Anti-FFR antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

FFR also known as Formyl Peptide Receptor is a G protein-coupled receptor with a molecular mass of approximately 40 kDa. It is mainly expressed on the surface of immune cells like neutrophils and monocytes. The receptor mediates cellular response to N-formylmethionine-containing peptides which arise from bacterial and mitochondrial proteins. When these peptides bind to FFR they trigger a signaling cascade that promotes cell movement or chemotaxis.

Biological function summary

This receptor plays a significant role in host defense mechanisms by guiding the immune cells to sites of infection or tissue damage. FFR acts as part of a receptor complex interacting with various intracellular signaling molecules to mediate chemotactic responses. It contributes to the regulation of inflammatory pathways by promoting the recruitment of immune cells to inflamed tissues thereby facilitating rapid immune responses.

Pathways

The receptor interacts with the MAPK/ERK and PI3K/Akt signaling pathways which are pivotal in cellular processes like growth survival and movement. FFR activation leads to the recruitment of Ras and PI3-kinase which in turn activate downstream effectors in these pathways. The receptor works closely with proteins like Rac and Cdc42 which are essential for the regulation of the actin cytoskeleton during cell migration.

Associated diseases and disorders

FFR has been implicated in conditions such as chronic inflammatory diseases and ischemia-reperfusion injury. The excessive activation of FFR through continuous recruitment of immune cells can lead to tissue damage seen in chronic inflammation. In ischemia-reperfusion injury FFR contributes to increased damage by attracting neutrophils to the affected area. The receptor's activity is also linked to proteins involved in the inflammatory response such as IL-8 and TNF-alpha which further exacerbate tissue damage.