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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 (28) and many more products for this protein.
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In this meta-analysis, genetic datasets demonstrate that TREM2 is a potent risk factor for Parkinson's Disease.
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.
results indicate that TREM-2 might act as a negative immuno-regulatory molecule...and partially predicts prognosis in lung cancer patients
Authors find, using a cell-free coat protein (show GOLPH3 Proteins) 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.
Mutations in TREM2 gene are known to cause Nasu-Hakola disease.
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.
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
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.
A central role of TREM2 is in the regulation of microglia response to acute neurotoxic insults.
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.
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