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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 Proteins (14) and many more products for this protein.
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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.
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
This study shown that Peripheral TREM2 mRNA levels are higher in AD and are associated with AD-related cognitive deficits and hippocampal atrophy.
The data of this study provided evidence that the A192T variant in TREM2 could contribute risk for Alzheimer's disease.
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.
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.
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 ELISA Kits) 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.
TREM2 protects against cerebral ischemia/reperfusion injury through the aspect of post-ischemic inflammatory response and neuronal apoptosis.
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 ELISA Kits) play opposite roles in microglia activation.
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.
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 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) 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.
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