TREML2 Proteins, Antibodies, cDNA Clones Research Reagents

TREML2 (Triggering Receptor Expressed On Myeloid Cells Like 2) is a protein coding gene located on human chromosome 6p21.1. TREML2 is also known as TLT2, TLT-2, C6orf76 and dJ238O23.1. The human TREML2 gene encodes a 35127 Da protein containing 321 amino acids. The TREML2 protein is biasedly expressed in bone marrow, lymph node and other tissues. Among its related pathways are Innate Immune System and Class I MHC mediated antigen processing and presentation. NCR2 is an important paralog of TREML2 gene. TREML2 is associated with some diseases, including Polycystic Lipomembranous Osteodysplasia With Sclerosing Leukoencephalopathy 1.

TREML2 Protein (1)

    TREML2 Antibody (3)

      TREML2 cDNA Clone (26)


      TREML2 Lysate (1)

        TREML2 Background

        Trem-like transcript 2 protein, also known as Triggering receptor expressed on myeloid cells-like protein 2, TREML2 and TLT2, is a single-pass type I membrane protein that contains one Ig-like V-type (immunoglobulin-like) domain. TREML2 is detected in cultured B cells, T cell leukemia and monocyte leukemia. TREML2 is expressed constitutively on CD8 T-cells and induced on CD4 T-cells after activation. TREML2 is a cell surface receptor that may play a role in the innate and adaptive immune response. TREML2 acts as a counter-receptor for CD276 and interaction with CD276 on T-cells enhances T-cell activation. Murine B7-H3 is specifically bound to Triggering receptor expressed on myeloid cells (TREM)-like transcript 2 (TLT-2, TREML2). TREML2 was expressed on CD8(+) T cells constitutively and on activated CD4(+) T cells. Stimulation with B7-H3 transfectants preferentially up-regulated the proliferation and IFN-gamma production of CD8(+) T cells. Transduction of TREML2 into T cells resulted in enhanced IL-2 and IFN-gamma production via interactions with B7-H3. There may be a direct interaction between B7-H3 and TREML2 that preferentially enhances CD8(+) T cell activation.

        TREML2 References

        • Mungall A.J. et al., 2003, Nature. 425: 805-11.
        • Clark HF. et al., 2003, Genome Res. 13: 2265-70.
        • The MGC Project Team. et al., 2004, Genome Res. 14:2121-7.
        • Hashiguchi M., et al., 2008, Proc. Natl.Acad. Sci. USA.105:10495-500.
        • Leitner,J. et al., 2009, Eur J Immunol. 39 (7):1754-64.

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