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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 Antikörper (192) und TREM2 Kits (28) und viele weitere Produktgruppen zu diesem Protein an.
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Authors find, using a cell-free coat protein (zeige GOLPH3 Proteine) 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 (zeige PLCG2 Proteine), ABI3 (zeige ABI3 Proteine), 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 (zeige HELLS Proteine) near TREM2 is seen in the superior temporal gyrus of patients with Alzheimer's disease
Our work identifies the TREM2-APOE (zeige APOE Proteine) 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 (zeige RCC1 Proteine), supporting the idea that proper TREM2 function is important to counteract disease progression.
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
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 (zeige TREML2 Proteine) play opposite roles in microglia activation.
Our study suggests that Vps35 (zeige vps35 Proteine)/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 (zeige WNT2 Proteine)/beta-catenin (zeige CTNNB1 Proteine) 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.
TREM2 protects from Alzheimer's disease by enabling microglia to surround and alter Abeta (zeige APP Proteine) plaque structure, thereby limiting neuritic damage.
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