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Four SNPs in IFNGR2, IL12RB1, IL12RB2, and IL23R were found to be associated with the MAP infection status of the resource population.
IL23R (rs10889677) polymorphism did not show any association with rheumatic heart disease in South Indian population
Study confirms an association between IL12B and IL23R genetic polymorphism and psoriasis vulgaris (with a protective effect of minor alleles).
The IL23R gene rs10889677 A allele confers increased risk of ankylosing spondylitis (AS) in Europeans, but its role in Asian populations needs further exploration.
these findings suggest that the variants +2199 A/C IL-23R and -197 G/A IL-17A could contribute to rheumatoid arthritis development in the studied population
Data show that interleukin-23 receptor (IL-23R) single nucleotide polymorphism (SNP) rs11465817 contributes to the risk of recurrent oral ulceration (ROU) in Chinese.
Findings indicate that IL17A -197 G/A and IL23R H3Q are not associated with susceptibility to MM. However, IL-17 and IL-23R polymorphisms may affect severity, bone lesions, and extra-medullary disease in patients with MM.
This study provides evidence for three alcohol-induced ONFH susceptibility genes (NOS3, ABCB1 and IL23R) in Chinese males and polymorphisms of them may be associated with alcohol-induced ONFH risk.
genetic association studies in population in southwest China: Data suggest that SNPs in STAT4 (rs7574865), IL23R (rs11209032), and STAT3 (rs744166) are associated with occurrence, severity, and immunosuppressive therapy outcomes of aplastic anemia in the population studied. (STAT = signal transducer and activator of transcription) [article includes Meta-Analysis]
Study provides a comprehensive examination of the available evidence for the association between polymorphisms in the IL-23R gene and ulcerative colitis (UC). The meta-analysis suggests that IL-23R gene polymorphisms are associated with UC susceptibility, especially in Caucasians.
Data indicate that the interleukin-23 receptor (IL-23R) SNPs rs11209026, p.Arg381Gln; rs41313262 p.Val362Ile were not associated with susceptibility to inflammatory bowel disease (IBD) in Chinese Han population.
Interleukin-23 receptor cytokine-binding homology region balances the ratio of Th17/Th9/Treg cells in collagen-induced arthritis.
our study provides the evidence that functional IL-23R rs1884444 G/T and IL-17F rs763780 A/G polymorphisms may be a new genetic susceptibility factor to SLE, especially in the Polish population.
IL23R rs10889677 and IL17A rs2275913 were not associated with the susceptibility to Necrotizing enterocolitis (NEC). In conclusion, data suggest that a variant of IL17F (rs763780) may contribute to the development of NEC.
this meta-analysis suggests that each allele of IL-23R, including rs7519847, rs17375018 and rs11209032 was negatively associated with uveitis; however, homozygote models, including the rs17375018 GG genotype and rs11209032 AA genotype, were significantly associated with uveitis
an evaluation of what is currently known about the protective role of R381Q variant in IL-23R gene in immune-based diseases (Review).
Th17 cells expressed consistent high levels of the IL-12Rbeta1 subunit, which appeared a better predictor of responsiveness to IL-23 than the expression of the IL-23R subunit.
We conclude that variants in IL-23A and IL-23R genes were associated with the risk of multiple sclerosis or other inflammatory demyelinating diseases.
IL-23 R (rs7517847) and LEP (rs7799039) polymorphisms were associated with an increased risk but not affecting the clinical presentation of HCC among Egyptian patients
In a Turkish population, IL23R polymorphism is a risk factor for UC and is protective against CD.
The current study emphasizes the lack of association of IL23R and IL17 polymorphisms with rheumatoid arthritis susceptibility in the Algerian population. However, the data showed the relationship between IL23R and IL17A polymorphisms and the production of the different RF isotypes in rheumatoid arthritis patients
Results suggest that the use of vectors carrying Soluble Interleukin-23 Receptor (sIL-23R) to block the interleukin-23/IL-23R interaction may be a new therapeutic strategy for the treatment of multiple sclerosis.
RBPJ binds and trans-activates the Il23r promoter and induces IL-23R expression and represses anti-inflammatory IL-10 production in Th17 cells.
Epithelial IL-23R signaling enables protective IL-22 responses in experimental colitis.
Study highlights the importance of IL-23R expression level and the instability of Foxp3+ regulatory T cells in the development of inflammatory bowel diseases.
Differential splicing generates antagonistic soluble IL-23R (sIL-23R) variants, which might limit IL-23-mediated immune responses. Here, ectodomain shedding of IL-23R was identified as an alternative pathway for the generation of sIL-23R.
Estrogen and progesterone decrease let-7f microRNA expression and increase IL-23/IL-23 receptor signaling and IL-17A production in patients with severe asthma.
Data show the contribution of IL-23/IL-23 receptor and IL-7/IL-7 receptor signaling in Th17 and Th1 cell dynamics during experimental autoimmune encephalomyelitis (EAE).
Study provides evidence that IL-23/IL-23R plays a critical role in brain ischemic injury
IL-23 plus T-cell receptor signalling results in significant upregulation of IL-23 receptor expressed predominantly on CD4(hi)CD8(hi)CD3(+)alphabetaTCR(+) thymocytes, and leads to RORgammat-dependent apoptosis.
Homeostatic IL-23 receptor signaling limits Th17 response through IL-22-mediated containment of commensal microbiota.
Characterization of potent IL-23R small-peptide modulator, 2305 (teeeqqly), that decreases inflammatory response.
Although they share a common subunit, IL-23 and IL-12 receptors are not expressed on the same cell populations
IL-23R+ innate lymphoid cells induce colitis via interleukin-22-dependent mechanism.
the balance between the enhancing and inhibitory effects of gamma-delta T cells is regulated by their level of IL-23R expression.
Identification of canonical tyrosine-dependent and non-canonical tyrosine-independent STAT3 activation sites in the intracellular domain of the interleukin 23 receptor.
study indicates the importance of IL-23 pathway in Th17 development and the negative regulation of Th17 development by IL23R-CHR
knock-out mice display decreased weight loss and reduced leukocyte infiltrate in dextran sulfate sodium-induced colitis
The IL-23 receptor is necessary for lymphoid hyperplasia, production of pathogenic autoantibodies, and infiltration of kidneys by IL-17-expressing cells in lupus-prone mice.
suppression of T-bet ameliorates EAE by limiting the differentiation of autoreactive Th1 cells, as well as inhibiting pathogenic Th17 cells via regulation of IL-23R.
IL-23R deficiency inhibited terminal differentiation of interleukin 17-producing effector T helper cells.
The protein encoded by this gene is a subunit of the receptor for IL23A/IL23. This protein pairs with the receptor molecule IL12RB1/IL12Rbeta1, and both are required for IL23A signaling. This protein associates constitutively with Janus kinase 2 (JAK2), and also binds to transcription activator STAT3 in a ligand-dependent manner.
, interleukin 23 receptor
, interleukin-23 receptor-like
, IL-23 receptor
, interleukin 23 receptor-like