IL22RA1 _ IL22R (N_term)
- Known as:
- IL22RA1 _ IL22R (N_term)
- Catalog number:
- AP30417PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IL22RA1 _ IL22R (N_term)
Related genes to: IL22RA1 _ IL22R (N_term)
- Gene:
- IL22RA1 NIH gene
- Name:
- interleukin 22 receptor subunit alpha 1
- Previous symbol:
- IL22R
- Synonyms:
- CRF2-9
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-16
- Date modifiied:
- 2015-12-11
Related products to: IL22RA1 _ IL22R (N_term)
Related articles to: IL22RA1 _ IL22R (N_term)
- The increased prevalence of inflammatory skin diseases such as atopic dermatitis, hidradenitis suppurativa, acne, lupus erythematosus in African American (AA) compared to White Non-Hispanic population is well recognized. However, the underlying mechanisms are largely unknown. Here we analyzed proteome in healthy skin biopsies from AA and White Non-Hispanic volunteers using Olink Explore 384 Inflammation biomarker panel. Among proteins with higher expression in AA skin were IRAK1, IL1A, IL4, IL22RA1. It is known that IL1A binding to IL1R1 receptor results in recruitment of signaling adapter MyD88 and IL1R1-associated kinases including IRAK1, a key signal transducer involved in activation of downstream NF-κB and MAPK signaling cascades. We confirmed the increased IRAK1 expression as well as activation of NF-κB and extracellular signal-regulated kinase1/2 signaling in both AA adult and neonatal skin by western blot analysis of relevant proteins (p65/RelA, IKKs, IκBα, extracellular signal-regulated kinase1/2) phosphorylation at specific activating sites. We also confirmed the overexpression of previously reported differentially expressed in AA skin pro-inflammatory genes such as IL1A, TNFα, fold change ER1G in our sets of AA healthy adult and neonatal skin using qRT-PCR. Overall, our study suggests the importance of further analysis of molecular landscape of healthy AA skin to assess how it may contribute to the increased risk of certain inflammatory diseases within the AA population. - Source: PubMed
Publication date: 2026/05/14
Trubetskoy DimitriGrudzien Patrick KKlopot AnnaTsoi Lam CKundu Roopal VPerez White Bethany EBudunova Irina - Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy with limited targeted treatment options and poor clinical outcomes. We developed an AI-driven multi-omics pipeline that links prognostic modeling to multitarget drug repurposing for ESCC. Summary-data-based Mendelian randomization was integrated with bulk transcriptomic datasets to identify esophageal cancer-related druggable genes that are differentially expressed. Cox regression and non-negative matrix factorization were then used to define prognostic genes and molecular subgroups, and a Lasso Cox model with SHapley Additive explanation provided an interpretable prognostic signature. Single-cell RNA sequencing analysis mapped the hub genes interleukin 22 receptor subunit alpha 1 (IL22RA1) and family with sequence similarity 221 member A (FAM221A) to epithelial cell populations and associated them with proliferative and DNA repair programs, supporting their role in tumor progression, supporting their role in ESCC progression. To translate these targets into a therapeutic strategy, we applied machine learning-based drug sensitivity prediction, ADMET-AI toxicity, pharmacokinetic profiling, and molecular docking, which converged on the checkpoint kinase inhibitor AZD7762 (3-(carbamoylamino)-5-(3-fluorophenyl)-N-[(3S)-piperidin-3-yl] thiophene-2-carboxamide) as a promising multitarget inhibitor of IL22RA1 and FAM221A. In vitro assays confirmed that IL22RA1 and FAM221A promote ESCC cell proliferation, migration, and invasion. Taken together, this AI-driven multi-omics framework delivers a prognostic model, defines biologically distinct ESCC subgroups, and nominates AZD7762 as a rational multitarget drug repurposing candidate, providing a precision oncology strategy. - Source: PubMed
Publication date: 2026/05/26
Zhuang ZhanYu ShaobinPeng KaimingZhang PeipeiYu JingchuanLin JihongKang Mingqiang - Vulvovaginal candidiasis (VVC) affects >75% of women, with considerable morbidity and high medical cost burden. While Type 17 cytokines (IL-17, IL-22) are critical for oral and dermal immunity to C. albicans, their role in VVC has been less clear. Th17 gene signatures are potently upregulated in VVC, yet impairment of individual Th17 components (IL-17A, IL-17R subunits, IL-22) does not worsen disease. Rather, estrogen activity is tightly linked to VVC, leading to a paradigm that hormonal pathways, rather than immune defense, dominate susceptibility. Here, we reveal a previously unappreciated role for IL-1/Type 17 in VVC that operates independently of estrogenic hormones. In contrast to mice lacking IL-17A, IL-17RA, IL-22, or IL-22R individually, mice lacking IL-17RA and IL-22RA1 together (Il17raIl22ra1-/-) exhibited high fungal loads and exacerbated tissue damage and inflammation during estrogen-induced VVC. In human vulvar epithelial cells, IL-17 and IL-22 drive synergistic signaling. IL-1R signaling but surprisingly not IL-23 was upstream of this response. Il17raIl22ra1-/- mice expressed high IL-1β yet did not control disease, indicating that IL-1 is upstream but not downstream of Type 17 responses. Unexpectedly, Type 17-dependent control occurred in the absence of exogenous estrogen administration and persisted even when estrus was prevented by progesterone treatment. Collectively, these data indicate that susceptibility to VVC is driven not only by estrogen sensitization but through combinatorial loss of IL-17 and IL-22. - Source: PubMed
Publication date: 2026/05/07
Coleman Bianca MCook Melissa EKhan Md RobinVogel Amanda KWells Anthony JMiao JianVyas Shachi PTaylor Tiffany CAggor Felix E YPonde Nicole ODey IpsitaZou HenryJašarević EldinPeters Brian MGaffen Sarah L - The aim of the present study is to compare cold adaptation mechanisms between cold-tolerant Hezuo and cold-sensitive Bama pigs. - Source: PubMed
Publication date: 2026/03/11
Li YajuanGao XiaoliZhang YatingGun Shuangbao - Bullous pemphigoid is a chronic autoimmune blistering disease characterized by subepidermal blisters and caused by autoantibodies against BP180 and BP230. Although type 2 inflammation is considered relevant to its pathogenesis, the full spectrum of immune dysregulation in BP remains incompletely defined. - Source: PubMed
Publication date: 2025/12/14
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