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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 (28) and TREM2 Proteins (14) and many more products for this protein.
Showing 10 out of 192 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 3 Pubmed References
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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Human Monoclonal TREM2 Primary Antibody for CyTOF, FACS - ABIN4900551
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
Show all 2 Pubmed References
Human Monoclonal TREM2 Primary Antibody for CyTOF, FACS - ABIN4900550
Kawabori, Kacimi, Kauppinen, Calosing, Kim, Hsieh, Nakamura, Yenari: Triggering receptor expressed on myeloid cells 2 (TREM2) deficiency attenuates phagocytic activities of microglia and exacerbates ischemic damage in experimental stroke. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2015
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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
Mouse (Murine) Monoclonal TREM2 Primary Antibody for IA, FACS - ABIN2191861
Koga, Inui, Inoue, Kim, Suematsu, Kobayashi, Iwata, Ohnishi, Matozaki, Kodama, Taniguchi, Takayanagi, Takai: Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis. in Nature 2004
Mouse (Murine) Polyclonal TREM2 Primary Antibody for ELISA, WB - ABIN4362238
Takahashi, Prinz, Stagi, Chechneva, Neumann: TREM2-transduced myeloid precursors mediate nervous tissue debris clearance and facilitate recovery in an animal model of multiple sclerosis. in PLoS medicine 2007
Mouse (Murine) Monoclonal TREM2 Primary Antibody for FACS - ABIN2476937
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
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 Antibodies) 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 Antibodies), ABI3 (show ABI3 Antibodies), 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 Antibodies) near TREM2 is seen in the superior temporal gyrus of patients with Alzheimer's disease
Our work identifies the TREM2-APOE (show APOE Antibodies) 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 Antibodies), supporting the idea that proper TREM2 function is important to counteract disease progression.
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 Antibodies) play opposite roles in microglia activation.
Our study suggests that Vps35 (show vps35 Antibodies)/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 Antibodies)/beta-catenin (show CTNNB1 Antibodies) 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