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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 Kits (31) and TREM2 Proteins (20) and many more products for this protein.
Showing 10 out of 196 products:
Human Polyclonal TREM2 Primary Antibody for CyTOF, FACS - ABIN4899382
Quan, Cooper, Potter, Roberts, Cheng, Jarvis: TREM-2 binds to lipooligosaccharides of Neisseria gonorrhoeae and is expressed on reproductive tract epithelial cells. in Mucosal immunology 2008
Show all 9 Pubmed References
Human Polyclonal TREM2 Primary Antibody for FACS, ICC - ABIN4899381
Cooper-Knock, Green, Altschuler, Wei, Bury, Heath, Wyles, Gelsthorpe, Highley, Lorente-Pons, Beck, Doyle, Otero, Traynor, Kirby, Shaw, Hide: A data-driven approach links microglia to pathology and prognosis in amyotrophic lateral sclerosis. in Acta neuropathologica communications 2017
Show all 3 Pubmed References
Human Monoclonal TREM2 Primary Antibody for FACS - ABIN4897941
Hall, Agrawal: Increased TREM-2 expression on the subsets of CD11c+cells in the lungs and lymph nodes during allergic airway inflammation. in Scientific reports 2017
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Human Monoclonal TREM2 Primary Antibody for CyTOF, FACS - ABIN4900550
Wu, Byers, Jin, Agapov, Alexander-Brett, Patel, Cella, Gilfilan, Colonna, Kober, Brett, Holtzman: TREM-2 promotes macrophage survival and lung disease after respiratory viral infection. in The Journal of experimental medicine 2015
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Human Monoclonal TREM2 Primary Antibody for ELISA, SimWes - ABIN449602
Roussos, Katsel, Fam, Tan, Purohit, Haroutunian: The triggering receptor expressed on myeloid cells 2 (TREM2) is associated with enhanced inflammation, neuropathological lesions and increased risk for Alzheimer's dementia. in Alzheimer's & dementia : the journal of the Alzheimer's Association 2015
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Mouse (Murine) Monoclonal TREM2 Primary Antibody for FACS - ABIN2476936
Humphrey, Daws, Spusta, Niemi, Torchia, Lanier, Seaman, Nakamura: TREM2, a DAP12-associated receptor, regulates osteoclast differentiation and function. in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2006
Human Polyclonal TREM2 Primary Antibody for FACS, IF (p) - ABIN749678
Satoh, Kawana, Yamamoto, Ishida, Saito, Arima: A survey of TREM2 antibodies reveals neuronal but not microglial staining in formalin-fixed paraffin-embedded postmortem Alzheimer's brain tissues. in Alzheimer's research & therapy 2014
Our data establish a critical link between oAbeta1-42, a major pathological component of Alzheimer's disease and TREM2
Data indicate a novel role for PS1 (show PSEN1 Antibodies) in regulating TREM2 intracellular trafficking and pathophysiological function.
Homozygous TREM2 R47C carrier presenting with an FTD (show FTL Antibodies) rather than an Alzheimer's disease phenotype.
Our results suggest that deficiency of microglial TREM2 leads to heightened tau pathology coupled with widespread increases in activated neuronal stress kinases
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.
TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 (show TLR4 Antibodies) signaling pathway and osteoclasts activation
ADAM17 (show ADAM17 Antibodies) 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.
In rheumatoid arthritis (RA), the expression of TREM-2 was reduced at first and then up-regulated after stimulation by TNF-alpha (show TNF Antibodies). TREM-2 also inhibited the activation of TNF-alpha (show TNF Antibodies) induced of inflammation in RA-fibroblast-like synovial cells (FLSs) by the p38 (show CRK Antibodies) pathway.
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.
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.
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.
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
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.
Overexpression of TREM2 downregulated the levels of IL-1beta (show IL1B Antibodies), ameliorated T396 expression, inhibited the activity of GSK-3beta, and improved sickness behavior. Increased Arg1 (show ARG1 Antibodies) expression and a high level of synaptophysin (show SYP Antibodies) were also observed in the transgenic mice following TREM2 overexpression.
These studies of the role of TREM2 in neuroinflammation and neurodegeneration suggest that impairing microglial TREM2 signaling reduces pure tauopathy.
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.
TREM2 protects against cerebral ischemia/reperfusion injury through the aspect of post-ischemic inflammatory response and neuronal apoptosis.
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.
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