TREM2, Polyclonal Antibody

Triggering receptor expressed on myeloid cells 2; TREM-2; Triggering receptor expressed on monocytes 2; TREM2

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit Ig

Rabbit

This TREM2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 22-50 amino acids from the N-terminal region of human TREM2.

Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab)

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.

Vial Concentration: 0.5 (lot specific)

Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

Small volumes of anti-TREM2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

TREM2 is a membrane protein
that forms a receptor signaling complex with TYROBP. The encoded
protein 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).

Immunology

Western Blot (WB), ELISA (EIA)

WB~~1:1000

TREM2 Antibody (N-term) western blot analysis in MDA-MB435 cell line lysates (35ug/lane).This demonstrates the TREM2 antibody detected the TREM2 protein (arrow).

25447

triggering receptor expressed on myeloid cells 2

triggering receptor expressed on myeloid cells 2

Triggering receptor expressed on myeloid cells 2

TREM-2  [Similar Products]

TREM2_HUMAN

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. [provided by RefSeq, Nov 2012]

TREM2: May have a role in chronic inflammations and may stimulate production of constitutive rather than inflammatory chemokines and cytokines. Forms a receptor signaling complex with TYROBP and triggers activation of the immune responses in macrophages and dendritic cells. Defects in TREM2 are a cause of polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL); also known as presenile dementia with bone cysts or Nasu-Hakola disease (NHD). PLOSL is a recessively inherited disease characterized by a combination of psychotic symptoms rapidly progressing to presenile dementia and bone cysts restricted to wrists and ankles. PLOSL has a global distribution, although most of the patients have been diagnosed in Finland and Japan, with an estimated population prevalence of 2x10(-6) in the Finns. 3 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral

Chromosomal Location of Human Ortholog: 6p21.1

Cellular Component: intracellular membrane-bound organelle; plasma membrane; integral to membrane; extracellular region

Molecular Function: peptidoglycan binding; lipopolysaccharide binding; receptor activity

Biological Process: axon guidance; positive regulation of peptidyl-tyrosine phosphorylation; detection of lipopolysaccharide; detection of peptidoglycan; innate immune response; positive regulation of calcium-mediated signaling; humoral immune response; positive regulation of antigen processing and presentation of peptide antigen via MHC class II

Disease: Polycystic Lipomembranous Osteodysplasia With Sclerosing Leukoencephalopathy

Stefano, L., et al. J. Neurochem. 110(1):284-294(2009)
Ford, J.W., et al. Curr. Opin. Immunol. 21(1):38-46(2009)

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