functionally associated with mastitis susceptibility or resilience. - Source: PubMed
Publication date: 2026/05/17
Vanzin AliceBisutti VittoriaCánovas ÁngelaCecchinato AlessioGallo LuigiGiannuzzi DianaPegolo Sara - The American College of Medical Genetics and Genomics (ACMG) recommends Tier-3 reproductive carrier screening for 97 genes associated with autosomal recessive conditions (AR genes). Gene selection for screening is based on a gene carrier frequency (GCF) of ≥1/200 in the Genome Aggregation Database (gnomAD)v2 populations and disease severity. The utility of ACMG Tier-3 in the Middle Eastern population is unclear as this ancestral group was not represented in the gnomADv2. We utilized genome data from 14,392 individuals in the Qatar Genome Project to estimate the carrier frequency of autosomal recessive conditions in the Middle Eastern population. The frequency of 136,624 Pathogenic/Likely Pathogenic variants in 2,987 AR genes from ClinVar was analyzed to estimate the GCF in the Qatari cohort. Genes with GCF≥1/200 were curated by an expert panel for the severity of corresponding conditions. We identified 69 genes with GCF≥1/200 associated with moderate to profound clinical presentations, 53 of which were unique to the Middle Eastern population. Common variants were observed with high frequency for individual genes such as IL2RA that suggested the presence of founder effects not described previously. Simulation studies predicted that inclusion of the ancestry-specific genes increased the chance of detecting at-risk couples from 3.85% to 8.15% in the Middle Eastern population. This study highlights the limitations of relying on global datasets to accurately identify the candidate genes for carrier screening in different populations. Our findings provide a framework for targeted, population-specific carrier screening programs in regions not represented in the large genome datasets. - Source: PubMed
Publication date: 2026/05/14
Nkrumah EstherAl-Mulla HajerBashar AryanSoman VishalSaad ChadiWang JohnDarabi HeliaYatsenko Svetlana ARajkovic AleksandarChandran UmaMbarek HamdiAarabi Mahmoud - NSCLC remains a leading cause of cancer-related mortality, with limited biomarkers to guide surgical and immunotherapeutic intervention. This study leveraged two complementary plasma proteomics platforms, SomaScan (7596 proteins) and NULISA (250 inflammation-related proteins) to profile 87 timepoints from 56 NSCLC patients, collected pre- and post-surgery and pre- and post-ICI therapy. Robust biomarker selection used adaptive Lasso regression and the Stabl algorithm, with inter- and intra-cohort validation via orthogonal nELISA proteomics. Twenty-one differentially detectable plasma proteins were identified across treatment contexts. Surgical resection induced measurable proteomic changes: non-recurrent patients had higher circulating MUC16 and lower IL36G post-surgery, while recurrent patients showed elevated COX7A2L, FGF19, and SPOCK2, alongside lower FCER2, FCRLA, and SLITRK2. Among ICI-treated patients, responders had lower baseline levels of IL-6, CCL19, IL-2RA, CD200R1, CRP, LIF, PDCD1, CCL7, and SPP1, implicating systemic inflammation and immune regulation in treatment sensitivity. CEACAM5, PTX3, FGF23, and AREG were elevated in patients with worse clinical outcomes and poorer overall survival. MUC16, IL36G, CCL19, and IL-6 were independently validated by nELISA. Cross-platform comparison highlighted the complementary strengths of SomaScan's broad proteomic coverage and NULISA's sensitivity for low-abundance proteins. This integrated approach reveals distinct plasma signatures associated with surgical recurrence, ICI response, and prognosis in NSCLC. - Source: PubMed
Publication date: 2026/05/12
Yaghoubi Naei VahidKilgallon AaronMendes GwendolineWijerathna-Yapa AkilaDutta SanjayLawler ClaraO'Leary ConnorMullally WilliamMonkman JamesMansfield JamesHedou JulienAdams Mark NO'Byrne KenWarkiani Majid EKulasinghe Arutha - Recent studies have advanced understanding of chromosomal organization and its role in gene regulation, yet most analyses focus on short-range interactions (<2 Mb), limiting insight into broader architecture. The relationships between topologically associating domains (TADs), sub-TAD loops, cross-TAD interactions, and chromosomal compartmentalization remain poorly understood. Here, using high-resolution Hi-C analysis, we identify extensive multi-megabase and interchromosomal interactions (metaloops) in T lymphocytes that organize into meta-TAD associations (metadomains). These metaloops connect distal promoters and regulatory elements of genes functionally important in T cells, including Ctla4, Ikzf2, Il2ra, Ets1, and Foxo1. Reanalysis of mouse and human datasets confirms their reproducibility and dependence on superenhancers. Genome-wide clustering reveals three distinct interchromosomal hubs, including a superenhancer-enriched hub linked to T cell-specific gene activation. Integrative analysis of regulatory genomics data identifies factors associated with short- versus long-range interactions. This study introduces a broadly applicable computational framework and reveals features of T cell genome organization. - Source: PubMed
Publication date: 2026/05/07
Dolsten GabrielWang Zhong-MinHuang XiaoSong SusieWilson Michael JBing Xin YangKe WenfanCafiero Thomas RNelson Amy NFernando SebastianPloss AlexanderSchedl PaulLevine Michael SViny Aaron DRudensky Alexander YPritykin Yuri - Regulatory T cells (Tregs) prevent autoimmunity through suppressive functions largely programmed by the transcription factor FOXP3. Healthy humans express approximately equivalent levels of two major alternatively spliced isoforms of FOXP3: a full-length version containing all coding exons (FOXP3-FL) and a version lacking exon 2 (FOXP3-ΔE2). However, sole FOXP3-ΔE2 expression causes lethal IPEX syndrome, and the FOXP3-ΔE2 isoform is elevated in several autoimmune diseases. These observations strongly suggest defects in suppression by FOXP3-ΔE2 Tregs which we investigated here using Foxp3-ΔE2 mice. In an influenza virus infection model, Foxp3-ΔE2 mice had an increased magnitude of the CD8 T cell response during acute and memory formation phases of infection. Transcriptomic and chromatin accessibility analyses of homeostatic Foxp3-ΔE2 Tregs revealed impaired Treg programming, including reduced expression of inhibitory molecules such as and chemokine receptors. Decreased cell surface CD25 expression on Foxp3-ΔE2 Tregs was associated with reduced IL-2 responsiveness in Foxp3-ΔE2 Tregs and, reciprocally, increased IL-2 responsiveness in CD8 T cells from Foxp3-ΔE2 mice. Additionally, altered chemokine receptor expression resulted in diminished localization of Foxp3-ΔE2 Tregs to the T cell zone of the inflamed lymph node. Thus, Treg programming by the Foxp3-ΔE2 isoform impairs suppressive function, resulting in failure to restrain CD8 T cells and aberrant immune responses. - Source: PubMed
Publication date: 2026/04/23
Weinstein Kristin NBishop Zoe HShamskhou Elya ABarry Finnegan NChandrashekar HarshiniVerdezoto Gabrielade Leon MarissaAlbe Joseph RKoval AndrewZhou BaohuaDomeier Phillip PGerner Michael YCampbell DanielZiegler Steven F