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Gene Review

Mtpn  -  myotrophin

Rattus norvegicus

Synonyms: Gcdp, Granule cell differentiation protein, Myotrophin, Protein V-1
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Disease relevance of Mtpn

  • To investigate the physiological role of this protein, we examined the effect of V-1 overexpression on cell toxicity induced by nitric oxide (NO) used at low concentrations [1].
  • To define the characteristics of each transcript and its pathophysiological significance, we examined transcripts of myotrophin in SHR heart during progression of hypertrophy [2].
  • Our data strongly suggest that myotrophin appears to be a candidate gene for cardiac hypertrophy and heart failure [2].
  • The gene encoding myotrophin has been cloned and expressed in E. coli [2].
  • It is also suggested that V-1 expression is increased by hypertension in DS rat atrium [3].
  • Myotrophin-induced myocyte growth and initiation of hypertrophy thus require nuclear co-translocation of myotrophin and p65, in a manner that depends crucially on the myotrophin hairpin loops [4].

Psychiatry related information on Mtpn


High impact information on Mtpn


Biological context of Mtpn

  • Taken together, these results indicate that V1 protein plays an important role in protection against cell death induced by NO at low levels by promoting the synthesis of BH(4) [1].
  • Moreover, these findings suggest the up-regulation of V1 expression as a possible therapeutic target for protection against the insult of NO-induced oxidative stress [1].
  • Equilibrium folding and stability of myotrophin: a model ankyrin repeat protein [7].
  • V-1 acts as a positive and coordinate regulator of gene expression of catecholamine biosynthetic enzymes in PC12D cells [8].
  • Recently, myotrophin gene has been mapped and shown to be a novel gene localized in human chromosome 7q-33 [2].

Anatomical context of Mtpn


Associations of Mtpn with chemical compounds

  • Overexpression of V-1 prevents nitric oxide-induced cell death: involvement of enhanced tetrahydrobiopterin biosynthesis [1].
  • High K(+)-induced dopamine secretion in V-1 overexpressing clones was shown to be markedly potentiated compared with control clones carried with a vector alone [11].
  • Western blotting showed that in cultured bovine adrenal medullary cells, dexamethasone, a synthetic glucocorticoid, inhibited expression of V-1, and that this inhibition was prevented by RU-486, a glucocorticoid receptor antagonist [8].
  • Genistein attenuated the [3H]leucine incorporation induced by myotrophin [6].
  • The effect of myotrophin on the stimulation of PKC activity and [3H]leucine incorporation was abolished by pretreatment with either staurosporine or H-7, two selective, pharmacological PKC inhibitors [6].

Other interactions of Mtpn

  • The increased BH(4) synthesis by V-1 overexpression was dose dependently inhibited by pretreatment with diaminohydroxypyrimidine (DAHP), an inhibitor of GTP-cyclohydrolase I, which is the rate-limiting enzyme for the biosynthesis of BH(4), concomitantly with the loss of protective effect afforded by V-1 overexpression [1].
  • Our data showed that both cyclic stretch and exposure to high pressure caused significant increase in the transcript levels of myotrophin followed by expression of beta-myosin heavy chain and atrial natriuretic factor associated with an increase in myocardial protein synthesis [12].
  • Neuronal activity and neurotrophic factors, known to be involved in granule cell differentiation, are major physiologic regulators of CREB function [13].
  • The results demonstrate that a dramatic increase in the tonic NMDA receptor-channel activity occurs during the stages of granule cell differentiation, migration and synaptogenesis, which is driven by endogenous glutamate release and regulated by NMDA receptor density and local glutamate uptake [14].

Analytical, diagnostic and therapeutic context of Mtpn

  • Northern blot analysis of myotrophin mRNA showed multiple transcripts [2].
  • One of the proteins, V-1, was isolated using a liquid-chromatography system, and its amino acid sequence was determined by analysis of the purified protein [15].
  • V-1 expression was shown to be increased in the atrial myocytes of these DS rats, but not in the sympathetic axons, when assayed by immunohistochemistry [3].
  • Our successive studies were conducted to evaluate the pathophysiological significance of myotrophin; a solid-phase radioimmunoassay technique was developed for quantifying the protein in hypertrophied and normal hearts [16].
  • As measured in the behaviorally tested rats, antisense treatment resulted in a reduced binding of radiolabeled AVP in the septum, but not in other limbic brain areas (receptor autoradiography), and an increased amount of V1 receptor mRNA (reverse transcriptase PCR), indicating translational arrest and ongoing transcriptional activity [5].


  1. Overexpression of V-1 prevents nitric oxide-induced cell death: involvement of enhanced tetrahydrobiopterin biosynthesis. Yuyama, K., Yamamoto, H., Nakamura, K., Nishizaki, I., Yamakuni, T., Song, S.Y., Sora, I., Nagatsu, T., Yamamoto, T. J. Neurosci. Res. (2003) [Pubmed]
  2. Characterization and functional significance of myotrophin: a gene with multiple transcripts. Adhikary, G., Gupta, S., Sil, P., Saad, Y., Sen, S. Gene (2005) [Pubmed]
  3. Expression of V-1, a novel catecholamine biosynthesis regulatory protein, is enhanced by hypertension in atrial myocytes of Dahl salt-sensitive rats. Yamakuni, T., Hashimoto, M., Sakagami, H., Yamamoto, T., Kobayashi, M., Fujii, Y., Yamamoto, H., Rohra, D.K., Hiwatashi, Y., Honma, T., Kondo, H., Shido, O., Ohizumi, Y. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  4. Nuclear co-translocation of myotrophin and p65 stimulates myocyte growth. Regulation by myotrophin hairpin loops. Das, B., Gupta, S., Vasanji, A., Xu, Z., Misra, S., Sen, S. J. Biol. Chem. (2008) [Pubmed]
  5. V1 vasopressin receptor antisense oligodeoxynucleotide into septum reduces vasopressin binding, social discrimination abilities, and anxiety-related behavior in rats. Landgraf, R., Gerstberger, R., Montkowski, A., Probst, J.C., Wotjak, C.T., Holsboer, F., Engelmann, M. J. Neurosci. (1995) [Pubmed]
  6. Increased protein kinase C activity in myotrophin-induced myocyte growth. Sil, P., Kandaswamy, V., Sen, S. Circ. Res. (1998) [Pubmed]
  7. Equilibrium folding and stability of myotrophin: a model ankyrin repeat protein. Mosavi, L.K., Williams, S., Peng Zy, Z.Y. J. Mol. Biol. (2002) [Pubmed]
  8. Glucocorticoid inhibits expression of V-1, a catecholamine biosynthesis regulatory protein, in cultured adrenal medullary cells. Hiwatashi, Y., Kurahashi, Y., Hatada, R., Ueno, S., Honma, T., Yanagihara, N., Yanase, H., Iwanaga, T., Ohizumi, Y., Yamakuni, T. FEBS Lett. (2002) [Pubmed]
  9. Nuclear magnetic resonance assignment and secondary structure of an ankyrin-like repeat-bearing protein: myotrophin. Yang, Y., Rao, N.S., Walker, E., Sen, S., Qin, J. Protein Sci. (1997) [Pubmed]
  10. Down-regulation of an ankyrin repeat-containing protein, V-1, during skeletal muscle differentiation and its re-expression in the regenerative process of muscular dystrophy. Furukawa, Y., Hashimoto, N., Yamakuni, T., Ishida, Y., Kato, C., Ogashiwa, M., Kobayashi, M., Kobayashi, T., Nonaka, I., Mizusawa, H., Song, S.Y. Neuromuscul. Disord. (2003) [Pubmed]
  11. V-1, a catecholamine biosynthesis regulatory protein, positively controls catecholamine secretion in PC12D cells. Yamakuni, T., Yamamoto, T., Ishida, Y., Yamamoto, H., Song, S.Y., Adachi, E., Hiwatashi, Y., Ohizumi, Y. FEBS Lett. (2002) [Pubmed]
  12. Regulation of myotrophin gene by pressure overload and stretch. Sil, P., Gupta, S., Young, D., Sen, S. Mol. Cell. Biochem. (2004) [Pubmed]
  13. Enhanced CREB phosphorylation in immature dentate gyrus granule cells precedes neurotrophin expression and indicates a specific role of CREB in granule cell differentiation. Bender, R.A., Lauterborn, J.C., Gall, C.M., Cariaga, W., Baram, T.Z. Eur. J. Neurosci. (2001) [Pubmed]
  14. The developmental onset of NMDA receptor-channel activity during neuronal migration. Rossi, D.J., Slater, N.T. Neuropharmacology (1993) [Pubmed]
  15. A rat cerebellar protein containing the cdc10/SWI6 motif. Taoka, M., Yamakuni, T., Song, S.Y., Yamakawa, Y., Seta, K., Okuyama, T., Isobe, T. Eur. J. Biochem. (1992) [Pubmed]
  16. Quantification of myotrophin from spontaneously hypertensive and normal rat hearts. Sil, P., Mukherjee, D., Sen, S. Circ. Res. (1995) [Pubmed]
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