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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 (198) et TREM2 Protéines (20) et beaucoup plus de produits pour cette protéine.
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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.
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.
This study demonstrated that Lower DNA methylation at TREM2 intron 1 caused higher TREM2 mRNA expression in the leukocytes of Alzheimer's disease subjects versus controls and may be a biomarker for Alzheimer's disease.
investigated consequences of TREM2 loss of function on microglia transcriptome; microglia lacking TREM2 migrate less towards apoptotic neurons, and outgrowth of microglial processes towards sites of damage in the somatosensory cortex is slowed; the apparent lack of chemotactic stimulation upon depletion of TREM2 is consistent with stable expression profile of genes characterizing the homoeostatic signature of microglia
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.
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.
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 (Montrer TREML2 Kits ELISA) play opposite roles in microglia activation.
Our study suggests that Vps35/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 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