TCTP expression is highly regulated and responds to numerous extracellular signals and intracellular conditions. For example, TCTP levels vary considerably in response to tissue specific growth factors, cytokines, and stress signals including those triggered by heat shock, starvation,7-Epitaxol pro-apoptotic conditions, the presence of environmental pollutants and heavy metals, and by changes in cellular calcium -mediated homeostasis. Despite its broad regulation and abundance, knowledge of TCTP function has remained elusive. The best classification of TCTP’s role in cellular function places the protein into two groups: i) functions associated with cell growth, division, and death and ii) immunity/allergic-related functions. Initially, evidence of a role for TCTP in cell death arose from variations in the cell’s phenotype under conditions in which the protein was either overexpressed or its gene was knocked down, resulting in enhancement of the action of anti-apoptotic players or in prevention of pro-apoptotic components from triggering cell death, respectively. Other evidence establishes a role for TCTP in cell proliferation. This includes i) the regulation of the GTPase activity of the Drosophila Ras homologue Rheb, a direct target of TSC1/2 tumor suppressors responsible for tuberous sclerosis, ii) the stabilization of the GDP form of the translational elongation factor eEF1A, and iii) progression through cytokinesis by a mechanism that involves phosphorylation of TCTP by the polo-like kinase and,Cephalomannine consequently, reduction of the microtubule-stabilizing activity of TCTP,. In agreement with a role for TCTP in cell growth and proliferation, this protein is overexpressed in tumor cells and its inhibition by antisense or siRNA promotes apoptosis or, in other cases, induces the reorganization of cells into specific structures when the malignant phenotype has been suppressed. In addition, TCTP exhibits extracellular function by acting as an IgE-dependent histaminereleasing factor ]. As shown, fluids secreted from human lung macrophages were able to induce Ca2+-dependent HRF release from basophiles and mast cells in an IgE-dependent manner.