| Field | Specification |
|---|---|
| Mfr No | |
| Alternative Names | Triggering receptor expressed on myeloid cells 2|TREM-2|Triggering receptor expressed on monocytes 2|TREM2 |
| Assay Time | |
| Detection Method | |
| Detection Range | |
| Product Type | |
| Reactivity | |
| Sample Type(s) | cell or tissue lysate, Other liquid samples |
| Sensitivity | |
| Species | |
| Storage | |
| Target | |
| UniProt # |
Background
human TREM2 (Triggering receptor expressed on myeloid cells 2) is a molecular target commonly studied in neuroscience and cardiovascular research. Receptors translate extracellular cues into intracellular signaling programs and may be regulated through expression, ligand binding, shedding, and endocytosis.
Biological role and mechanism
The biological role of TREM2 is typically understood in terms of its molecular category and interaction network. Depending on the model system, it may participate in cell–cell communication, intracellular signaling, enzymatic processing, or regulation of gene expression programs. Mechanistic interpretation is often strengthened by considering upstream regulators and downstream readouts rather than relying on a single marker.
Expression and abundance of TREM2 can vary by tissue, cell type, and physiological state. In many systems, levels are influenced by factors such as developmental stage, immune activation, metabolic status, and cellular stress. Because sample matrix and pre-analytical handling can affect measured concentrations, interpretation is typically strongest when experiments keep collection and processing consistent across groups.
Nomenclature and related terms
TREM2 (Triggering receptor expressed on myeloid cells 2) may also be referenced as Triggering receptor expressed on myeloid cells 2, TREM-2, and Triggering receptor expressed on monocytes 2 in the literature or in databases. When comparing results across studies, confirm that the reported analyte refers to the same molecule, species context, and molecular form (e.g., precursor vs mature protein, or soluble vs membrane-associated forms).
Why it matters in research
- Understanding how TREM2 relates to neuronal signaling and synaptic function, neuroinflammation, neurodegeneration models, and brain–body communication in neuroscience and cardiovascular research.
- Interpreting shifts in TREM2 levels alongside other pathway components or complementary markers.
- Connecting molecular changes to phenotypes such as inflammation, remodeling, metabolism shifts, or cell-state transitions (context-dependent).
Molecular forms and interpretation
For some targets, isoforms, proteolytic processing, or post-translational modifications (such as phosphorylation or glycosylation) can influence function and apparent abundance. If multiple molecular forms are expected in your model, align interpretation with the form most relevant to the biological question.
Disease and translational relevance
TREM2 has been investigated across diverse physiological and disease contexts, and changes in its abundance have been reported in areas aligned with neuroscience and cardiovascular studies. These associations are interpreted as research findings rather than diagnostic or therapeutic claims, and they should be evaluated alongside model-specific covariates and study design.
Can’t Find What You’re Looking For? We can help you source the best match or customize an ELISA solution for your study. Options may include alternative target synonyms, different species reactivity, sample type/matrix compatibility (serum/plasma/lysate/supernatant), assay format (sandwich/competitive), sensitivity/range, detection chemistry (colorimetric/fluorescent/chemiluminescent), plate format (pre-coated/uncoated, strips vs full plate), and bulk or custom packaging. Click Talk to a Scientist to submit a request form, email us at support@biohippo.com, or explore our Research Services for additional support. Our team will be in contact with you shortly.
Cerebrospinal Fluid sTREM-2, GFAP, and β-S100 in Symptomatic Sporadic Alzheimer’s Disease: Microglial, Astrocytic, and APOE Contributions Along the Alzheimer’s Disease Continuum
IF: 4.16 Journal: Journal of Alzheimer's Disease Cited Date: 2023-04-14