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Human Polyclonal IL23A Primary Antibody für IHC (p), WB - ABIN541529
Oppmann, Lesley, Blom, Timans, Xu, Hunte, Vega, Yu, Wang, Singh, Zonin, Vaisberg, Churakova, Liu, Gorman, Wagner, Zurawski, Liu, Abrams, Moore, Rennick, de Waal-Malefyt, Hannum, Bazan, Kastelein: Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. in Immunity 2001
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Human Monoclonal IL23A Primary Antibody für IHC (fro), IHC (p) - ABIN614363
Katsifis, Rekka, Moutsopoulos, Pillemer, Wahl: Systemic and local interleukin-17 and linked cytokines associated with Sjögren's syndrome immunopathogenesis. in The American journal of pathology 2009
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Human Polyclonal IL23A Primary Antibody für IF, WB - ABIN541528
Hunter: New IL-12-family members: IL-23 and IL-27, cytokines with divergent functions. in Nature reviews. Immunology 2005
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Human Polyclonal IL23A Primary Antibody für ELISA, ICC - ABIN4324980
Li, Yao, Mariscal, Wu, Hülse, Pedersen, Helin, Waisman, Vinkel, Thomsen, Avgustinova, Benitah, Lovato, Norsgaard, Mortensen, Veng, Rozell, Brakebusch: Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation. in Nature communications 2018
Human Monoclonal IL23A Primary Antibody für FACS - ABIN4896157
Bao, Zheng, Li, Huang, Chen, Cheng, Li, Lu, Zhu, Ling, Yu, Chen, Shi: Role of interleukin-23 in monocyte-derived dendritic cells of HBV-related acute-on-chronic liver failure and its correlation with the severity of liver damage. in Clinics and research in hepatology and gastroenterology 2018
Human Monoclonal IL23A Primary Antibody für CyTOF, FACS - ABIN4899476
Duluc, Joo, Ni, Yin, Upchurch, Li, Xue, Klucar, Zurawski, Zurawski, Oh: Induction and activation of human Th17 by targeting antigens to dendritic cells via dectin-1. in Journal of immunology (Baltimore, Md. : 1950) 2014
rs2066808 polymorphism located near the IL-23A gene could increase the genetic risk of premature coronary artery disease in Mexican population.
IL-23-regulated miRNAs in T cells from patients with ankylosing spondylitis (AS) could alter the expression of downstream target molecules and thereby contribute to the immunopathogenesis of AS.
Persistent IL-23 generation of liver inflammatory macrophages responding to damaged hepatocytes after chronic hepatitis B virus (HBV) infection altered macrophage function for hepatocellular carcinoma promotion.
these data propose that, in humans, strength of TCR/CD28/Akt activation serves as a rheostat tuning the magnitude of Th17 development driven by IL-23 and IL-1beta.
IL-12 and IL-23 heterodimers are increased in Giant-cell arteritis (GCA) lesions and decrease with glucocorticoid treatment. p19 and p35 subunits are much more abundant than p40, indicating an independent role for these subunits or their potential association with alternative subunits.
Genetically determined high activities of the TNF-alpha, IL23/IL17, and NF-kappaB pathways were associated with increased risk of ankylosing spondylitis.
LMO4 appears to mediate IL-23-related responses in psoriatic keratinocytes and is a potential therapeutic target in psoriasis.
The interleukins IL-23/IL-17 immune axis has been detected as an important factor in the immunopathogenesis of ankylosing spondylitis (AS) [Review].
These results demonstrate a key role for IL-23 in HT pathogenesis and provide a potential therapeutic strategy against IL-23 or its signaling pathway in HT.
IL-23 secreted by myeloid-derived suppressor cells (MDSCs) can activate the androgen receptor pathway in prostate tumour cells, promoting cell survival and proliferation in androgen-deprived conditions; results reveal that MDSCs promote castration-resistant prostate cancer by acting in a non-cell autonomous manner; treatments that block IL-23 can oppose MDSC-mediated resistance to castration in prostate cancer
Binding affinities of these molecules with IL23 are estimated through protein-protein docking by employing ZDOCK, ClusPro and RosettaDock...Subsequent molecular dynamics simulations too favored prospective of best ranked molecule to have therapeutic implications in autoimmune and inflammatory diseases
IL23A expression in nonmuscle invasive bladder urothelial carcinoma was significantly higher than that in muscle invasive bladder urothelial carcinoma. Expression of IL23A was negatively correlated with the clinical stage of bladder urothelial carcinoma and had a positive correlation with prognosis.
IL23 and IL17 have roles in the pathogenesis of Tunisian pemphigus foliaceus
Effect of polymorphisms in IL-12B p40, IL-17A and IL-23 A/G genes on the response of psoriatic patients to narrowband UVB.
Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation.
IL-23 binding to its receptor promotes the migration and invasion of gastric cancer cells by inducing epithelial-to-mesenchymal transition through the STAT3 signaling pathway.
TNF-alpha plays an important role for the autocrine stimulation of IL-23 production by 6-sulfo LacNAc(+) dendritic cells.
The expression of IL-17 and IL-12 in patients with lupus miliaris disseminatus faciei is reported in patients and healthy controls.
SIGIRR is both a negative regulator of TLR4 and a positive regulator of TLR7/8.
interleukin 23 (IL-23)/T-helper 17 (TH 17) immune axis has been identified as a major immune pathway in psoriasis disease pathogenesis
Our study demonstrates that in dendritic cells infected with Lymphocytic choriomeningitis virus, TLR activation with bacterial PAMPs resulted in reduced IL-12 and IL-23 expression compared to non-infected cells.
Blocking the IL-23 cytokine activity decreased liver cancer development in murine model.
Our work uncovers the IL-23-IL-22 signaling as a regulator of atherosclerosis that restrains expansion of pro-atherogenic microbiota and argues for informed use of cytokine blockers to avoid cardiovascular side effects driven by microbiota and inflammation.
IL-23p19 is a key cytokine responsible for induction of Leishmania-specific Th17 cells that play an important role for progressive disease in susceptible BALB/c mice
these findings show a feed-forward mechanism involving STAT4 and T-BET that modulates the outcome of IL-23 signaling in innate lymphoid cells
It has been shown in a genetic psoriasis model that N-WASP controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter.
JunB has an essential role in IL-23-dependent pathogenicity of Th17 cells
HO-1 enhanced STAT3 phosphorylation, which enriched to Il12b and Il23a loci and negatively regulated their transcription. These findings demonstrate the underlying mechanism through which a nutritional can interfere with the immune response. CUR silences IL-23/Th17-mediated pathology by enhancing HO-1/STAT3 interaction in dendritic cells.
This study defines a critical IL-36/IL-23/IL-22 cytokine network instrumental for antimicrobial peptide production and host defense in intestinal mucosa damage using a mouse inflammatory bowel disease model.
IL-23 drives differentiation of peripheral gamma-delta 17 T cells from adult bone marrow-derived precursors.
In mice on a C57BL/6 background, neither IL-23p19 nor IL-17A plays a role for immune protection against L. major in the physiological context of natural infections.
The hormone levels are significantly reduced and lymphocytic infiltration in the lacrimal gland in ovariectomized mice, whereas the frequency of Th17 cells in the blood and spleen and IL-17A and IL-23 expression in the lacrimal glands are increased, leading to reduced tear production and positive fluorescein staining in the cornea.
this study unveiled the role of IL-23-dependent IL-17 induction in LdCen-/- parasite-induced immunity and subsequent protection against visceral leishmaniasis
Results reveal the importance of the IL-23/IL-17 inflammatory axis in secondary brain injury after intracerebral hemorrhage.
RIG-I expression is markedly increased in the affected skin derived from psoriasis patients and from both IL-23- and imiquimod -induced psoriasis-like mouse model.
results show that IL-23 accounts for the main aspects of human and murine lupus including the expansion of double negative T cells, decreased IL-2, and increased IL-17 production
this study shows that IL-23 but not IL-1 contributes to the IL-17A expression induced by subacute O3 exposure
IL-23 released by keratinocytes in response to endogenous TLR4 ligands causes skin DCs, which selectively express IL-23R, to up-regulate their endogenous IL-23 production and drive an IL-22 response in naive CD4(+) T cells that mediates epidermal thickening.
In mice overexpressing IL23, enthesis-resident gamma/delta T cells accumulate in the enthesis, ciliary body, and aortic valve.
These results provide genetic information about both swine IL-23 the IL-23 receptor alpha (IL-23Ralpha) and IL-12 receptor beta1 (IL-12Rbeta1), which allows for better understanding of interleukin systems involved in pig immunity.
cloning and characterization of interleukin-17 expressed gene sequence from mRNA obtained from intestinal tissue and interleukin-23 expressed gene sequence from mRNA obtained from peripheral blood mononuclear cells
This study examined effects of in vitro exposure to solutions of hay dust, lipopolysaccharides, or beta-glucan on cytokine expression in pulmonary mononuclear cells isolated from healthy horses and horses with recurrent airway obstruction.
The acute pulmonary neutrophilia characteristic of recurrent airway obstruction was not associated with an increase in expression of chemokines in pulmonary mononuclear cells from disease-susceptible horses.
This gene encodes a subunit of the heterodimeric cytokine interleukin 23 (IL23). IL23 is composed of this protein and the p40 subunit of interleukin 12 (IL12B). The receptor of IL23 is formed by the beta 1 subunit of IL12 (IL12RB1) and an IL23 specific subunit, IL23R. Both IL23 and IL12 can activate the transcription activator STAT4, and stimulate the production of interferon-gamma (IFNG). In contrast to IL12, which acts mainly on naive CD4(+) T cells, IL23 preferentially acts on memory CD4(+) T cells.
IL-23 subunit alpha
, JKA3 induced upon T-cell activation
, interleukin 23 p19 subunit
, interleukin-23 subunit alpha
, interleukin-23 subunit p19
, interleukin-six, G-CSF related factor
, IL-23 p19 subunit
, Interleukin-23 p19 subunit
, interleukin 23 p19