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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 (179) and TREM2 Proteins (13) and many more products for this protein.
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silencing TREM-2 downregulated the expression levels of Bcl2 and PCNA, and upregulated the expression levels of Bax and caspase-3 in renal cell carcinoma cells. Depletion of TREM-2 inactivated PI3K/Akt pathway through increasing the expression of PTEN. TREM-2 acts as an oncogene in the development of renal cell carcinoma and can be considered as a novel therapeutic factor in the treatment of renal cell carcinoma.
TREM2 expression is significantly upregulated in human masticatory mucosa during wound healing
this study shows that activation of TREM-2 may restrain h-MSC (show MSC ELISA Kits) immune activation and promote differentiation for tissue repair
The TREM family members are also considered to involve in Alzheimer's disease (AD) and cerebrospinal fluid (CSF (show CSF2 ELISA Kits)) soluble form of TREM2 (sTREM2) levels has also been associated with respond to progression of disease.
Study provides evidence that TREM2 mRNA is upregulated in the human hippocampus affected by Alzheimer's disease (AD). Findings also suggest that 5hmC may play a role in regulating TREM2 mRNA expression in AD hippocampus.
The study suggests that TREM2 may work as an oncogene (show RAB1A ELISA Kits) and a new effective therapeutic target for glioma treatment.
CSF (show CSF2 ELISA Kits) concentrations of soluble TREM2 are higher in Alzheimer's disease than in controls
Variant p.R47H of TREM2 was not associated with Parkinson's disease
Our results corroborate and extend previous findings, concluding that the variant rs75932628-T (p.R47H) in TREM2 is not a risk factor for leucoaraiosis or Parkinson's disease in the Han Chinese population.
the minor T allele at TREM2 (p.R47H, rs75932628) showed nominally significant association with AD risk (OR 5 5.73, 95% CI 5 1.80-18.25, P 5 .0232), whereas no significant association for risk of frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease.
This study showed that TREM-2 deficiency restricts the inflammatory response, thereby decreasing organ damage and mortality.
TREM2 attenuates tau kinase activity through restriction of neuroinflammation, and thus protects against tau pathology.
TREM2 is involved in prion (show PRNP ELISA Kits)-induced microglial activation but does not noticeably modulate the pathogenesis of experimental prion (show PRNP ELISA Kits) infections.
These findings provide a novel interpretation of Brucella intracellular growth through inhibition of NO production produced by TREM-2-mediated activated macrophages.
TREM-1 (show TREM1 ELISA Kits)/TREM-3 macrophage expression improved host defense against Klebsiella-derived pneumosepsis, whereas TREM-2 did not have a role.
These findings place TREM2 as a key regulator of microglia activation in vivo in response to tissue damage
TREM-2 has a protective effect on inflammatory response of endotoxin-induced acute lung injury in mice.
results support a role of DAP12 (show TYROBP ELISA Kits) in stabilizing TREM2-CTF (show NFIA ELISA Kits), thereby protecting against excessive pro-inflammatory responses.
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.
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.
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