Recombinant Mouse TREM-2 Protein (His Tag)

Name: Recombinant Mouse TREM-2 Protein (His Tag)
Brand: Beta LifeScience
SKU: BLPSN-4643
Availability: InStock

Collections: Other recombinant proteins, Recombinant proteins

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Product Overview

Tag	His
Host Species	Mouse
Accession	NP_112544.1
Synonym	TREM-2, Trem2a, Trem2b, Trem2c
Background	Triggering receptor expressed on myeloid cells 2 ( TREM2 ) is a single Ig domain receptor. It is expressed on macrophages and dendritic cells but not on granulocytes or monocytes. Its expression is most abundant in the basal ganglia, corpus callosum, medulla oblongata and spinal cord, and microglial cells are the major TREM2-producing cell type in the central nervous system (CNS). TREM2 may play a role in chronic inflammations and may stimulate production of constitutive rather than inflammatory chemokines and cytokines. TREM2 forms a receptor signaling complex with TYROBP and triggers activation of the immune responses in macrophages and dendritic cells. It also associates with the signal adapter protein, DAP12, which has a cytoplasmic ITAM, leading to the subsequent activation of cytoplasmic tyrosine kinases. TREM2 is both required and sufficient for competent uptake of apoptotic neuronal cells. TREM2 and TREM2-L form a receptor-ligand pair connecting microglia with apoptotic neurons, directing removal of damaged cells to allow repair. Deficiency of the adapter protein DAP12 or its associated receptor TREM2 is associated with abnormal osteoclast development in humans. Defects in TREM2 are causes of PLOSL, also known as NHD. In addition, TREM2 signaling is also an important pathway to promote healing of wounds in the colon where stem cell replacement is necessary.
Description	A DNA sequence encoding the mouse TREM2 (NP_112544.1) extracellular domain (Met 1-Pro 168) was expressed, with a C-terminal His tag.
Source	HEK293
Predicted N Terminal	Leu 19
AA Sequence	Met 1-Pro 168
Molecular Weight	The recombinant mouse TREM2 consists of 161 a.a. with the predicted molecular mass of 18 kDa. As a result of glycosylation, the apparent molecular mass of rmTREM2 is approximately 30-40 kDa in SDS-PAGE under reducing conditions.
Purity	>95% as determined by SDS-PAGE
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Bioactivity	Please contact us for detailed information
Formulation	Lyophilized from sterile PBS, pH 7.4.
Stability	The recombinant proteins are stable for up to 1 year from date of receipt at -70°C.
Usage	For Research Use Only
Storage	Store the protein under sterile conditions at -20°C to -80°C. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.

Target Details

Target Function	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.
Subcellular Location	[Isoform 1]: Cell membrane; Single-pass type I membrane protein.; [Isoform 2]: Secreted.
Database References	KEGG: mmu:83433 STRING: 10090.ENSMUSP00000024791 UniGene: Mm.261623
Tissue Specificity	Expressed in the brain, specifically in microglia (at protein level). Expressed in macrophages (at protein level). Expressed at higher levels in the CNS, heart and lung than in lymph nodes or in other non-lymphoid tissues such as kidney, liver and testis.

Gene Functions References

The present study provide novel evidence that overexpression of TREM2 protects against MPTP-induced PD progression via modulation of microglial function through inhibiting TRAF6/TLR4-mediated activation of the MAPK and NF-kappaB signaling pathways. PMID: 29407460
Our data establish a critical link between oAbeta1-42, a major pathological component of Alzheimer's disease and TREM2 PMID: 29587871
These data suggest that the Alzheimer's disease-associated TREM2 R47H variant increases risk for Alzheimer's disease by conferring a loss of TREM2 function and enhancing neuritic dystrophy around plaques. PMID: 29859094
Data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function. PMID: 29611543
whereas complete TREM2 deficiency protected against tau-mediated microglial activation and atrophy, TREM2 haploinsufficiency elevated expression of proinflammatory markers and exacerbated atrophy at a late stage of disease. The differential effects of partial and complete loss of TREM2 on microglial function and tau pathology PMID: 30232263
TREM2 plays a crucial role in altering the proinflammatory M1 microglia to M2 phenotype and has beneficial effects in the immune pathogenesis of Parkinson's disease. PMID: 29621548
Overexpression of TREM2 downregulated the levels of IL-1beta, ameliorated T396 expression, inhibited the activity of GSK-3beta, and improved sickness behavior. Increased Arg1 expression and a high level of synaptophysin were also observed in the transgenic mice following TREM2 overexpression. PMID: 29689568
These studies of the role of TREM2 in neuroinflammation and neurodegeneration suggest that impairing microglial TREM2 signaling reduces pure tauopathy. PMID: 29073081
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
TREM2 protects against cerebral ischemia/reperfusion injury through the aspect of post-ischemic inflammatory response and neuronal apoptosis. PMID: 28592261
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
TREM2 deficiency influences both acute and chronic responses to traumatic brain injury, with altered macrophage response early on and improved functional outcome at later time points. PMID: 26976047
A central role of TREM2 is in the regulation of microglia response to acute neurotoxic insults. PMID: 28189343
Loss of TREM2 reduces the ability of microglia to engulf amyloid beta-peptide. PMID: 27402340
TREM2 and TREML2 play opposite roles in microglia activation. PMID: 27143430
Our study suggests that Vps35/retromer is responsible for recycling of Trem2 in the regulation of microglial function such as proinflammatory responses, whereas R47H mutation impairs Trem2 trafficking, which might contribute to Alzheimer disease. PMID: 27717139
sTREM2 plays a crucial role in regulating microglial cell survival and inflammatory responses. PMID: 28209725
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
This study demonstrate a critical role of TREM2-mediated Wnt/beta-catenin pathway in microglial viability and suggest that modulating this pathway therapeutically may help to combat the impaired microglial survival. PMID: 28077724
Triggering receptor expressed on myeloid cells 2 (TREM2) is an immunoglobulin-like receptor of the TREM family and is expressed on activated macrophages, immature dendritic cells, osteoclasts, and microglia. PMID: 28398927
TREM2 deficiency may disrupt the formation of a neuroprotective microglia barrier that regulates amyloid compaction and insulation PMID: 27196974
TREM2 deficiency has opposing effects on Alzheimer's disease-related pathologies at early and late stages of disease progression. PMID: 28100745
TREM2 protects from Alzheimer's disease by enabling microglia to surround and alter Abeta plaque structure, thereby limiting neuritic damage. PMID: 27091843
Recent studies have revealed that activated microglia in the spinal dorsal horn exacerbate neuropathic pain, which has suggested that suppression of microglial activity should be considered as a therapeutic target. However, only a few molecules have been identified as regulators of microglial activity. In this study, we focused on a receptor complex of TREM2 and DAP12, both of which are expressed by microglia and have bee PMID: 27798193
The authors demonstrate that a TREM2 loss-of-function mutation causes brain-wide metabolic alterations pointing toward a possible function of microglia in regulating brain glucose metabolism. PMID: 28559417
flow cytometry analyses indicated significantly lower surface expression of T66M TREM2 variant than wild type or other TREM2 variants PMID: 28490631
Study found that TREM2 was upregulated in the brain of P301S mice, an animal model of tau pathology, during disease progression and showed that TREM2 overexpression rescued spatial cognitive impairments and ameliorated neuropathologies including neuronal and synaptic loss as well as tau hyperphosphorylation. PMID: 26802771
This study showed that TREM-2 deficiency restricts the inflammatory response, thereby decreasing organ damage and mortality. PMID: 27253382
TREM2 attenuates tau kinase activity through restriction of neuroinflammation, and thus protects against tau pathology. PMID: 26364736
TREM2 is involved in prion-induced microglial activation but does not noticeably modulate the pathogenesis of experimental prion infections. PMID: 25816748
These findings provide a novel interpretation of Brucella intracellular growth through inhibition of NO production produced by TREM-2-mediated activated macrophages. PMID: 25563793
TREM-1/TREM-3 macrophage expression improved host defense against Klebsiella-derived pneumosepsis, whereas TREM-2 did not have a role. PMID: 25860078
These findings place TREM2 as a key regulator of microglia activation in vivo in response to tissue damage PMID: 25631124
TREM-2 has a protective effect on inflammatory response of endotoxin-induced acute lung injury in mice. PMID: 24916365
results support a role of DAP12 in stabilizing TREM2-CTF, thereby protecting against excessive pro-inflammatory responses. PMID: 25957402
Corpus callosum microglia normally expand with age, but aged Trem2(-/-) mice had fewer microglia with an abnormal morphology which failed to amplify transcripts indicative of activation, phagocytosis, and lipid catabolism in response to myelin damage. PMID: 25893602
Data (including data from studies using knockout mice) suggest that TREM2 is expressed on alveolar macrophages and lung mucosa and plays role innate immunity during pneumococcal pneumonia; knockout of TREM2 increases phagocytosis and survival. PMID: 24945405
viral replication increases lung macrophage levels of intracellular and cell surface TREM-2, and this action prevents macrophage apoptosis PMID: 25897174
TREM2 knockdown reduced microglial activation, decreased phagocytosis of injured neurons and worsened stroke damage. PMID: 25716838
Upon infection with Escherichia coli, the otherwise beneficial effect of an exaggerated early immune response in TREM-2(-/-) animals was counteracted by a 50% reduction in bacterial phagocytosis. PMID: 25477281
important role for TREM2 in inflammatory macrophages and neuroinflammation PMID: 25732305
TREM2 detects damage-associated lipid patterns associated with neurodegeneration, sustaining the microglial response to beta-amyloid accumulation. PMID: 25728668
TREM2 promotes adipogenesis and diet-induced obesity by upregulating adipogenic regulators in conjunction with inhibiting the Wnt10b/beta-catenin signaling pathway. PMID: 25114293
It may play a protective role against aging-related neuroinflammation and cognitive impairment. PMID: 24368090
These data suggest that TREM2 is important for the microglial response to Amyloid-beta deposition PMID: 24893973
Results suggest that an epigenetic mechanism involving an aluminum-triggered, NF-kB-sensitive, miRNA-34a-mediated down-regulation of triggering receptor expressed in myeloid cells 2 (TREM2) expression may impair phagocytic responses. PMID: 23778113
TREM-2-mediated bacterial killing is dependent on the activation of PI3K/Akt signaling. PMID: 24383713
TREM2 protein is expressed only in microglia/macrophages and is developmentally downregulated in a region-dependent manner. PMID: 23977213
TREM2 governs Kupffer cell activation and explains belr1 genetic resistance to malaria liver stage infection. PMID: 24218563
Trem-2 plays an important role in the host defense response to sepsis by enhancing bacterial clearance. PMID: 23721075

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