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TREM2 encodes a membrane protein that forms a receptor signaling complex with the TYRO protein tyrosine kinase binding protein. Additionally we are shipping TREM2 Antibodies (192) and TREM2 Kits (24) and many more products for this protein.
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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.
Data show that protein-altering changes are in PLCG2 (show PLCG2 Proteins), ABI3 (show ABI3 Proteins), and TREM2 genes highly expressed in microglia and highlight an immune-related protein-protein interaction network in Alzheimer's disease.
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.
Increased DNA methylation (show HELLS Proteins) near TREM2 is seen in the superior temporal gyrus of patients with Alzheimer's disease
Our work identifies the TREM2-APOE (show APOE Proteins) 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.
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 (show RCC1 Proteins), supporting the idea that proper TREM2 function is important to counteract disease progression.
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
Rare coding variants of TREM2 may play an important role in AD in Han Chinese.
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.
link three genetic risk factors for Alzheimer's disease and reveal a possible mechanism by which mutant TREM2 increases risk of AD
Loss of TREM2 reduces the ability of microglia to engulf amyloid beta-peptide.
TREM2 and TREML2 (show TREML2 Proteins) play opposite roles in microglia activation.
Our study suggests that Vps35 (show vps35 Proteins)/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.
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.
This study demonstrate a critical role of TREM2-mediated Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) pathway in microglial viability and suggest that modulating this pathway therapeutically may help to combat the impaired microglial survival.
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.
TREM2 deficiency may disrupt the formation of a neuroprotective microglia barrier that regulates amyloid compaction and insulation
TREM2 deficiency has opposing effects on Alzheimer's disease-related pathologies at early and late stages of disease progression.
TREM2 protects from Alzheimer's disease by enabling microglia to surround and alter Abeta (show APP Proteins) plaque structure, thereby limiting neuritic damage.
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 (show TYROBP Proteins), both of which are expressed by microglia and have bee
This gene encodes a membrane protein that forms a receptor signaling complex with the TYRO protein tyrosine kinase binding protein. The encoded protein functions in immune response and may be involved in chronic inflammation by triggering the production of constitutive inflammatory cytokines. Defects in this gene are a cause of polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL). Alternative splicing results in multiple transcript variants encoding different isoforms.
triggering receptor expressed on myeloid cells 2
, triggering receptor expressed on monocytes 2
, triggering receptor expressed on myeloid cells 2a
, triggering receptor expressed on myeloid cells 2b
, triggering receptor expressed on myeloid cells 2c