Human IL23A blocking peptide (CDBP1589)

Synthetic Human IL23A blocking peptide for BL

Product Overview
Blocking peptide for anti-IL-23 antibody
Target
IL-23
Nature
Synthetic
Species Reactivity
Human
Tag/Conjugate
Unconjugated
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
Procedure
None
Format
Liquid
Concentration
200 μg/ml
Size
50 μg
Buffer
PBS containing 0.02% sodium azide
Preservative
0.02% Sodium Azide
Storage
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
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. [provided by RefSeq, Jul 2008]
Function
cytokine activity; contributes_to interleukin-23 receptor binding;
Synonyms
IL23A; interleukin 23, alpha subunit p19; interleukin-23 subunit alpha; IL 23; IL 23A; IL23P19; interleukin six; G CSF related factor; P19; SGRF; IL-23-A; IL-23p19; IL-23 subunit alpha; interleukin 23 p19 subunit; interleukin-23 subunit p19; JKA3 induced upon T-cell activation; interleukin-six, G-CSF related factor; IL-23; IL-23A; MGC79388;

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References


2D Visualization of the Psoriasis Transcriptome Fails to Support the Existence of Dual-Secreting IL-17A/IL-22 Th17 T Cells

FRONTIERS IN IMMUNOLOGY

Authors: Le, Stephanie T.; Merleev, Alexander A.; Luxardi, Guillaume; Shimoda, Michiko; Adamopoulos, Lannis E.; Tsoi, Lam C.; Wang, Jenny Z.; Alexanian, Claire; Raychaudhuri, Siba P.; Hwang, Samuel T.; Gudjonsson, Johann; Marusina, Alina, I; Maverakis, Emanual

The present paradigm of psoriasis pathogenesis revolves around the IL-23/IL-17A axis. Dual-secreting Th17 T cells presumably are the predominant sources of the psoriasis phenotype-driving cytokines, IL-17A and IL-22. We thus conducted a meta-analysis of independently acquired RNA-seq psoriasis datasets to explore the relationship between the expression of 1L17A and IL22. This analysis failed to support the existence of dual secreting IL-17A/IL-22 Th17 cells as a major source of these cytokines. However, variable relationships amongst the expression of psoriasis susceptibility genes and of IL17A, IL22, and IL23A were identified. Additionally, to shed light on gene expression relationships in psoriasis, we applied a machine learning nonlinear dimensionality reduction strategy (t-SNE) to display the entire psoriasis transcriptome as a 2-dimensonal image. This analysis revealed a variety of gene clusters, relevant to psoriasis pathophysiology but failed to support a relationship between IL17A and IL22. These results support existing theories on alternative sources of IL-17A and IL-22 in psoriasis such as a Th22 cells and non-T cell populations.

A Role for RUNX3 in Inflammation-Induced Expression of IL23A in Gastric Epithelial Cells

CELL REPORTS

Authors: Hor, Yit Teng; Voon, Dominic Chih-Cheng; Koo, Jason Kin Wai; Wang, Huajing; Lau, Wen Min; Ashktorab, Hassan; Chan, Shing Leng; Ito, Yoshiaki

RUNX3 functions as a tumor suppressor in the gastric epithelium, where its inactivation is frequently observed during carcinogenesis. We identified IL23A as a RUNX3 target gene in gastric epithelial cells. This was confirmed in a series of in vitro analyses in gastric epithelial cell lines. In elucidating the underlying regulatory network, we uncovered a prominent role for the TNF-alpha/NF-kappa B pathway in activating IL23A transcription. Moreover, the activating effect of TNF-alpha was markedly augmented by the infection of Helicobacter pylori, the primary cause of human gastritis. Of note, H. pylori utilized the CagA/SHP2 pathway to activate IL23A, as well as the induction of the NOD1 pathway by iE-DAP. Importantly, RUNX3 synergized strongly with these physiologically relevant stimuli to induce IL23A. Lastly, we present evidence for the secretion of IL23A by gastric epithelial cells in a form that is distinct from canonical IL-23 (IL23A/IL12B).

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