Anti-TREM1 antibody [EPR26207-34] - BSA and Azide free

Supplementary info

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

Activity summary

Triggering receptor expressed on myeloid cells 1 (TREM1) is a transmembrane receptor involved in amplifying inflammatory responses. TREM1 is known alternatively as CD354. This protein has a molecular mass of approximately 30 kDa and is expressed on the surface of neutrophils monocytes and macrophages. The receptor participates in innate immune responses and acts as an amplifier for inflammatory signals. It is often found in tissues that are engaged in inflammatory processes including lungs and intestines.

Biological function summary

TREM1 significantly enhances the immune response by activating myeloid cells. It does not form a standalone unit; instead it works with the adapter protein DNAX-activating protein of 12 kDa (DAP12) which pairs with TREM1 to transduce signals that promote cytokine and chemokine release. Through this interaction the receptor plays a role in the defense against bacterial infection boosting the body's immune response during pathogen assault. This function positions TREM1 as an important player in the regulation of acute inflammation.

Pathways

TREM1 engages significantly in the Toll-like receptor (TLR) signaling pathway and NF-kB pathway. In these pathways TREM1 interacts with various proteins that include TLRs and DAP12 intensifying inflammatory responses. The integration of TREM1 within these pathways suggests that it acts as an important modulator of inflammation capable of enhancing TLR-mediated signals for a stronger immune response.

Associated diseases and disorders

TREM1 connections extend to sepsis and inflammatory bowel disease (IBD). In the context of sepsis TREM1 expression correlates with increased inflammation and poor prognosis where it interacts with proteins involved in inflammatory pathways such as TNF-α. Concerning IBD TREM1's role in promoting inflammation links it to the pathogenesis of this disease where it could influence the severity and progression of IBD-related inflammation. Given these relationships therapeutic strategies targeting TREM1 could hold potential in modulating these conditions.