Triggering Receptor Expressed On Myeloid Cells 2 (TREM2) Kits ELISA

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 (197) et TREM2 Protéines (20) et beaucoup plus de produits pour cette protéine.

list all ELISA KIts Gène GeneID UniProt
TREM2 54209 Q9NZC2
TREM2 83433 Q99NH8
TREM2 301227  
Comment commander chez anticorps-enligne
  • +1 877 302 8632
  • +1 888 205 9894 (toll-free)
  • Commandez enligne
  • orders@anticorps-enligne.fr

Top TREM2 Kits ELISA sur anticorps-enligne.fr

Showing 3 out of 31 products:

Catalogue No. Reactivité Sensibilité Gamme Images Quantité Fournisseur Livraison Prix Détails
Humain 25.5 pg/mL 62.5 pg/mL - 4000 pg/mL 96 Tests Connectez-vous pour afficher 13 to 16 Days
$736.84
Détails
Souris 6.5 pg/mL 15.6 pg/mL - 1000 pg/mL 96 Tests Connectez-vous pour afficher 13 to 16 Days
$757.89
Détails
Rat 3.9 pg/mL 15.6-1000 pg/mL Typical standard curve 96 Tests Connectez-vous pour afficher 13 to 16 Days
$910.56
Détails

Plus Kits ELISA pour TREM2 partenaires d'interaction

Human Triggering Receptor Expressed On Myeloid Cells 2 (TREM2) interaction partners

  1. Trem2 R47H variant activates a cryptic splice site that generates miss-spliced transcripts leading to Trem2 haploinsufficiency only in mice but not in humans

  2. Peripheral TREM2 originating from erythromyeloid cells significantly determines Alzheimer's disease neuropathology in Down syndrome subjects.

  3. Our data establish a critical link between oAbeta1-42, a major pathological component of Alzheimer's disease and TREM2

  4. Data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function.

  5. Homozygous TREM2 R47C carrier presenting with an FTD rather than an Alzheimer's disease phenotype.

  6. Our results suggest that deficiency of microglial TREM2 leads to heightened tau pathology coupled with widespread increases in activated neuronal stress kinases

  7. 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.

  8. TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

  9. ADAM17 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.

  10. In rheumatoid arthritis (RA), the expression of TREM-2 was reduced at first and then up-regulated after stimulation by TNF-alpha. TREM-2 also inhibited the activation of TNF-alpha induced of inflammation in RA-fibroblast-like synovial cells (FLSs) by the p38 pathway.

  11. 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.

  12. 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.

  13. 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.

  14. 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.

  15. 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

  16. This study shown that Peripheral TREM2 mRNA levels are higher in AD and are associated with AD-related cognitive deficits and hippocampal atrophy.

  17. The data of this study provided evidence that the A192T variant in TREM2 could contribute risk for Alzheimer's disease.

  18. 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.

  19. Recent studies have advanced our understanding of TREM2 biology and microglial activities in aging and neurodegenerative brains, providing new insights into TREM2 functions in amyloid plaque maintenance, microglial envelopment of plaque, microglia viability, and the identification of novel TREM2 ligands.

  20. In this meta-analysis, genetic datasets demonstrate that TREM2 is a potent risk factor for Parkinson's Disease.

Mouse (Murine) Triggering Receptor Expressed On Myeloid Cells 2 (TREM2) interaction partners

  1. Trem2 R47H variant activates a cryptic splice site that generates miss-spliced transcripts leading to Trem2 haploinsufficiency only in mice but not in humans

  2. Triggering receptor expressed on myeloid cells 2 (TREM2) knockout(-/-) mice displayed repetitive behavior and altered sociability.

  3. Transcriptome analysis revealed that our Trem2-/- mouse line (Velocigene allele) results in exaggerated Treml1 upregulation. In contrast, aberrantly high Treml1 expression was absent in the Trem2 knockout line generated by the Colonna lab and the Jackson Labs CRISPR/Cas9 Trem2 knockout line.

  4. The present study provide novel evidence that overexpression of TREM2 protects against MPTP-induced PD progression via modulation of microglial function through inhibiting TRAF6/TLR4-mediated activation of the MAPK and NF-kappaB signaling pathways.

  5. Our data establish a critical link between oAbeta1-42, a major pathological component of Alzheimer's disease and TREM2

  6. 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.

  7. Data indicate a novel role for PS1 in regulating TREM2 intracellular trafficking and pathophysiological function.

  8. 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

  9. 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.

  10. Overexpression of TREM2 downregulated the levels of IL-1beta, ameliorated T396 expression, inhibited the activity of GSK-3beta, and improved sickness behavior. Increased Arg1 expression and a high level of synaptophysin were also observed in the transgenic mice following TREM2 overexpression.

  11. These studies of the role of TREM2 in neuroinflammation and neurodegeneration suggest that impairing microglial TREM2 signaling reduces pure tauopathy.

  12. 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.

  13. TREM2 protects against cerebral ischemia/reperfusion injury through the aspect of post-ischemic inflammatory response and neuronal apoptosis.

  14. 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.

  15. 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.

  16. A central role of TREM2 is in the regulation of microglia response to acute neurotoxic insults.

  17. Loss of TREM2 reduces the ability of microglia to engulf amyloid beta-peptide.

  18. TREM2 and TREML2 play opposite roles in microglia activation.

  19. 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.

  20. sTREM2 plays a crucial role in regulating microglial cell survival and inflammatory responses.

TREM2 profil antigène

Antigen Summary

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.

Gene names and symbols associated with TREM2

  • triggering receptor expressed on myeloid cells 2 (TREM2) anticorps
  • triggering receptor expressed on myeloid cells 2 (trem2) anticorps
  • trem-like transcript 2 protein (LOC100228399) anticorps
  • triggering receptor expressed on myeloid cells 2 (Trem2) anticorps
  • TREM-2 anticorps
  • TREM-A1 anticorps
  • TREM-B1 anticorps
  • TREM2 anticorps
  • Trem2a anticorps
  • Trem2b anticorps
  • Trem2c anticorps

Protein level used designations for TREM2

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

GENE ID SPECIES
419920 Gallus gallus
748470 Pan troglodytes
100126214 Xenopus (Silurana) tropicalis
100228399 Taeniopygia guttata
719740 Macaca mulatta
54209 Homo sapiens
83433 Mus musculus
301227 Rattus norvegicus
608965 Canis lupus familiaris
100737974 Sus scrofa
506467 Bos taurus
Fournisseurs de qualité sélectionnés pour TREM2 (TREM2) Kits ELISA
Avez-vous cherché autre chose?