Date published: 2025-9-14

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FcRH2 Activators

Fc Receptor-like 2 (FcRH2), also known as IRTA2, is a protein encoded by the FCRL2 gene in humans. FcRH2 is part of the larger family of Fc receptor-like molecules, which share structural characteristics with classical Fc receptors and are predominantly expressed on B cells and related immune cells. FcRH2 has been implicated in the modulation of B cell signaling and the maintenance of immune homeostasis. It is characterized by its immunoglobulin-like domains and a transmembrane region that implicates it in cellular signaling pathways. The expression of FcRH2 is subject to regulation by a variety of internal cell mechanisms and external stimuli, reflecting its role in the dynamic immune environment. Understanding the regulation of FcRH2 expression is crucial for deciphering the complex interactions within the immune system and how B cells adjust their responses to external signals.

A number of chemical compounds have been identified as potential activators of FcRH2 expression, although the precise mechanisms by which they exert this effect are often complex and multifaceted. For instance, molecules like lipopolysaccharide (LPS) can act as potent stimulants of immune cell activity, possibly leading to the upregulation of FcRH2 as part of the broader immune response. Similarly, compounds such as phorbol 12-myristate 13-acetate (PMA) can activate protein kinase C, triggering a cascade of intracellular events that may culminate in increased FcRH2 expression. Other compounds, such as forskolin, retinoic acid, and 5-azacytidine, may influence FcRH2 expression through their roles in modulating intracellular signaling pathways, affecting gene transcription directly or altering the epigenetic landscape. These activators are of interest in the context of immunological research as they shed light on the regulatory networks that govern the immune system's behavior. While these insights are valuable for the scientific understanding of immune regulation, it is crucial to consider that the direct link between these chemicals and the induction of FcRH2 expression requires rigorous experimental validation.

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