Triggering Receptor Expressed on Myeloid Cells-Like Protein 1 (TREML1) is a single-pass type I membrane protein. TREML1 precursor contains a 15 amino acid signal peptide; a 147 amino acid extracellular domain with an Ig-like V-type (immunoglobulin-like) domain; and 128 amino acid cytoplasmic domain. It can be expressed exclusively in platelets and megakaryocytes (MKs). It is a cell surface receptor that may play a role in the innate and adaptive immune response. TREML1 Sequestered in cytoplasmic vesicles in resting platelets. TREML1 be transported to the cell surface after stimulation by thrombin. Soluble fragments can be released into the serum by proteolysis. The phosphorylated TREML1 can interact with PTPN6 and PTPN11. TREML1 may participate in maintaining vascular hemostasis and regulating coagulation and inflammation at sites of injury.
Trem-like transcript 2 protein (TLT2), also known as Triggering receptor expressed on myeloid cells-like protein 2, TLT2 and C6orf76, is single-pass type I membrane protein. TREML2 contains one Ig-like V-type domain, which can be induced in CD4 T-cell by concanavalin-A. As a cell surface receptor, TREML2 may play a role in the innate and adaptive immune response. TREML2 also acts as a counter-receptor for CD276 and interaction with CD276 on T-cells enhances T-cell activation. It has shown that TREML2 may be involved in the innate immune response based on its expression profile and the fact that it is up-regulated in response to inflammation.
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 which contains oneIg-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 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 maybe a direct interaction between B7-H3 and TREML2 that preferentially enhances CD8(+) T cell activation.
Tribbles homolog 2, also known as TRB-2, and Trib2, is a member of the protein kinase superfamily and Tribbles subfamily (Trib1, Trib2, Trib3). The identification of tribbles as regulators of signal processing systems and physiological processes, including development, together with their potential involvement in diabetes and cancer, has generated considerable interest in these proteins. Tribbles have been reported to regulate activation of a number of intracellular signalling pathways with roles extending from mitosis and cell activation to apoptosis and modulation of gene expression. Tribbles controls the timing of mitosis in the prospective mesoderm, allowing cell-shape changes to be completed. This mechanism for coordinating cell division and cell-shape changes may have helped Drosophila to evolve its mode of rapid early development. Trib2 was identified as a downregulated transcript in leukemic cells undergoing growth arrest. Trib2-transduced bone marrow cells exhibited a growth advantage and readily established factor-dependent cell lines. Trib2-reconstituted mice uniformly developed fatal transplantable acute myelogenous leukemia (AML).
Tribbles homolog 3, also known as Neuronal cell death-inducible putative kinase, p65-interacting inhibitor of NF-kappa-B, SINK and TRIB3, is a Nucleus protein which belongs to theprotein kinase superfamily and CAMK Ser/Thr protein kinase family and Tribbles subfamily. Highest expression Of TRIB3 is in liver, pancreas, peripheral blood leukocytes and bone marrow. It is also highly expressed in a number of primary lung, colon and breast tumors. TRIB3 is expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney. TRIB3 disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. TRIB3 may bind directly to and mask the 'Thr-308' phosphorylation site in AKT1. It binds to ATF4 and inhibits its transcriptional activation activity. TRIB3 interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. It interacts with MAPK kinases and regulates activation of MAP kinases. It may play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. TRIB3 does not display kinase activity.
E3 ubiquitin-protein ligase.
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