IL22RA1 _ IL22R (N_term)
- Known as:
- IL22RA1 _ IL22R (N_term)
- Catalog number:
- AP07312PU-N
- Product Quantity:
- 50 µg
- 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)
- Interleukin-22 (IL-22) is a cytokine that regulates tissue inflammation and repair, primarily through activation of STAT3 signaling. Although its protective effects in acute pancreatitis (AP) are well established, the specific contribution of its receptor, IL-22Ra1, and the underlying signaling mechanisms remain incompletely defined. Notably, the C-terminal region of IL-22Ra1, although devoid of tyrosine residues, has been reported to promote STAT3 activation through unconventional mechanisms. Here, we investigated the role of IL-22Ra1 and its C-terminal (STAT3-associated) domain in a mouse model of caerulein-induced AP. We show that deletion of the C-terminal region of IL-22Ra1 markedly reduces STAT3 activation in the pancreas, confirming its role in amplifying canonical signaling. Unexpectedly, this reduction does not worsen pancreatic injury. In contrast, both IL-22- and IL-22Ra1-deficient mice develop more severe pancreatitis, characterized by increased serum amylase levels, exacerbated inflammatory responses, and enhanced tissue damage. Notably, IL-22Ra1 deficiency results in a more severe phenotype than IL-22 deficiency alone, indicating that IL-22Ra1 mediates protective effects beyond IL-22 signaling. Consistently, acinar-to-ductal metaplasia during the regenerative phase is impaired in both IL-22- and IL-22Ra1-deficient mice but preserved upon C-terminal truncation. Together, these findings identify IL-22Ra1 as a central regulator of pancreatic protection through mechanisms that are independent of maximal STAT3 activation and extend beyond IL-22 itself, suggesting the involvement of additional IL-22Ra1 ligands. These results support the exploration of receptor-activating strategies, such as agonistic antibodies, to promote tissue protection and regeneration. - Source: PubMed
Publication date: 2026/07/28
Puigdevall LénaStewardson ClaraDhulst LysaHendrickx EmilieDumoutier Laure - To assess the involvement of long non-coding RNA (lncRNA) Antisense Noncoding RNA in the INK4 Locus (ANRIL) in subconjunctival fibrosis after glaucoma filtration surgery (GFS). - Source: PubMed
Publication date: 2026/07/22
Jiang LeiWu YifengShu YujieFan FangliDeng Zhen - Giant cell arteritis (GCA) is a clinically heterogeneous disease, which complicates both diagnosis and management. This study aimed to identify genetic risk factors associated with GCA clinical manifestations and evaluate their utility for defining clinical phenotypes. - Source: PubMed
Publication date: 2026/07/03
Borrego-Yaniz GonzaloFuentes-Moreno VeraOrtiz-Fernández LourdesHernández-Rodríguez JoséMackie Sarah LVaglio AugustoCastañeda SantosSolans RoserMestre-Torres JaumeKhalidi NaderLangford Carol AYtterberg StevenBeretta LorenzoGovoni MarcelloEmmi GiacomoCimmino Marco AWitte TorstenNeumann ThomasHolle JuliaSchönau VerenaPugnet GregoryPapo ThomasHaroche JulienMahr AlfredMouthon LucMolberg ØyvindDiamantopoulos Andreas PVoskuyl AlexandreDaikeler ThomasBerger Christoph TMolloy Eamonn Svan Sleen YannickSorensen LouiseLuqmani Raashid Ortego-Centeno NorbertoBrouwer ElisabethLamprecht PeterKlapa SebastianSalvarani CarloMerkel Peter ACid María CIles Mark MGonzález-Gay Miguel AMorgan Ann WMartin JavierMárquez Ana - Proliferative diabetic retinopathy (PDR) is one of the leading causes of blindness in working-age adults. We have previously shown that the risk of PDR is significantly elevated in individuals with intrauterine exposure to famine. However, the genetic mechanisms mediating this association remain unknown. The aim of the current study was to investigate the molecular underpinnings of famine-related PDR by performing genome-wide association (GWAS) and interaction studies (GWIS). - Source: PubMed
Publication date: 2026/06/25
Fedotkina OlenaBegum Most ChampaTrinh Xuan TungÖzgumus TurkulerÅkerlund MikaelNilsson PeterSpindola Leticia MariaLyssenko Valeriya - 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