ST2/IL-33R (H2) rabbit mAb

Suppression of tumorigenicity (ST)2 is an interleukin (IL)-1 receptor family member and due to alternative splicing and 3’ processing at RNA level, ST2 is expressed as soluble (sST2) as well as trans-membrane (ST2L) isoforms (1).  Originally identified in 1989 as an orphan receptor, the ST2 ligand was identified to be IL-33 in 2005 (2).  IL-33 is mechanically induced in cardiac fibroblasts and antagonizes hypertrophic stimuli. Analysis of rat neonatal cardiac fibroblasts and cardiomyocytes indicate that gene expression of IL-33 and sST2 was more than 5-fold greater in cardiac fibroblasts than in cardiomyocytes (3,4). Expression sST2 is markedly increased as early as 1 hr following mechanical strain in cultured myocytes and in patients with acute myocardial infarction (5). 

In addition, IL-33 behaves as a chromatin-related nuclear interleukin, and act as transcriptional repressor when overexpressed in cells (4). IL-33 production may be augmented by inflammation (6). IL-33 has been demonstrated to participate in several forms of inflammatory diseases and to influence tumorigenesis. IL-33 was identified to be pro-cancer mediator, since the activation pathway of IL-33/ST2 could promote metastasis (7).