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These results provide a new pathway of Th1 (show HAND1 ELISA Kits) response regulation where IL-12 (show IL12A ELISA Kits) secreted by dendritic cellss is consumed by a sub-population of IL-12Rbeta2-expressing Treg cells.
in neonatal mice, IL-12 (show IL12A ELISA Kits) uses IL-12Rbeta2 to counter IL-13Ralpha1 expression in addition to promoting Th1 (show HAND1 ELISA Kits) differentiation
Data indicate that delayed induction of the IL-12Rbeta2 receptor component after STAT1 (show STAT1 ELISA Kits) activation helped ensure that Treg cells do not readily complete STAT4 (show STAT4 ELISA Kits)-dependent Th1 (show HAND1 ELISA Kits) cell development and lose their ability to suppress effector T cell proliferation.
Signaling through the IL-35 receptor required the transcription factors STAT1 (show STAT1 ELISA Kits) and STAT4 (show STAT4 ELISA Kits).
Data show that T(H)1 differentiation was impaired in Il2 (show IL2 ELISA Kits)(-/-) T cells but was restored by IL-12Rbeta2 expression.
gamma rays cause a decrease in IFN-gamma (show IFNG ELISA Kits), IL-12p70, IL-12 (show IL12A ELISA Kits) receptor beta2, and STAT4 (show STAT4 ELISA Kits) and an increase in IL-4 (show IL4 ELISA Kits) in natural killer cells
Freshly isolated ex vivo T helper (Th)17 cells display restricted expression from Il12rb2 due to the presence of repressive chromatin remodeling.
T-bet mediates STAT1 (show STAT1 ELISA Kits)-dependent processes of T(H)1 development, including the induction of IL-12Rbeta2.
NO activates soluble guanylyl cyclase, leading to the up-regulation of cGMP, which selectively induces the expression of IL-12 (show IL12A ELISA Kits) receptor beta2.
Contrary to the expectation that the absence of IL-12RB2 would protect from experimental autoimmune encephalitis, IL-12RB2-deficient mice develop earlier and more severe disease, with extensive demyelination and central nervous system inflammation.
inhibition of the H3K27 demethylase (show MBD2 ELISA Kits) JMJD3 (show Kdm6b ELISA Kits) in naive CD4 (show CD4 ELISA Kits) T cells demonstrates how critically important molecules required for T cell differentiation, such as JAK2 (show JAK2 ELISA Kits) and IL12RB2, are regulated by H3K27me3.
this study identified susceptibility single nucleotide polymorphisms in IL12RB2 with Behcet's disease in Han Chinese
In ankylosing spondylitis, conditional analysis identified rs11209032 as the probable causal single-nucleotide polymorphism within a 1.14 kb putative enhancer between IL23R (show IL23R ELISA Kits) and IL12RB2. The rs11209032 single-nucleotide polymorphism downstream of IL23R (show IL23R ELISA Kits) forms part of an enhancer, allelic variation of which may influence Th1 (show TH1L ELISA Kits)-cell numbers.
The results of this case-control study suggest that IL-12A (show IL12A ELISA Kits), IL-12B (show IL12B ELISA Kits), IL12RB1 (show IL12RB1 ELISA Kits), IL12RB2 and IL23R (show IL23R ELISA Kits) make no genetic contribution to the susceptibility of Takayasu arteritis in Chinese populations
study confirmed the relationship of IL12RB2 polymorphisms with primary biliary cholangitis (PBC (show DLAT ELISA Kits)) susceptibility; provided evidence that IL12RB2 polymorphisms are associated with liver cirrhosis and an increased concentration of disease-specific anti-mitochondrial antibodies in sera of PBC (show DLAT ELISA Kits) patients
this study shows that single nucleotide polymorphisms of the IL23R-IL12RB2 region are associated with Behcet's disease in a Northern Chinese Han population
IL12RB2 polymorphisms correlate with risk of lung adenocarcinoma.
The effects of rs3762315 and rs3762316 single nucleotide polymorphisms in 5' flanking region on IL12RB2 transcription
Estrogen receptor beta 2 (show ESR2 ELISA Kits) regulates IL12RB2 expression via p38 MAPK (show MAPK14 ELISA Kits) signaling and inhibits non-small-cell lung cancer proliferation and invasion.
IL12RB2 polymorphism is associated with systemic lupus erythematosus in the Chinese population.
Four SNPs in IFNGR2 (show IFNGR2 ELISA Kits), IL12RB1 (show IL12RB1 ELISA Kits), IL12RB2, and IL23R (show IL23R ELISA Kits) were found to be associated with the MAP infection status of the resource population.
The protein encoded by this gene is a type I transmembrane protein identified as a subunit of the interleukin 12 receptor complex. The coexpression of this and IL12RB1 proteins was shown to lead to the formation of high-affinity IL12 binding sites and reconstitution of IL12 dependent signaling. The expression of this gene is up-regulated by interferon gamma in Th1 cells, and plays a role in Th1 cell differentiation. The up-regulation of this gene is found to be associated with a number of infectious diseases, such as Crohn's disease and leprosy, which is thought to contribute to the inflammatory response and host defense. Several transcript variants encoding different isoforms and non-protein coding transcripts have been found for this gene.
interleukin 12 receptor, beta 2
, interleukin 12 receptor beta-2
, interleukin-12 receptor subunit beta-2
, interleukin-12 receptor subunit beta-2-like
, IL-12 receptor subunit beta-2
, IL-12R subunit beta-2
, interferon response to microorganisms
, interleukin-12 receptor beta-2 chain
, interleukin-12 receptor beta 2
, IL-12 receptor beta-2