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TREM2 encodes a membrane protein that forms a receptor signaling complex with the TYRO protein tyrosine kinase binding protein. Zusätzlich bieten wir Ihnen TREM2 Kits (24) und TREM2 Proteine (14) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 192 products:
Human Polyclonal TREM2 Primary Antibody für FACS, ICC - 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
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Human Monoclonal TREM2 Primary Antibody für EIA, WB - ABIN336080
NDiaye, Branda, Branda, Nevarez, Colonna, Lowell, Hamerman, Seaman: TREM-2 (triggering receptor expressed on myeloid cells 2) is a phagocytic receptor for bacteria. in The Journal of cell biology 2009
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Human Monoclonal TREM2 Primary Antibody für 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 für 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 Polyclonal TREM2 Primary Antibody für IHC, ELISA - ABIN190752
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 für EIA, IP - ABIN1109326
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
Human Polyclonal TREM2 Primary Antibody für 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
SNPs involved in pathways related to virus cellular entry and vesicular trafficking were overrepresented, suggesting that cerebrospinal fluid soluble TREM2 levels could be an informative phenotype for Alzheimer disease
Rare coding variants of TREM2 may play an important role in AD in Han Chinese.
These data demonstrate that cerebrospinal fluid soluble TREM2 levels are increased in the early symptomatic phase of Alzheimer's disease, probably reflecting a corresponding change of the microglia activation status in response to neuronal degeneration.
link three genetic risk factors for Alzheimer's disease and reveal a possible mechanism by which mutant TREM2 increases risk of AD
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.
TREM2 deficiency may disrupt the formation of a neuroprotective microglia barrier that regulates amyloid compaction and insulation
flow cytometry analyses indicated significantly lower surface expression of T66M TREM2 variant than wild type or other TREM2 variants
silencing TREM-2 downregulated the expression levels of Bcl2 (zeige BCL2 Antikörper) and PCNA (zeige PCNA Antikörper), and upregulated the expression levels of Bax (zeige BAX Antikörper) and caspase-3 (zeige CASP3 Antikörper) in renal cell carcinoma (zeige MOK Antikörper) cells. Depletion of TREM-2 inactivated PI3K (zeige PIK3CA Antikörper)/Akt (zeige AKT1 Antikörper) pathway through increasing the expression of PTEN (zeige PTEN Antikörper). TREM-2 acts as an oncogene (zeige RAB1A Antikörper) in the development of renal cell carcinoma (zeige MOK Antikörper) and can be considered as a novel therapeutic factor in the treatment of renal cell carcinoma (zeige MOK Antikörper).
TREM2 expression is significantly upregulated in human masticatory mucosa during wound healing
this study shows that activation of TREM-2 may restrain h-MSC (zeige MSC Antikörper) immune activation and promote differentiation for tissue repair
TREM2 and TREML2 (zeige TREML2 Antikörper) play opposite roles in microglia activation.
Our study suggests that Vps35 (zeige vps35 Antikörper)/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.
This study demonstrate a critical role of TREM2-mediated Wnt (zeige WNT2 Antikörper)/beta-catenin (zeige CTNNB1 Antikörper) 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 has opposing effects on Alzheimer's disease-related pathologies at early and late stages of disease progression.
TREM2 protects from Alzheimer's disease by enabling microglia to surround and alter Abeta (zeige APP Antikörper) plaque structure, thereby limiting neuritic damage.
Recent studies have revealed that activated microglia in the spinal dorsal horn exacerbate neuropathic pain, which has suggested that suppression of microglial activity should be considered as a therapeutic target. However, only a few molecules have been identified as regulators of microglial activity. In this study, we focused on a receptor complex of TREM2 and DAP12 (zeige TYROBP Antikörper), both of which are expressed by microglia and have bee
The authors demonstrate that a TREM2 loss-of-function mutation causes brain-wide metabolic alterations pointing toward a possible function of microglia in regulating brain glucose metabolism.
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