ANTI-RICK

All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry.

The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit .

RIPK2 (receptor-interacting serine-threonine kinase 2) is a member of the kinase family called RIP, which has seven members. It is an intracellular protein, and its C-terminal contains CARD (caspase activation and recruit domain). This gene is localized to human chromosome 8q21, and codes for a protein composed of 531 amino acids, and with a molecular weight of 61kDa. An alternatively spliced variant of this gene is called RIP2β, which lacks the C-terminal CARD and the intermediate region. It only contains a part of the kinase domain present at the N-terminal.

RIPK2 (receptor-interacting serine-threonine kinase 2) plays a role in both innate and adaptive immune pathways. It also interacts with T-cell receptor (TCR) complex, and is a part of the signaling pathway. It is a part of the Toll-like receptor (TLR), Nod, IL (interleukin)-1R receptors and IL-12 transduction pathways. Studies in Chinese population suggest that variants in this gene might be linked to susceptibility to systemic lupus erythematosus (SLE). It stimulates the activity of caspase-8 and thus, promotes CD95-mediated apoptosis. It facilitates the maturation of IL-1β, by interacting with caspase-1. It is essential for the proliferation of keratinocytes. In glucocorticoid-treated patients, its expression is suppressed, which leads to decreased re-epithelialization of wounds. It plays a part in the tumorigenesis of human colon cancer, and might have potential as a marker for the aggressiveness of human colon cancer.