Recombinant Human Triggering receptor expressed on myeloid cells 2 (TREM2), partial

Code CSB-MP024405HU
Size $660
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Greater than 90% as determined by SDS-PAGE.
Target Names
Uniprot No.
Research Area
Alternative Names
TREM 2; TREM-2; TREM2; TREM2_HUMAN; TREM2a; TREM2b; TREM2c; Trggering receptor expressed on myeloid cells 2; Trggering receptor expressed on myeloid cells 2a; Triggering receptor expressed on monocytes 2; Triggering receptor expressed on myeloid cells 2
Homo sapiens (Human)
Mammalian cell
Expression Region
Target Protein Sequence
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
22.5 kDa
Protein Length
Tag Info
N-terminal 10xHis-tagged and C-terminal Myc-tagged
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
18-28 business days
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

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Target Background

Forms a receptor signaling complex with TYROBP which mediates signaling and cell activation following ligand binding. Acts as a receptor for amyloid-beta protein 42, a cleavage product of the amyloid-beta precursor protein APP, and mediates its uptake and degradation by microglia. Binding to amyloid-beta 42 mediates microglial activation, proliferation, migration, apoptosis and expression of pro-inflammatory cytokines, such as IL6R and CCL3, and the anti-inflammatory cytokine ARG1. Acts as a receptor for lipoprotein particles such as LDL, VLDL, and HDL and for apolipoproteins such as APOA1, APOA2, APOB, APOE, APOE2, APOE3, APOE4, and CLU and enhances their uptake in microglia. Binds phospholipids (preferably anionic lipids) such as phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol and sphingomyelin. Regulates microglial proliferation by acting as an upstream regulator of the Wnt/beta-catenin signaling cascade. Required for microglial phagocytosis of apoptotic neurons. Also required for microglial activation and phagocytosis of myelin debris after neuronal injury and of neuronal synapses during synapse elimination in the developing brain. Regulates microglial chemotaxis and process outgrowth, and also the microglial response to oxidative stress and lipopolysaccharide. It suppresses PI3K and NF-kappa-B signaling in response to lipopolysaccharide; thus promoting phagocytosis, suppressing pro-inflammatory cytokine and nitric oxide production, inhibiting apoptosis and increasing expression of IL10 and TGFB. During oxidative stress, it promotes anti-apoptotic NF-kappa-B signaling and ERK signaling. Plays a role in microglial MTOR activation and metabolism. Regulates age-related changes in microglial numbers. Triggers activation of the immune responses in macrophages and dendritic cells. Mediates cytokine-induced formation of multinucleated giant cells which are formed by the fusion of macrophages. In dendritic cells, it mediates up-regulation of chemokine receptor CCR7 and dendritic cell maturation and survival. Involved in the positive regulation of osteoclast differentiation.
Gene References into Functions
  1. Our data establish a critical link between oAbeta1-42, a major pathological component of Alzheimer's disease and TREM2 PMID: 29587871
  2. Data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function. PMID: 29611543
  3. Homozygous TREM2 R47C carrier presenting with an FTD rather than an Alzheimer's disease phenotype. PMID: 29748150
  4. Our results suggest that deficiency of microglial TREM2 leads to heightened tau pathology coupled with widespread increases in activated neuronal stress kinases PMID: 29037207
  5. In the current study, we evaluated the rs75932628 polymorphism in the Chinese Han population. However, we did not detect any rs75932628-T in our cohort, indicating that the single nucleotide polymorphism of TREM2 may not be a genetic marker to assess the risk of LOAD in the Chinese Han population. PMID: 29256968
  6. TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation PMID: 27934908
  7. ADAM17 is the main sheddase for the generation of human triggering receptor expressed in myeloid cells (hTREM2) ectodomain and cleaves TREM2 after Histidine 157. Findings reveal a link between shedding of TREM2 and its regulation during inflammatory conditions or chronic neurodegenerative disease in which activity or expression of sheddases might be altered. PMID: 28923481
  8. In rheumatoid arthritis (RA), the expression of TREM-2 was reduced at first and then up-regulated after stimulation by TNF-alpha. TREM-2 also inhibited the activation of TNF-alpha induced of inflammation in RA-fibroblast-like synovial cells (FLSs) by the p38 pathway. PMID: 28869414
  9. TREM2 is shed by proteases of the ADAM (a disintegrin and metalloproteinase domain containing protein) family C-terminal to histidine 157, a position where an AD-associated coding variant has been discovered (p.H157Y) in the Han Chinese population. PMID: 28855300
  10. Selective partial inhibition of cleavage of triggering receptor expressed on myeloid cells 2 TREM2 at H157-Ser158 bond might provide a potential therapeutic strategy for carriers of the Alzheimer's disease-associated H157Y variant and possibly for individuals with wild-type TREM2. PMID: 28855301
  11. This article suggests a potential explanation of why TREM2-deficient microglia are unable to respond to neurotoxic plaques in the Alzheimer's disease brain and highlight a further need to understand microglial biology. PMID: 28978423
  12. This study demonstrated that Lower DNA methylation at TREM2 intron 1 caused higher TREM2 mRNA expression in the leukocytes of Alzheimer's disease subjects versus controls and may be a biomarker for Alzheimer's disease. PMID: 28412600
  13. investigated consequences of TREM2 loss of function on microglia transcriptome; microglia lacking TREM2 migrate less towards apoptotic neurons, and outgrowth of microglial processes towards sites of damage in the somatosensory cortex is slowed; the apparent lack of chemotactic stimulation upon depletion of TREM2 is consistent with stable expression profile of genes characterizing the homoeostatic signature of microglia PMID: 28483841
  14. This study shown that Peripheral TREM2 mRNA levels are higher in AD and are associated with AD-related cognitive deficits and hippocampal atrophy. PMID: 28453482
  15. The data of this study provided evidence that the A192T variant in TREM2 could contribute risk for Alzheimer's disease. PMID: 28376694
  16. Results suggest that TREM2 plays a critical role in inflammation and neuronal cell survival and in neurogenesis. Study showed that TREM2 is a soluble protein transported by macrophages through ventricle walls and choroid plexus, and then enters the brain parenchyma via radial glial cells. TREM2 protein is essential for neuroplasticity and myelination. A lack of TREM2 protein may accelerate aging. PMID: 27662313
  17. Recent studies have advanced our understanding of TREM2 biology and microglial activities in aging and neurodegenerative brains, providing new insights into TREM2 functions in amyloid plaque maintenance, microglial envelopment of plaque, microglia viability, and the identification of novel TREM2 ligands. PMID: 28442216
  18. In this meta-analysis, genetic datasets demonstrate that TREM2 is a potent risk factor for Parkinson's Disease. PMID: 26365049
  19. High amount of TREM2 mRNA expression in leukocytes is specific to SCZ but not MDD and that changes in TREM2 mRNA expression may be a trait biomarker for SCZ. PMID: 27130565
  20. Its genetic variation contributes to pathogenesis of Alzheimer disease. PMID: 28789839
  21. results indicate that TREM-2 might act as a negative immuno-regulatory molecule...and partially predicts prognosis in lung cancer patients PMID: 27102437
  22. sTREM2 is increased in dominantly inherited Alzheimer's disease after amyloid deposition and neuronal injury PMID: 27974666
  23. Authors find, using a cell-free coat protein complex II (COPII) vesicle budding reaction, that mutant TREM2 is exported efficiently from the ER. Mutant TREM2 becomes sensitive to cleavage by endoglycosidase D under conditions that inhibit recycling to the ER, indicating that it normally reaches a post-ER compartment. PMID: 28768830
  24. Mutations in TREM2 gene are known to cause Nasu-Hakola disease. PMID: 28214109
  25. TREM2 upregulation in the frontal cortex in AD is a late event and may not play a role early in the development of AD pathogenesis and the onset of clinical dementia. PMID: 28365005
  26. Our results suggest that TREM2 expression is increased in Alzheimer's disease and support previous findings that suggest that p.R47H variant affects TREM2 function by altering binding properties of the receptor rather than expression. PMID: 27887626
  27. Data show that protein-altering changes are in PLCG2, ABI3, and TREM2 genes highly expressed in microglia and highlight an immune-related protein-protein interaction network in Alzheimer's disease. PMID: 28714976
  28. Study found that rare variation in TREM2, including two variants within the extracellular Ig-like domain, may be associated with risk for Alzheimer's disease; suggests that impaired overall and cell surface expression of TREM2 may contribute to risk for Alzheimer's disease. PMID: 27589997
  29. Increased DNA methylation near TREM2 is seen in the superior temporal gyrus of patients with Alzheimer's disease PMID: 27522519
  30. results indicated thatTREM2 p.H157Y was associated with an increased risk of Alzheimer's Disease PMID: 27501831
  31. Our work identifies the TREM2-APOE pathway as a major regulator of microglial functional phenotype in neurodegenerative diseases and serves as a novel target that could aid in the restoration of homeostatic microglia. PMID: 28930663
  32. Found increased Alzheimer's disease risk associated with several TREM2 variants, and show that these variants decreased or markedly increased binding to TREM2 ligands. Results suggest that TREM2 signaling helps protect against Alzheimer's disease but can cause harm in excess, supporting the idea that proper TREM2 function is important to counteract disease progression. PMID: 27520774
  33. SNPs involved in pathways related to virus cellular entry and vesicular trafficking were overrepresented, suggesting that cerebrospinal fluid soluble TREM2 levels could be an informative phenotype for Alzheimer disease PMID: 26754641
  34. Its mutation plays a role in pathogenesis of Alzheimer's disease. PMID: 27084067
  35. Rare coding variants of TREM2 may play an important role in AD in Han Chinese. PMID: 27067662
  36. These data demonstrate that cerebrospinal fluid soluble TREM2 levels are increased in the early symptomatic phase of Alzheimer's disease, probably reflecting a corresponding change of the microglia activation status in response to neuronal degeneration. PMID: 26941262
  37. link three genetic risk factors for Alzheimer's disease and reveal a possible mechanism by which mutant TREM2 increases risk of AD PMID: 27477018
  38. Microglia in Alzheimer's disease (AD) patients carrying TREM2 risk variants and TREM2-deficient mice with AD-like pathology have abundant autophagic vesicles, as do TREM2-deficient macrophages under growth-factor limitation or endoplasmic reticulum (ER) stress. Study concludes that TREM2 enables microglial responses during AD by sustaining cellular energetic and biosynthetic metabolism. PMID: 28802038
  39. TREM2 deficiency may disrupt the formation of a neuroprotective microglia barrier that regulates amyloid compaction and insulation PMID: 27196974
  40. flow cytometry analyses indicated significantly lower surface expression of T66M TREM2 variant than wild type or other TREM2 variants PMID: 28490631
  41. silencing TREM-2 downregulated the expression levels of Bcl2 and PCNA, and upregulated the expression levels of Bax and caspase-3 in renal cell carcinoma cells. Depletion of TREM-2 inactivated PI3K/Akt pathway through increasing the expression of PTEN. TREM-2 acts as an oncogene in the development of renal cell carcinoma and can be considered as a novel therapeutic factor in the treatment of renal cell carcinoma. PMID: 27779645
  42. TREM2 expression is significantly upregulated in human masticatory mucosa during wound healing PMID: 28005267
  43. this study shows that activation of TREM-2 may restrain h-MSC immune activation and promote differentiation for tissue repair PMID: 26079507
  44. The TREM family members are also considered to involve in Alzheimer's disease (AD) and cerebrospinal fluid (CSF) soluble form of TREM2 (sTREM2) levels has also been associated with respond to progression of disease. PMID: 27769848
  45. Study provides evidence that TREM2 mRNA is upregulated in the human hippocampus affected by Alzheimer's disease (AD). Findings also suggest that 5hmC may play a role in regulating TREM2 mRNA expression in AD hippocampus. PMID: 27051467
  46. The study suggests that TREM2 may work as an oncogene and a new effective therapeutic target for glioma treatment. PMID: 26506595
  47. CSF concentrations of soluble TREM2 are higher in Alzheimer's disease than in controls PMID: 26754172
  48. Variant p.R47H of TREM2 was not associated with Parkinson's disease PMID: 26651418
  49. Our results corroborate and extend previous findings, concluding that the variant rs75932628-T (p.R47H) in TREM2 is not a risk factor for leucoaraiosis or Parkinson's disease in the Han Chinese population. PMID: 26758262
  50. the minor T allele at TREM2 (p.R47H, rs75932628) showed nominally significant association with AD risk (OR 5 5.73, 95% CI 5 1.80-18.25, P 5 .0232), whereas no significant association for risk of frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease. PMID: 25936935

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Involvement in disease
Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL)
Subcellular Location
[Isoform 1]: Cell membrane; Single-pass type I membrane protein.; [Isoform 2]: Secreted.; [Isoform 3]: Secreted.
Tissue Specificity
Expressed in the brain, specifically in microglia and in the fusiform gyrus (at protein level). Expressed on macrophages and dendritic cells but not on granulocytes or monocytes. In the CNS strongest expression seen in the basal ganglia, corpus callosum,
Database Links

HGNC: 17761

OMIM: 221770

KEGG: hsa:54209

STRING: 9606.ENSP00000362205

UniGene: Hs.435295

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