The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

TPR  -  translocated promoter region, nuclear...

Homo sapiens

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of TPR


High impact information on TPR

  • Several classes of protein domains have been identified that are either designed for or are capable of interacting with protein C-termini - these include PDZ and TPR domains [6].
  • The PPR motif - a TPR-related motif prevalent in plant organellar proteins [7].
  • FKBP51 is composed of three domains: two consecutive FKBP domains and a three-unit repeat of the TPR (tetratricopeptide repeat) domain [8].
  • We found that in vitro translated TPR bound to in vitro translated Nup98 and, via Nup98, to Nup96 [9].
  • TPR (translocated promoter region) is a protein that forms filamentous structures extending from nuclear pore complexes (NPCs) to intranuclear sites [9].

Chemical compound and disease context of TPR

  • At the highest dose of phenylephrine, the increase in MAP and TPR from predrug baselines was significantly attenuated during the heat stress [DeltaMAP 8.4 +/- 1.2 mmHg; DeltaTPR 0.96 +/- 0.85 peripheral resistance units (PRU)] compared with normothermia (DeltaMAP 15.4 +/- 1.4 mmHg, DeltaTPR 7.13 +/- 1.18 PRU; all P < 0.001) [10].

Biological context of TPR

  • We show also the involvement of TPR in the generation of another TRK-T oncogene [11].
  • The resulting hybrid mRNA contains 598 nucleotides of the TPR gene and 1148 nucleotides of the TRK proto-oncogene [11].
  • The thyroid TRK oncogenes are activated by recombination with at least three different genes: the gene coding for tropomyosin and TPR, both on chromosome 1,and TFG on chromosome 3 [12].
  • Nifedipine reduced total peripheral resistance (TPR; 1744 +/- 398 versus 1290 +/- 215 dyne-s/cm5) and increased arterial compliance (ACL; 1.234 +/- 0.253 versus 1.776 +/- 0.415 mL/mm Hg) [13].
  • With both drugs, changes in MAP were not associated with significant changes in cardiac output (p greater than 0.10 for both drugs), but correlated with changes in systemic resistance (TPR); r = 0.84, p less than 0.001 for AA and r = 0.71, p less than 0.001 for CEI [14].

Anatomical context of TPR

  • This characteristic staining pattern of the TPR network was considerably enhanced when a myc-tagged pyruvate kinase-6kDa fusion protein was overexpressed in HeLa cells [9].
  • In this paper, we report (1) the cDNA structure of TRK-T2, (2) evidence that TRK-T2 is generated by different rearrangements in two thyroid tumors, and (3) a detailed analysis of the three different TPR/NTRK1 rearrangements [12].
  • Collectively, these findings suggest a novel TPR signaling pathway in OLGs and a potential role for this signaling during OLG maturation and myelin production [15].
  • Analysis of hybrid cells containing TPR-MET demonstrated that both the upstream and downstream portions of MET are conserved in this rearrangement and that oncogene activation occurred by an insertion of TPR sequences into the MET locus [16].
  • Using Western blotting, the temporal patterns of cleavage of three nuclear matrix proteins (lamin B, NUMA and the nucleoporin TPR) were compared in HL60 cells induced to undergo apoptosis after irradiation, heat shock or treatment with etoposide [17].

Associations of TPR with chemical compounds

  • Ramipril also decreased TPR (1740 +/- 292 versus 1437 +/- 290 dyne-s/cm5) and increased ACL (1.214 +/- 0.190 versus 1.569 +/- 0.424 mL/mm Hg), but with this agent, the change in arterial compliance was explained solely on the basis of a reduction in distending pressure [13].
  • Atenolol, in contrast, did not affect either TPR or ACL [13].
  • Despite the well documented involvement of thromboxane A(2) receptor (TPR) signaling in the pathogenesis of thrombotic diseases, there are currently no rationally designed antagonists available for clinical use [18].
  • Results suggested that reduction of blood pressure by lofexidine depended on lack of increase in TPR in response to reduction of cardiac output; the hemodynamic pattern of this centrally acting adrenergic blocker closely resembled that reported for beta blockers [19].
  • In addition to the NTPase domain, these proteins typically contain DNA-binding or protein-binding domains, superstructure-forming repeats, such as WD40 and TPR, and enzymatic domains involved in signal transduction, including adenylate cyclases and kinases [20].

Other interactions of TPR

  • The nucleoporin Nup98 associates with the intranuclear filamentous protein network of TPR [9].
  • Alternatively, inhibition of endogenous TPR signaling led to reduced MBP expression [15].
  • Although the TPR4 mutant fully complemented the cells, it showed a reduced interaction with FANCA, suggesting that this TPR may also be of functional importance [21].
  • Using Saccharomyces cerevisiae two-hybrid screening, we identified tetratricopeptide repeat 1 (TPR1), a 292-amino-acid protein with three TPR motifs, as a Galpha16-binding protein [22].
  • We have also observed that LGN, a Galphai-interacting protein with seven TPR motifs, binds Ha-Ras [22].
  • These results suggest that HSP mRNA export escapes stress inhibition via HSF1-mediated recruitment of the nuclear pore-associating protein TPR to HSP genes, thereby functionally connecting the first and last nuclear steps of the gene expression pathway, transcription and mRNA export [23].

Analytical, diagnostic and therapeutic context of TPR

  • The distance between NTRK1 and its oncogenic partner TPR was determined by two-color fluorescence in situ hybridization and two-dimensional microscopy [24].
  • Comparative sequence alignments indicate that members of this protein family contain multiple SH3 and TPR domains that are likely involved in the formation of protein complexes [25].
  • Molecular cloning and expression of a transformation-sensitive human protein containing the TPR motif and sharing identity to the stress-inducible yeast protein STI1 [26].
  • Characterizations of the VOx/TiO2 catalysts were carried out with XRD, laser Raman spectroscopy, and TPR [27].
  • During TM, there was a greater decrease in SBP due to a concomitantly greater decrease in TPR compared with the control group during eyes-closed relaxation (SBP: -3.0 vs. +2.1 mm Hg, p < .04; TPR: -1.0 vs. +0.3 mm Hg/liter per minute, p < .03) [28].


  1. Locus of control predicts appraisals and cardiovascular reactivity to a novel active coping task. Weinstein, S.E., Quigley, K.S. Journal of personality. (2006) [Pubmed]
  2. TPR-MET oncogenic rearrangement: detection by polymerase chain reaction amplification of the transcript and expression in human tumor cell lines. Soman, N.R., Wogan, G.N., Rhim, J.S. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  3. Nucleolar localization of the nucleophosmin-anaplastic lymphoma kinase is not required for malignant transformation. Mason, D.Y., Pulford, K.A., Bischof, D., Kuefer, M.U., Butler, L.H., Lamant, L., Delsol, G., Morris, S.W. Cancer Res. (1998) [Pubmed]
  4. Expression and characterization of a magnetosome-associated protein, TPR-containing MAM22, in Escherichia coli. Okuda, Y., Fukumori, Y. FEBS Lett. (2001) [Pubmed]
  5. Regional and cellular specificity of the expression of TPRD, the tetratricopeptide Down syndrome gene, during human embryonic development. Rachidi, M., Lopes, C., Gassanova, S., Sinet, P.M., Vekemans, M., Attie, T., Delezoide, A.L., Delabar, J.M. Mech. Dev. (2000) [Pubmed]
  6. Functional diversity of protein C-termini: more than zipcoding? Chung, J.J., Shikano, S., Hanyu, Y., Li, M. Trends Cell Biol. (2002) [Pubmed]
  7. The PPR motif - a TPR-related motif prevalent in plant organellar proteins. Small, I.D., Peeters, N. Trends Biochem. Sci. (2000) [Pubmed]
  8. Structure of the large FK506-binding protein FKBP51, an Hsp90-binding protein and a component of steroid receptor complexes. Sinars, C.R., Cheung-Flynn, J., Rimerman, R.A., Scammell, J.G., Smith, D.F., Clardy, J. Proc. Natl. Acad. Sci. U.S.A. (2003) [Pubmed]
  9. The nucleoporin Nup98 associates with the intranuclear filamentous protein network of TPR. Fontoura, B.M., Dales, S., Blobel, G., Zhong, H. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  10. Phenylephrine-induced elevations in arterial blood pressure are attenuated in heat-stressed humans. Cui, J., Wilson, T.E., Crandall, C.G. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2002) [Pubmed]
  11. TRK-T1 is a novel oncogene formed by the fusion of TPR and TRK genes in human papillary thyroid carcinomas. Greco, A., Pierotti, M.A., Bongarzone, I., Pagliardini, S., Lanzi, C., Della Porta, G. Oncogene (1992) [Pubmed]
  12. Chromosome 1 rearrangements involving the genes TPR and NTRK1 produce structurally different thyroid-specific TRK oncogenes. Greco, A., Miranda, C., Pagliardini, S., Fusetti, L., Bongarzone, I., Pierotti, M.A. Genes Chromosomes Cancer (1997) [Pubmed]
  13. Differential effects of chronic oral antihypertensive therapies on systemic arterial circulation and ventricular energetics in African-American patients. Cholley, B.P., Shroff, S.G., Sandelski, J., Korcarz, C., Balasia, B.A., Jain, S., Berger, D.S., Murphy, M.B., Marcus, R.H., Lang, R.M. Circulation (1995) [Pubmed]
  14. Constrasts and similarities of acute hemodynamic responses to specific antagonism of angiotensin II ([Sar1, Thr8] A II) and to inhibition of converting enzyme (captopril). Fouad, F.M., Ceimo, J.M., Tarazi, R.C., Bravo, E.L. Circulation (1980) [Pubmed]
  15. Characterization of thromboxane A(2) receptor signaling in developing rat oligodendrocytes: Nuclear receptor localization and stimulation of myelin basic protein expression. Ramamurthy, S., Mir, F., Gould, R.M., Breton, G.C. J. Neurosci. Res. (2006) [Pubmed]
  16. Analysis by pulsed field gel electrophoresis reveals complex rearrangements in two MET alleles in a chemically-treated human cell line, MNNG-HOS. Testa, J.R., Park, M., Blair, D.G., Kalbakji, A., Arden, K., Vande Woude, G.F. Oncogene (1990) [Pubmed]
  17. Different patterns of DNA fragmentation and degradation of nuclear matrix proteins during apoptosis induced by radiation, hyperthermia or etoposide. Dynlacht, J.R., Earles, M., Henthorn, J., Seno, J.D. Radiat. Res. (2000) [Pubmed]
  18. Differential mapping of the amino acids mediating agonist and antagonist coordination with the human thromboxane A2 receptor protein. Khasawneh, F.T., Huang, J.S., Turek, J.W., Breton, G.C. J. Biol. Chem. (2006) [Pubmed]
  19. Early hemodynamic and humoral effects of lofexidine. Fouad, F.M., Vidt, D.G., Williams, H., Tarazi, R.C., Bravo, E.L. Clin. Pharmacol. Ther. (1981) [Pubmed]
  20. STAND, a class of P-loop NTPases including animal and plant regulators of programmed cell death: multiple, complex domain architectures, unusual phyletic patterns, and evolution by horizontal gene transfer. Leipe, D.D., Koonin, E.V., Aravind, L. J. Mol. Biol. (2004) [Pubmed]
  21. Multiple TPR motifs characterize the Fanconi anemia FANCG protein. Blom, E., van de Vrugt, H.J., de Vries, Y., de Winter, J.P., Arwert, F., Joenje, H. DNA Repair (Amst.) (2004) [Pubmed]
  22. Identification of tetratricopeptide repeat 1 as an adaptor protein that interacts with heterotrimeric G proteins and the small GTPase Ras. Marty, C., Browning, D.D., Ye, R.D. Mol. Cell. Biol. (2003) [Pubmed]
  23. HSF1-TPR interaction facilitates export of stress-induced HSP70 mRNA. Skaggs, H.S., Xing, H., Wilkerson, D.C., Murphy, L.A., Hong, Y., Mayhew, C.N., Sarge, K.D. J. Biol. Chem. (2007) [Pubmed]
  24. Proximity of TPR and NTRK1 rearranging loci in human thyrocytes. Roccato, E., Bressan, P., Sabatella, G., Rumio, C., Vizzotto, L., Pierotti, M.A., Greco, A. Cancer Res. (2005) [Pubmed]
  25. Mutations in a gene encoding a novel SH3/TPR domain protein cause autosomal recessive Charcot-Marie-Tooth type 4C neuropathy. Senderek, J., Bergmann, C., Stendel, C., Kirfel, J., Verpoorten, N., De Jonghe, P., Timmerman, V., Chrast, R., Verheijen, M.H., Lemke, G., Battaloglu, E., Parman, Y., Erdem, S., Tan, E., Topaloglu, H., Hahn, A., Müller-Felber, W., Rizzuto, N., Fabrizi, G.M., Stuhrmann, M., Rudnik-Schöneborn, S., Züchner, S., Michael Schröder, J., Buchheim, E., Straub, V., Klepper, J., Huehne, K., Rautenstrauss, B., Büttner, R., Nelis, E., Zerres, K. Am. J. Hum. Genet. (2003) [Pubmed]
  26. Molecular cloning and expression of a transformation-sensitive human protein containing the TPR motif and sharing identity to the stress-inducible yeast protein STI1. Honoré, B., Leffers, H., Madsen, P., Rasmussen, H.H., Vandekerckhove, J., Celis, J.E. J. Biol. Chem. (1992) [Pubmed]
  27. Development of new vanadium-based oxide catalysts for decomposition of chlorinated aromatic pollutants. Cho, C.H., Ihm, S.K. Environ. Sci. Technol. (2002) [Pubmed]
  28. Acute effects of transcendental meditation on hemodynamic functioning in middle-aged adults. Barnes, V.A., Treiber, F.A., Turner, J.R., Davis, H., Strong, W.B. Psychosomatic medicine. (1999) [Pubmed]
WikiGenes - Universities