Triggering Receptor Expressed on Myeloid Cells 1 Human Recombinant
Triggering Receptor Expressed on Myeloid Cells 2 Human Recombinant
Triggering Receptor Expressed on Myeloid Cells 2 Human Recombinant, HEK
TREM2 Human Recombinant is a single, glycosylated, polypeptide chain (19-174 a.a) containing a total of 162 amino acids, having a molecular mass of 18.2 kDa.
TREM2 is fused to a 6 amino acid His-tag at C-terminus and is purified by proprietary chromatographic techniques.
Triggering Receptor Expressed on Myeloid Cells (TREM) is a family of cell surface receptors that play a crucial role in the immune response. The most well-known members of this family are TREM-1 and TREM-2. TREM-1 is primarily involved in amplifying inflammatory responses, while TREM-2 has a more regulatory role, often inhibiting inflammation .
Key Biological Properties: TREM-1 and TREM-2 are part of the immunoglobulin superfamily and are transmembrane proteins. They are involved in the regulation of inflammation and immune responses .
Expression Patterns and Tissue Distribution: TREM-1 is constitutively expressed on the surface of peripheral blood monocytes and neutrophils and is upregulated by toll-like receptor (TLR) ligands . TREM-2 is expressed on activated macrophages, immature dendritic cells, osteoclasts, and microglia .
Primary Biological Functions: TREM-1 amplifies the immune response by promoting the production of proinflammatory cytokines and chemokines . TREM-2, on the other hand, plays a role in immune surveillance, cell-cell interactions, and tissue debris clearance .
Role in Immune Responses and Pathogen Recognition: TREM-1 enhances the toll-like receptor (TLR)-4-induced inflammatory response, which is crucial for pathogen recognition and the subsequent immune response . TREM-2 is involved in the phagocytosis of apoptotic cells and tissue debris, thus playing a role in maintaining tissue homeostasis .
Mechanisms with Other Molecules and Cells: TREM-1 signals through the adapter protein DAP12, leading to the activation of downstream signaling pathways such as the MEK/ERK and NF-κB pathways . TREM-2 also signals through DAP12, activating the PI3K/Akt pathway, which promotes cell survival and phagocytosis .
Binding Partners and Downstream Signaling Cascades: TREM-1 and TREM-2 interact with various ligands, although the specific ligands for TREM-1 are not well-characterized . The activation of these receptors leads to the production of cytokines and chemokines, which amplify the immune response .
Regulatory Mechanisms Controlling Expression and Activity: The expression of TREM-1 is upregulated by TLR ligands, which are recognized during infections . TREM-2 expression is regulated by factors secreted in the extracellular environment, such as nucleotides and lipid mediators .
Transcriptional Regulation and Post-Translational Modifications: TREM-1 and TREM-2 are regulated at the transcriptional level by various cytokines and signaling pathways. Post-translational modifications, such as phosphorylation of DAP12, are crucial for the activation of downstream signaling pathways .
Biomedical Research: TREM-1 and TREM-2 are studied extensively for their roles in various diseases, including sepsis, autoimmune diseases, and cancers .
Diagnostic Tools: Elevated levels of soluble TREM-1 (sTREM-1) in the blood can serve as a biomarker for sepsis and other inflammatory conditions .
Therapeutic Strategies: Targeting TREM-1 and TREM-2 with specific inhibitors or activators holds potential for treating inflammatory diseases, autoimmune disorders, and cancers .
Role Throughout the Life Cycle: TREM-1 and TREM-2 play essential roles from development to aging. TREM-1 is involved in the acute inflammatory response, while TREM-2 is crucial for tissue homeostasis and the resolution of inflammation .
From Development to Aging and Disease: During development, TREM-2 is involved in the maturation of dendritic cells and osteoclasts . In aging, dysregulation of TREM-2 is associated with neurodegenerative diseases such as Alzheimer’s disease .