Invitrogen™ TCL1 Monoclonal Antibody (eBio1-21 (1-21)), eBioscience™

Description

Description: The eBio1-21 antibody reacts with human T cell leukemia/lymphoma 1 (TCL1), a 14 kDa proto-oncogene product with a suggested role in intracellular regulation of T cell signalling. TCL1 was identified as the oncogene located at the 14q32.1 chromosome breakpoint region in T-cell prolymphocytic leukemia (T-PLL). In T-PLL, TCL1 is overexpressed as a result of an inversion or a reciprocal translocation, by juxtaposition to the T-cell receptor promoter/enhancer elements. TCL1 binds to the pleckstrin homology domain of Akt (protein kinase B) family proteins, which facilitates Akt dimerization and activity. By increasing Akt activity TCL1 may enhance the serine/threonine phosphorylation of major Akt signaling substrates, such as Ikk complex, mTOR, BAD, p70S6 kinase, FOXO transcription factors, and GSK3beta. These substrates regulate cellular differentiation, growth, survival, and metabolism. Besides its tumorigenic role in T-PLL, TCL1 is normally expressed in the CD3-CD4-CD8- subset of thymic precursors in the T cell lineage, the plasmacytoid subset of dendritic cells, stimulated (not resting) mature T cells, and B cells up to the germinal center stage of maturation. TCL1 is inappropriately expressed by chromosome rearrangements that lead to pre-malignant clonal T cell expansions and mature T cell tumors. TCL1 shows a regulated expression pattern in chronic lymphocytic leukemia (CLL). Applications Reported: This eBio1-21 (1-21) antibody has been reported for use in int...

Overexpression of the TCL1 gene in humans has been implicated in the development of mature T cell leukemia, in which chromosomal rearrangements bring the TCL1 gene in close proximity to the T-cell antigen receptor (TCR)-alpha or TCR-beta regulatory elements (summarized by Virgilio et al., 1998). In normal T cells TCL1 is expressed in CD4-/CD8- cells, but not in cells at later stages of differentiation. TCL1 functions as a coactivator of the cell survival kinase AKT (Laine et al., 2000).