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Gene Review

Tnpo1  -  transportin 1

Mus musculus

Synonyms: AU021749, D13Ertd688e, IPO2, Importin beta-2, Karyopherin beta-2, ...
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Disease relevance of Tnpo1

  • To understand this discrepancy, we compared a local tumor model with a metastatic one using MIP-1 alpha-transfected B16 F10 melanoma cells [1].
  • HIV-1 protease, while the trigger of cataract formation, does not appear to be the protease responsible for cleavage of MIP or lens crystallins [2].
  • In contrast, IL-1 (0.1 to 2.5 ng/ml), IFN-gamma (10 micrograms/ml), and IL-10 (2.5 to 10 ng/ml) were able to induce the significant production of MIP-1 by the granuloma fibroblasts [3].
  • PURPOSE: Three different lens fiber cell intrinsic membrane proteins, MIP (Major Intrinsic Protein), MP19, and connexin50 (Cx50), have separately been implicated as causative candidates for congenital cataracts [4].
  • CD8+ cell-secreted CC-chemokines, MIP-1alpha, and MIP-beta have recently been identified as factors which suppress HIV [5].

High impact information on Tnpo1

  • These results suggest that TGF-beta may be capable of interfering with MIP-1 alpha's role as a stem cell inhibitor [6].
  • Comparison of this MIP-1 beta cDNA with our previously cloned MIP-1 alpha sequence reveals that the MIP-1 peptides, members of a growing family of potential inflammatory mediators, are distinct but highly homologous (58.9% sequence identity) products of different genes [7].
  • We recently reported the isolation of a novel monokine, macrophage inflammatory protein 1 (MIP-1), which causes local inflammatory responses in vivo, and induces superoxide production by neutrophils in vitro [7].
  • Furthermore, F-peptide phosphorylation modulates the interaction of hnRNP A1 with transportin Trn1 [8].
  • We demonstrate that PA is a potent activator of the inflammatory chemokines MIP (macrophage inflammatory protein)-1 alpha and MIP-1 beta (MIPs) mRNA expression in mouse macrophages in a dose- and time-dependent fashion and through a de novo protein synthesis-dependent process [9].

Biological context of Tnpo1

  • By contrast to these apparent "macrophage activating" properties of MIP 1, the cytokine failed to trigger the macrophage oxidative burst, or to up-regulate the expression of Ia on the macrophage surface [10].
  • These studies demonstrated constitutive expression of MCP-1 and differential up-regulation of MIP-1 on cytokine stimulation [3].
  • The mRNA levels of gamma E- and/or gamma F-crystallin and MIP, markers of lens cell differentiation, are drastically reduced, while expression of ICSBP, a gamma IFN-inducible transcriptional factor, is induced in the alpha ACry-gamma IFN transgenic mouse eyes [11].
  • METHODS: Study interaction of factors present in newborn mouse lens nuclear extracts with DNA fragments corresponding to mouse MIP gene 5' flanking sequence by electrophoresis mobility shift assay (EMSA) and DNase I footprinting [12].
  • Cross reaction of antibodies against liver gap junction protein (26K) with lens fiber junction protein (MIP) suggests structural homology between these tissue specific gene products [13].

Anatomical context of Tnpo1

  • MIP 1 treatment stimulated proliferation of mature tissue macrophages, and this effect was enhanced upon costimulations with either CSF-1 or granulocyte-macrophage-CSF [10].
  • Interestingly, normal noninflammatory fibroblasts from uninfected mice showed no significant production of MIP-1 or MCP-1 in response to these cytokines [3].
  • Thioglycollate-elicited peritoneal exudate macrophages incubated with native doublet MIP 1-secreted bioactive TNF and IL-6, as well as immunoreactive IL-1 alpha, and these effects were enhanced significantly when the cells were costimulated with IFN-gamma [10].
  • The expression of FGF-3 in the lens rapidly induced epithelial cells throughout the lens to elongate and to express fiber cell-specific proteins including MIP and beta-crystallins [14].
  • The role of MIP in lens fiber cell membrane transport [15].

Associations of Tnpo1 with chemical compounds

  • We report here the resolution of MIP-1 into component peptides by SDS-hydroxylapatite chromatography, and compare the NH2-terminal sequences of the two peptides, now referred to as MIP-1 alpha and MIP-1 beta [7].
  • Macrophage inflammatory protein 1 (MIP 1), initially purified from the conditioned medium of endotoxin-stimulated macrophages, is a low m.w. heparin-binding protein doublet comprising two peptides, MIP 1 alpha and MIP 1 beta [10].
  • Pretreatment with LPS or addition of MIP-1 inhibited the in vitro migration of ESb-MP cells toward various chemokines [16].
  • MIP has been hypothesized to be a gap junction protein, a membrane ion channel, a membrane water channel and a facilitator of glycerol transport and metabolism [15].
  • Finally, PGE inhibits PMA and IFN-gamma-induced JE and MIP-1-related mRNA expression [17].

Other interactions of Tnpo1

  • Macrophage inflammatory proteins MIP-1 and MIP-2 are involved in T cell-mediated neutrophil recruitment [18].
  • Expression levels of IL-1beta, interferon-gamma inducible protein, macrophage inflammatory protein-1 (MIP-1) alpha, and MIP-1beta genes were 10- to 17-fold higher on day 5 after transplantation in C57BL/6 grafts on C57BL/6-presensitized recipients than in C57BL/6 grafts on unprimed recipients [19].
  • This study examines the appearance of messenger RNA (mRNA) for cachectin/tumor necrosis factor (TNF), IL 1, and macrophage inflammatory proteins 1 and 2 (MIP-1 and MIP-2), as well as the mature peptides, in a model of wound healing using wound chambers [20].
  • Tagged prothymosin alpha shared domains with mobile proteins such as Ran, transportin, and karyopherin beta, which also traverse the nuclear membrane, and co-localized with active RNA polymerase II [21].
  • We have identified a novel CC chemokine family member, herein termed MIP-1 gamma in view of its similarity to existing members of the MIP-1 group [22].

Analytical, diagnostic and therapeutic context of Tnpo1

  • Flow cytometry showed a significant increase in CD8(+) cells in lungs of mice with MIP-1 alpha-transfected tumors 3 days after injection [1].
  • RESULTS: Examination of protein expression in c-Maf homozygous mutant mice revealed undetectable levels of CP49, CP115 and MIP protein. mRNA transcripts for these non-crystallin genes were observed at reduced levels in subsequent RT-PCR experiments [23].
  • However, Western blot analysis revealed that iNOS protein production by TRN was 2-fold lower than that produced by B6/J2 [24].


  1. Transfection of macrophage inflammatory protein 1 alpha into B16 F10 melanoma cells inhibits growth of pulmonary metastases but not subcutaneous tumors. van Deventer, H.W., Serody, J.S., McKinnon, K.P., Clements, C., Brickey, W.J., Ting, J.P. J. Immunol. (2002) [Pubmed]
  2. Cysteine protease activated by expression of HIV-1 protease in transgenic mice. MIP26 (aquaporin-0) cleavage and cataract formation in vivo and ex vivo. Mitton, K.P., Kamiya, T., Tumminia, S.J., Russell, P. J. Biol. Chem. (1996) [Pubmed]
  3. Production of monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha by inflammatory granuloma fibroblasts. Lukacs, N.W., Chensue, S.W., Smith, R.E., Strieter, R.M., Warmington, K., Wilke, C., Kunkel, S.L. Am. J. Pathol. (1994) [Pubmed]
  4. Temporal expression of three mouse lens fiber cell membrane protein genes during early development. Zhou, L., Chen, T., Church, R.L. Mol. Vis. (2002) [Pubmed]
  5. Macrophage inflammatory protein-1alpha (MIP-1alpha) expression plasmid enhances DNA vaccine-induced immune response against HIV-1. Lu, Y., Xin, K.Q., Hamajima, K., Tsuji, T., Aoki, I., Yang, J., Sasaki, S., Fukushima, J., Yoshimura, T., Toda, S., Okada, E., Okuda, K. Clin. Exp. Immunol. (1999) [Pubmed]
  6. Transforming growth factor beta: is it a downregulator of stem cell inhibition by macrophage inflammatory protein 1 alpha? Maltman, J., Pragnell, I.B., Graham, G.J. J. Exp. Med. (1993) [Pubmed]
  7. Resolution of the two components of macrophage inflammatory protein 1, and cloning and characterization of one of those components, macrophage inflammatory protein 1 beta. Sherry, B., Tekamp-Olson, P., Gallegos, C., Bauer, D., Davatelis, G., Wolpe, S.D., Masiarz, F., Coit, D., Cerami, A. J. Exp. Med. (1988) [Pubmed]
  8. Regulation of heterogenous nuclear ribonucleoprotein A1 transport by phosphorylation in cells stressed by osmotic shock. Allemand, E., Guil, S., Myers, M., Moscat, J., Cáceres, J.F., Krainer, A.R. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  9. The tryptophan catabolite picolinic acid selectively induces the chemokines macrophage inflammatory protein-1 alpha and -1 beta in macrophages. Bosco, M.C., Rapisarda, A., Massazza, S., Melillo, G., Young, H., Varesio, L. J. Immunol. (2000) [Pubmed]
  10. Macrophage inflammatory protein 1 modulates macrophage function. Fahey, T.J., Tracey, K.J., Tekamp-Olson, P., Cousens, L.S., Jones, W.G., Shires, G.T., Cerami, A., Sherry, B. J. Immunol. (1992) [Pubmed]
  11. gamma Interferon expression disrupts lens and retinal differentiation in transgenic mice. Egwuagu, C.E., Sztein, J., Chan, C.C., Mahdi, R., Nussenblatt, R.B., Chepelinsky, A.B. Dev. Biol. (1994) [Pubmed]
  12. The transcription factor Sp3 interacts with promoter elements of the lens specific MIP gene. Kim, S., Ge, H., Ohtaka-Maruyama, C., Chepelinsky, A.B. Mol. Vis. (1999) [Pubmed]
  13. Cross reaction of antibodies against liver gap junction protein (26K) with lens fiber junction protein (MIP) suggests structural homology between these tissue specific gene products. Traub, O., Willecke, K. Biochem. Biophys. Res. Commun. (1982) [Pubmed]
  14. Disregulation of ocular morphogenesis by lens-specific expression of FGF-3/int-2 in transgenic mice. Robinson, M.L., Ohtaka-Maruyama, C., Chan, C.C., Jamieson, S., Dickson, C., Overbeek, P.A., Chepelinsky, A.B. Dev. Biol. (1998) [Pubmed]
  15. The role of MIP in lens fiber cell membrane transport. Varadaraj, K., Kushmerick, C., Baldo, G.J., Bassnett, S., Shiels, A., Mathias, R.T. J. Membr. Biol. (1999) [Pubmed]
  16. Role of the autocrine chemokines MIP-1alpha and MIP-1beta in the metastatic behavior of murine T cell lymphoma. Menten, P., Saccani, A., Dillen, C., Wuyts, A., Struyf, S., Proost, P., Mantovani, A., Wang, J.M., Van Damme, J. J. Leukoc. Biol. (2002) [Pubmed]
  17. Differential regulation of interleukin-6, macrophage inflammatory protein-1, and JE/MCP-1 cytokine expression in macrophage cell lines. Martin, C.A., Dorf, M.E. Cell. Immunol. (1991) [Pubmed]
  18. Macrophage inflammatory proteins MIP-1 and MIP-2 are involved in T cell-mediated neutrophil recruitment. Appelberg, R. J. Leukoc. Biol. (1992) [Pubmed]
  19. T cell-dependent acceleration of chemoattractant cytokine gene expression during secondary rejection of allogeneic skin grafts. Kondo, T., Watarai, Y., Novick, A.C., Toma, H., Fairchild, R.L. Transplantation (1997) [Pubmed]
  20. Cytokine production in a model of wound healing: the appearance of MIP-1, MIP-2, cachectin/TNF and IL-1. Fahey, T.J., Sherry, B., Tracey, K.J., van Deventer, S., Jones, W.G., Minei, J.P., Morgello, S., Shires, G.T., Cerami, A. Cytokine (1990) [Pubmed]
  21. Mobility within the nucleus and neighboring cytosol is a key feature of prothymosin-alpha. Enkemann, S.A., Ward, R.D., Berger, S.L. J. Histochem. Cytochem. (2000) [Pubmed]
  22. MIP-1 gamma: molecular cloning, expression, and biological activities of a novel CC chemokine that is constitutively secreted in vivo. Poltorak, A.N., Bazzoni, F., Smirnova, I.I., Alejos, E., Thompson, P., Luheshi, G., Rothwell, N., Beutler, B. J. Inflamm. (1995) [Pubmed]
  23. Analysis of non-crystallin lens fiber cell gene expression in c-Maf -/- mice. DePianto, D.J., Blankenship, T.N., Hess, J.F., FitzGerald, P.G. Mol. Vis. (2003) [Pubmed]
  24. LPS stimulation of TNF-receptor deficient macrophages: a differential role for TNF-alpha autocrine signaling in the induction of cytokine and nitric oxide production. Clemons-Miller, A.R., Cox, G.W., Suttles, J., Stout, R.D. Immunobiology (2000) [Pubmed]
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