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TREM2 encodes a membrane protein that forms a receptor signaling complex with the TYRO protein tyrosine kinase binding protein. De plus, nous expédions TREM2 Anticorps (196) et TREM2 Protéines (20) et beaucoup plus de produits pour cette protéine.
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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 (Montrer PSEN1 Kits ELISA) in regulating TREM2 intracellular trafficking and pathophysiological function.
Homozygous TREM2 R47C carrier presenting with an FTD (Montrer FTL Kits ELISA) 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 (Montrer TLR4 Kits ELISA) signaling pathway and osteoclasts activation
ADAM17 (Montrer ADAM17 Kits ELISA) 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 (Montrer TNF Kits ELISA). TREM-2 also inhibited the activation of TNF-alpha (Montrer TNF Kits ELISA) induced of inflammation in RA-fibroblast-like synovial cells (FLSs) by the p38 (Montrer CRK Kits ELISA) 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 (Montrer IL1B Kits ELISA), ameliorated T396 expression, inhibited the activity of GSK-3beta, and improved sickness behavior. Increased Arg1 (Montrer ARG1 Kits ELISA) expression and a high level of synaptophysin (Montrer SYP Kits ELISA) 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