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Human Monoclonal IL23R Primary Antibody for FACS - ABIN4896718
Foucher, Blanchard, Preisser, Descamps, Ifrah, Delneste, Jeannin: IL-34- and M-CSF-induced macrophages switch memory T cells into Th17 cells via membrane IL-1α. in European journal of immunology 2015
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Human Monoclonal IL23R Primary Antibody for FACS - ABIN4896710
Shen, Zhang, Abraham, Cho: Age and CD161 expression contribute to inter-individual variation in interleukin-23 response in CD8+ memory human T cells. in PLoS ONE 2013
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Human Monoclonal IL23R Primary Antibody for FACS - ABIN4896714
Arnold, Gordon, Barker, Wilson: The activation status of human macrophages presenting antigen determines the efficiency of Th17 responses. in Immunobiology 2015
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Human Polyclonal IL23R Primary Antibody for IF (p), IHC (p) - ABIN686857
Wang, Zhong, Zheng, Li, Chen, Ma, Sun, Yan, Li: Damage effect of interleukin (IL)-23 on oxygen-glucose-deprived cells of the neurovascular unit via IL-23 receptor. in Neuroscience 2015
Mouse (Murine) Monoclonal IL23R Primary Antibody for FACS - ABIN4896726
Coffelt, Kersten, Doornebal, Weiden, Vrijland, Hau, Verstegen, Ciampricotti, Hawinkels, Jonkers, de Visser: IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis. in Nature 2015
Four SNPs in IFNGR2 (show IFNGR2 Antibodies), IL12RB1 (show IL12RB1 Antibodies), IL12RB2 (show IL12RB2 Antibodies), and IL23R were found to be associated with the MAP infection status of the resource population.
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 (show IL17A Antibodies) 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 (show IL17A Antibodies) -197 G/A and IL23R H3Q are not associated with susceptibility to MM. However, IL-17 (show IL17A Antibodies) 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 (show NANOS3 Antibodies), ABCB1 (show ABCB1 Antibodies) 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 (show STAT4 Antibodies) (rs7574865), IL23R (rs11209032), and STAT3 (show STAT3 Antibodies) (rs744166) are associated with occurrence, severity, and immunosuppressive therapy outcomes of aplastic anemia in the population studied. (STAT (show STAT1 Antibodies) = signal transducer and activator of transcription (show STAT1 Antibodies)) [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 (show IL17F Antibodies) rs763780 A/G polymorphisms may be a new genetic susceptibility factor to SLE, especially in the Polish population.
Results suggest that the use of vectors carrying Soluble Interleukin-23 Receptor (sIL (show STIL Antibodies)-23R) to block the interleukin-23/IL-23R interaction may be a new therapeutic strategy for the treatment of multiple sclerosis.
RBPJ (show RBPJ Antibodies) binds and trans-activates the Il23r promoter and induces IL-23R expression and represses anti-inflammatory IL-10 (show IL10 Antibodies) production in Th17 cells.
Epithelial IL-23R signaling enables protective IL-22 (show IL22 Antibodies) responses in experimental colitis.
Study highlights the importance of IL-23R expression level and the instability of Foxp3 (show FOXP3 Antibodies)+ regulatory T cells in the development of inflammatory bowel diseases.
Differential splicing generates antagonistic soluble IL-23R (sIL (show STIL Antibodies)-23R) variants, which might limit IL-23 (show IL23A Antibodies)-mediated immune responses. Here, ectodomain shedding of IL-23R was identified as an alternative pathway for the generation of sIL (show STIL Antibodies)-23R.
Estrogen and progesterone decrease let-7f microRNA expression and increase IL-23/IL-23 (show IL23A Antibodies) receptor signaling and IL-17A (show IL17A Antibodies) production in patients with severe asthma.
Data show the contribution of IL-23/IL-23 (show IL23A Antibodies) receptor and IL-7/IL-7 (show IL7 Antibodies) receptor signaling in Th17 and Th1 (show HAND1 Antibodies) cell dynamics during experimental autoimmune encephalomyelitis (EAE).
Study provides evidence that IL-23 (show IL23A Antibodies)/IL-23R plays a critical role in brain ischemic injury
IL-23 (show IL23A Antibodies) plus T-cell receptor signalling results in significant upregulation of IL-23 receptor expressed predominantly on CD4 (show CD4 Antibodies)(hi)CD8 (show CD8A Antibodies)(hi)CD3 (show CD3E Antibodies)(+)alphabetaTCR(+) thymocytes, and leads to RORgammat-dependent apoptosis.
Homeostatic IL-23 receptor signaling limits Th17 response through IL-22 (show IL22 Antibodies)-mediated containment of commensal microbiota.
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