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Gene Review

Fbxo32  -  F-box protein 32

Mus musculus

Synonyms: 4833442G10Rik, AI430017, ATROGIN1, Atrogin-1, F-box only protein 32, ...
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Disease relevance of Fbxo32


High impact information on Fbxo32


Chemical compound and disease context of Fbxo32

  • Muscle atrophy after 4 d of high-dose dexamethasone was associated with increased mRNA of enzymes involved in proteolytic pathways (atrogin-1, muscle ring finger 1, and cathepsin L) and increased chymotrypsin-like proteasomal activity [7].

Biological context of Fbxo32


Anatomical context of Fbxo32

  • FOXO3a transduction activated the atrogin-1 promoter in both cultured myocytes and mouse heart [10].
  • In cardiac myocyte cultures, transduction with constitutively active Akt or treatment with IGF suppressed atrogin-1 mRNA expression, whereas transduction with FOXO3a stimulated its expression [10].

Associations of Fbxo32 with chemical compounds

  • MAFbx associates with MyoD through an inverted LXXLL motif located in a series of helical leucine-charged residue-rich domains [11].
  • Similarly, whereas dexamethasone increased atrogene expression, pretreatment with the glucocorticoid receptor antagonist RU-486 failed to ameliorate the sepsis-induced increase in atrogin-1 and MuRF1 [12].
  • We investigated the differential expression of atrogin-1 and FBXO25 in fasted and dexamethasone-treated mice and also in rats with streptozotocin-induced diabetes [13].
  • We also demonstrate that mRNA levels of the ubiquitin ligases atrogin-1 and muscle ring finger-1 are upregulated in angiotensin II-infused WT, but not in IGF-1-transgenic, mice [14].

Physical interactions of Fbxo32

  • A core LXXLL motif sequence in MyoD is necessary for binding to MAFbx [11].

Regulatory relationships of Fbxo32


Other interactions of Fbxo32


Analytical, diagnostic and therapeutic context of Fbxo32

  • Furthermore, in transgenic mice overexpressing PGC-1alpha, denervation and fasting caused a much smaller decrease in muscle fiber diameter and a smaller induction of atrogin-1 and MuRF-1 than in control mice [8].
  • Additionally, peritonitis produced by cecal ligation and puncture increased atrogin-1 and MuRF1 mRNA in gastrocnemius (but not soleus or heart) by 8 h, which was sustained for 72 and 24 h, respectively [12].
  • Using a RT-PCR, we demonstrated that FBXO25 is highly expressed in brain, kidney, and intestine, whereas atrogin-1 expression is largely restricted to striate muscle [13].


  1. TNF-alpha acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle. Li, Y.P., Chen, Y., John, J., Moylan, J., Jin, B., Mann, D.L., Reid, M.B. FASEB J. (2005) [Pubmed]
  2. Atrogin-1/muscle atrophy F-box inhibits calcineurin-dependent cardiac hypertrophy by participating in an SCF ubiquitin ligase complex. Li, H.H., Kedar, V., Zhang, C., McDonough, H., Arya, R., Wang, D.Z., Patterson, C. J. Clin. Invest. (2004) [Pubmed]
  3. Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy. Gomes, M.D., Lecker, S.H., Jagoe, R.T., Navon, A., Goldberg, A.L. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  4. Tumor necrosis factor-alpha gene transfer induces cachexia and inhibits muscle regeneration. Coletti, D., Moresi, V., Adamo, S., Molinaro, M., Sassoon, D. Genesis (2005) [Pubmed]
  5. Atrogin-1 inhibits Akt-dependent cardiac hypertrophy in mice via ubiquitin-dependent coactivation of Forkhead proteins. Li, H.H., Willis, M.S., Lockyer, P., Miller, N., McDonough, H., Glass, D.J., Patterson, C. J. Clin. Invest. (2007) [Pubmed]
  6. Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy. Sandri, M., Sandri, C., Gilbert, A., Skurk, C., Calabria, E., Picard, A., Walsh, K., Schiaffino, S., Lecker, S.H., Goldberg, A.L. Cell (2004) [Pubmed]
  7. Myostatin gene deletion prevents glucocorticoid-induced muscle atrophy. Gilson, H., Schakman, O., Combaret, L., Lause, P., Grobet, L., Attaix, D., Ketelslegers, J.M., Thissen, J.P. Endocrinology (2007) [Pubmed]
  8. PGC-1{alpha} protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. Sandri, M., Lin, J., Handschin, C., Yang, W., Arany, Z.P., Lecker, S.H., Goldberg, A.L., Spiegelman, B.M. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  9. Structure and function of the upstream promotor of the human Mafbx gene: the proximal upstream promotor modulates tissue-specificity. Zhao, W., Wu, Y., Zhao, J., Guo, S., Bauman, W.A., Cardozo, C.P. J. Cell. Biochem. (2005) [Pubmed]
  10. The FOXO3a transcription factor regulates cardiac myocyte size downstream of AKT signaling. Skurk, C., Izumiya, Y., Maatz, H., Razeghi, P., Shiojima, I., Sandri, M., Sato, K., Zeng, L., Schiekofer, S., Pimentel, D., Lecker, S., Taegtmeyer, H., Goldberg, A.L., Walsh, K. J. Biol. Chem. (2005) [Pubmed]
  11. Degradation of MyoD mediated by the SCF (MAFbx) ubiquitin ligase. Tintignac, L.A., Lagirand, J., Batonnet, S., Sirri, V., Leibovitch, M.P., Leibovitch, S.A. J. Biol. Chem. (2005) [Pubmed]
  12. Hormone, cytokine, and nutritional regulation of sepsis-induced increases in atrogin-1 and MuRF1 in skeletal muscle. Frost, R.A., Nystrom, G.J., Jefferson, L.S., Lang, C.H. Am. J. Physiol. Endocrinol. Metab. (2007) [Pubmed]
  13. FBXO25, an F-box protein homologue of atrogin-1, is not induced in atrophying muscle. Maragno, A.L., Baqui, M.M., Gomes, M.D. Biochim. Biophys. Acta (2006) [Pubmed]
  14. Muscle-specific expression of IGF-1 blocks angiotensin II-induced skeletal muscle wasting. Song, Y.H., Li, Y., Du, J., Mitch, W.E., Rosenthal, N., Delafontaine, P. J. Clin. Invest. (2005) [Pubmed]
  15. Quantification of hormone-induced atrophy of large myotubes from C2C12 and L6 cells: atrophy-inducible and atrophy-resistant C2C12 myotubes. Sultan, K.R., Henkel, B., Terlou, M., Haagsman, H.P. Am. J. Physiol., Cell Physiol. (2006) [Pubmed]
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