TREM2 Antibody, Biotin conjugated
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Description
Research Findings and Mechanisms
Recent studies highlight the antibody’s role in modulating TREM2 signaling and therapeutic potential:
TREM2 Shedding Inhibition
Biotin-conjugated antibodies like ATV:TREM2 act as shedding blockers, preventing ADAM17-mediated cleavage of soluble TREM2. This preserves membrane-bound TREM2, enhancing signaling in microglia .
Therapeutic Applications in Alzheimer’s Disease (AD)
TREM2 loss-of-function variants are linked to AD. ATV:TREM2, a biotin-conjugated antibody engineered with a TfR-binding domain, demonstrates:
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Improved Brain Penetration: Enhanced blood-brain barrier transcytosis via TfR engagement .
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Microglial Activation: Increased proliferation and mitochondrial metabolism in iPSC-derived microglia .
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Reduced Amyloid Pathology: Boosted glucose metabolism and microglial activity in AD mouse models .
Critical Considerations
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Cross-Reactivity: Minimized in validated antibodies (e.g., <1% cross-reactivity with TREM1/TREM3) .
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Therapeutic Engineering: ATV:TREM2’s TfR-binding domain enables targeted delivery to the brain, bypassing systemic toxicity .
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Experimental Optimization: Dilutions vary by assay; optimization is required for specific protocols .
Product Specs
Buffer
Preservative: 0.03% Proclin 300
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
Typically, we can ship your order within 1-3 business days of receipt. Delivery timelines may vary depending on the purchase method and location. Please consult your local distributor for specific delivery timeframes.
Synonyms
TREM 2 antibody; TREM-2 antibody; TREM2 antibody; TREM2_HUMAN antibody; TREM2a antibody; TREM2b antibody; TREM2c antibody; Trggering receptor expressed on myeloid cells 2 antibody; Trggering receptor expressed on myeloid cells 2a antibody; Triggering receptor expressed on monocytes 2 antibody; Triggering receptor expressed on myeloid cells 2 antibody
Target Names
Uniprot No.
Target Background
Function
TREM2, or triggering receptor expressed on myeloid cells 2, is a transmembrane receptor expressed primarily on microglia, the resident immune cells of the central nervous system. It plays a crucial role in various cellular processes, including:
**1. Receptor Signaling:** TREM2 forms a receptor signaling complex with TYROBP, which mediates signaling and cell activation upon ligand binding.
**2. Amyloid-beta Protein 42 Recognition:** TREM2 acts as a receptor for amyloid-beta protein 42 (Aβ42), a cleavage product of the amyloid-beta precursor protein (APP). It facilitates the uptake and degradation of Aβ42 by microglia.
**3. Microglial Activation:** Binding to Aβ42 triggers microglial activation, leading to proliferation, migration, apoptosis, and the expression of pro-inflammatory cytokines like IL6R and CCL3, as well as the anti-inflammatory cytokine ARG1.
**4. Lipoprotein Particle Recognition:** TREM2 serves as a receptor for lipoprotein particles, such as LDL, VLDL, and HDL, and for apolipoproteins like APOA1, APOA2, APOB, APOE, APOE2, APOE3, APOE4, and CLU. It enhances their uptake in microglia.
**5. Phospholipid Binding:** TREM2 binds phospholipids, preferentially anionic lipids such as phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol, and sphingomyelin.
**6. Microglial Proliferation Regulation:** TREM2 acts as an upstream regulator of the Wnt/β-catenin signaling cascade, thereby modulating microglial proliferation.
**7. Phagocytosis:** TREM2 is essential for microglial phagocytosis of apoptotic neurons, myelin debris following neuronal injury, and neuronal synapses during synapse elimination in the developing brain.
**8. Chemotaxis and Process Outgrowth:** TREM2 regulates microglial chemotaxis, process outgrowth, and the microglial response to oxidative stress and lipopolysaccharide.
**9. Inflammatory Signaling Modulation:** TREM2 suppresses PI3K and NF-κB signaling in response to lipopolysaccharide, promoting phagocytosis, suppressing pro-inflammatory cytokine and nitric oxide production, inhibiting apoptosis, and increasing the expression of IL10 and TGFB. During oxidative stress, it promotes anti-apoptotic NF-κB and ERK signaling.
**10. MTOR Activation and Metabolism:** TREM2 plays a role in microglial MTOR activation and metabolism.
**11. Age-Related Microglial Changes:** TREM2 regulates age-related changes in microglial numbers.
**12. Immune Responses in Macrophages and Dendritic Cells:** TREM2 triggers activation of immune responses in macrophages and dendritic cells.
**13. Multinucleated Giant Cell Formation:** TREM2 mediates cytokine-induced formation of multinucleated giant cells, which are formed by the fusion of macrophages.
**14. Dendritic Cell Maturation and Survival:** In dendritic cells, TREM2 mediates upregulation of chemokine receptor CCR7, and dendritic cell maturation and survival.
**15. Osteoclast Differentiation:** TREM2 is involved in the positive regulation of osteoclast differentiation.
**1. Receptor Signaling:** TREM2 forms a receptor signaling complex with TYROBP, which mediates signaling and cell activation upon ligand binding.
**2. Amyloid-beta Protein 42 Recognition:** TREM2 acts as a receptor for amyloid-beta protein 42 (Aβ42), a cleavage product of the amyloid-beta precursor protein (APP). It facilitates the uptake and degradation of Aβ42 by microglia.
**3. Microglial Activation:** Binding to Aβ42 triggers microglial activation, leading to proliferation, migration, apoptosis, and the expression of pro-inflammatory cytokines like IL6R and CCL3, as well as the anti-inflammatory cytokine ARG1.
**4. Lipoprotein Particle Recognition:** TREM2 serves as a receptor for lipoprotein particles, such as LDL, VLDL, and HDL, and for apolipoproteins like APOA1, APOA2, APOB, APOE, APOE2, APOE3, APOE4, and CLU. It enhances their uptake in microglia.
**5. Phospholipid Binding:** TREM2 binds phospholipids, preferentially anionic lipids such as phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol, and sphingomyelin.
**6. Microglial Proliferation Regulation:** TREM2 acts as an upstream regulator of the Wnt/β-catenin signaling cascade, thereby modulating microglial proliferation.
**7. Phagocytosis:** TREM2 is essential for microglial phagocytosis of apoptotic neurons, myelin debris following neuronal injury, and neuronal synapses during synapse elimination in the developing brain.
**8. Chemotaxis and Process Outgrowth:** TREM2 regulates microglial chemotaxis, process outgrowth, and the microglial response to oxidative stress and lipopolysaccharide.
**9. Inflammatory Signaling Modulation:** TREM2 suppresses PI3K and NF-κB signaling in response to lipopolysaccharide, promoting phagocytosis, suppressing pro-inflammatory cytokine and nitric oxide production, inhibiting apoptosis, and increasing the expression of IL10 and TGFB. During oxidative stress, it promotes anti-apoptotic NF-κB and ERK signaling.
**10. MTOR Activation and Metabolism:** TREM2 plays a role in microglial MTOR activation and metabolism.
**11. Age-Related Microglial Changes:** TREM2 regulates age-related changes in microglial numbers.
**12. Immune Responses in Macrophages and Dendritic Cells:** TREM2 triggers activation of immune responses in macrophages and dendritic cells.
**13. Multinucleated Giant Cell Formation:** TREM2 mediates cytokine-induced formation of multinucleated giant cells, which are formed by the fusion of macrophages.
**14. Dendritic Cell Maturation and Survival:** In dendritic cells, TREM2 mediates upregulation of chemokine receptor CCR7, and dendritic cell maturation and survival.
**15. Osteoclast Differentiation:** TREM2 is involved in the positive regulation of osteoclast differentiation.
Gene References Into Functions
- Our data establish a critical link between oAbeta1-42, a major pathological component of Alzheimer's disease and TREM2. PMID: 29587871
- Data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function. PMID: 29611543
- Homozygous TREM2 R47C carrier presenting with an FTD rather than an Alzheimer's disease phenotype. PMID: 29748150
- Our results suggest that deficiency of microglial TREM2 leads to heightened tau pathology coupled with widespread increases in activated neuronal stress kinases. PMID: 29037207
- 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
- TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation. PMID: 27934908
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- The data of this study provided evidence that the A192T variant in TREM2 could contribute risk for Alzheimer's disease. PMID: 28376694
- 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
- 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
- In this meta-analysis, genetic datasets demonstrate that TREM2 is a potent risk factor for Parkinson's Disease. PMID: 26365049
- 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
- Its genetic variation contributes to pathogenesis of Alzheimer disease. PMID: 28789839
- results indicate that TREM-2 might act as a negative immuno-regulatory molecule...and partially predicts prognosis in lung cancer patients. PMID: 27102437
- sTREM2 is increased in dominantly inherited Alzheimer's disease after amyloid deposition and neuronal injury. PMID: 27974666
- 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
- Mutations in TREM2 gene are known to cause Nasu-Hakola disease. PMID: 28214109
- 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
- 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
- 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
- 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
- Increased DNA methylation near TREM2 is seen in the superior temporal gyrus of patients with Alzheimer's disease. PMID: 27522519
- results indicated thatTREM2 p.H157Y was associated with an increased risk of Alzheimer's Disease. PMID: 27501831
- 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
- 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
- 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
- Its mutation plays a role in pathogenesis of Alzheimer's disease. PMID: 27084067
- Rare coding variants of TREM2 may play an important role in AD in Han Chinese. PMID: 27067662
- 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
- link three genetic risk factors for Alzheimer's disease and reveal a possible mechanism by which mutant TREM2 increases risk of AD. PMID: 27477018
- 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
- TREM2 deficiency may disrupt the formation of a neuroprotective microglia barrier that regulates amyloid compaction and insulation. PMID: 27196974
- flow cytometry analyses indicated significantly lower surface expression of T66M TREM2 variant than wild type or other TREM2 variants. PMID: 28490631
- 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
- TREM2 expression is significantly upregulated in human masticatory mucosa during wound healing. PMID: 28005267
- this study shows that activation of TREM-2 may restrain h-MSC immune activation and promote differentiation for tissue repair. PMID: 26079507
- 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
- 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
- The study suggests that TREM2 may work as an oncogene and a new effective therapeutic target for glioma treatment. PMID: 26506595
- CSF concentrations of soluble TREM2 are higher in Alzheimer's disease than in controls. PMID: 26754172
- Variant p.R47H of TREM2 was not associated with Parkinson's disease. PMID: 26651418
- 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
- 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
Database Links
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,
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