Involved in calcium binding and microtubule stabilization. (updated: Sept. 12, 2018)
The data and differentiation stages presented below come from the proteomic study and analysis performed by our partners of the GReX consortium, more details are available in their published work.
No sequence conservation computed yet.
Total structural coverage: 0%
No model available.
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The reference OMIM entry for this protein is 600763
Tumor protein, translationally-controlled 1; tpt1
Translationally controlled tumor protein; tctp
Histamine-releasing factor, immunoglobulin e-dependent; hrf
CLONING
MacDonald et al. (1995) stated that several in vivo systems are used to study human allergic disease. A favored model is the late response in humans that occurs hours after the immediate reaction to allergen challenge. The pathophysiologic events, such as decreased airway function, are characterized by infiltration of inflammatory cells and by the presence of mediators such as histamine, which are findings similar to those observed in people with chronic allergic diseases such as asthma. The histamine released in this late-phase reaction (LPR) results from activation of basophils that, along with eosinophils and lymphocytes, infiltrate tissues during this response. Because the allergen that initiated the response is no longer present, 2 questions required study: the nature of the agent that triggers the release of inflammatory mediators from the basophils in the LPR, and the basis for the observation that only about half of allergic individuals experience an LPR. MacDonald et al. (1995) identified and purified an immunoglobulin E (IgE;
147180)-dependent histamine-releasing factor, which they symbolized HRF, produced by lymphocytes of atopic children and present in biologic fluids of allergic patients. Amino-terminal sequencing revealed extensive homology to the mouse protein p21 and identity to its human homolog, p23, described by Bohm et al. (1989) and Bohm et al. (1991).
GENE FUNCTION
MacDonald et al. (1995) showed that both human and mouse recombinant HRF proteins caused histamine release from human basophils of a subpopulation of donors, and this release was dependent on IgE. Polyclonal antibodies raised in the rabbit against recombinant mouse Hrf recognized and removed the biologic activity of both recombinant and native HRF. HRF identifies heterogeneity of IgE, which may be a genetically determined polymorphism, may be due to differential glycosylation of the IgE molecule, or may be based on interactions with the alternatively spliced forms of human IgE reported to be present in human atopic serum (Zhang et al., 1992; see
147180). Amzallag et al. (2004) found that secretion of TPT1 proceeded by a nonclassical pathway independent of the endoplasmic reticulum and Golgi apparatus. Secreted TPT1 appeared to originate from preexisting pools. Amzallag et al. (2004) determined that TSAP6 (STEAP3;
609671) interacted with TPT1 in several protein interaction assays, and the 2 proteins codistributed to small vesicles called exosomes at the plasma membrane and around the nucleus in several human cell lines. Overexpression of TSAP6 increased the level of TPT1 in exosome preparations and consistently enhanced TPT1 secretion. Hsu et al. (2007) demonstrated that a conserved protein, TCTP, is an essential component of the tuberous sclerosis (see TSC1,
605284)-RHEB (
601293) pathway. Reducing Drosophila Tctp levels reduced cell size, cell number, and organ size, which mimics Drosophila Rheb mutant phenotypes. Drosophila Tctp is genetically epistatic to Tsc1 and Rheb, but acts upstream of S6K (see
608938), a downstream target of Rheb. Drosophila Tctp directly associated with Rheb and displayed guanine nucleotide exchange activity with it in vivo and in vitro. Human TCTP showed similar biochemical properties compared to Drosophila Tctp and could rescue Drosophila Tctp mutant phenotypes, suggesting that the function of TCTP in the TSC pathway is evolutionarily conserved. Hsu et al. (2007) concluded that their studies ident ...
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Subscribe to this protein entry history
June 30, 2020: Protein entry updated
Automatic update: OMIM entry 600763 was added.
Oct. 19, 2018: Additional information
Initial protein addition to the database. This entry was referenced in Bryk and co-workers. (2017).