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

TRIM63  -  tripartite motif containing 63, E3...

Homo sapiens

Synonyms: E3 ubiquitin-protein ligase TRIM63, IRF, Iris RING finger protein, MURF-1, MURF1, ...
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 TRIM63


Psychiatry related information on TRIM63

  • The IRF also showed the fewest significant differences between the means of the estimated MMPI scale scores and those that actually were obtained [6].

High impact information on TRIM63

  • Expression of the E3 ligase MuRF1, a mediator of muscle atrophy, was increased in MIKK mice [7].
  • Maxicircle-encoded guide RNAs (gRNAs) for cytochrome b and maxicircle unidentified reading frames 2 and 3 (MURF2 and MURF3) were isolated by hybrid selection and sequenced [8].
  • Uridine additions and deletions in the 5' ends of the COIII, MURF2, and MURF3 transcripts create new N-terminal amino acid sequences that are conserved between species, and new AUG initiation codons in several cases [9].
  • Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy [10].
  • This perspective will focus on the signalling pathways that control skeletal muscle atrophy and hypertrophy, including the recently identified ubiquitin ligases muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx), as a basis to develop targets for pharmacologic intervention in muscle disease [11].

Biological context of TRIM63


Anatomical context of TRIM63

  • To investigate the functional significance of this interaction, we expressed green fluorescent protein fusion constructs encoding defined fragments of titin's M-line region and MURF-1 in cardiac myocytes [12].
  • Consistent with our in vitro binding data implicating MURF-1 with nuclear functions, endogenous MURF-1 also was detected in the nuclei of some myocytes [12].
  • Functional properties of the titin/connectin-associated proteins, the muscle-specific RING finger proteins (MURFs), in striated muscle [2].
  • MURF-2 is developmentally down-regulated and is assembled at the M-line region of the sarcomere and with microtubules [2].
  • MuRF1 reduced steady-state troponin I levels when coexpressed in COS-7 cells and increased degradation of endogenous troponin I protein in cardiomyocytes [14].

Associations of TRIM63 with chemical compounds

  • Changes in overall proteolysis with Dex and IGF-I correlated tightly with changes in atrogin-1 mRNA content, but not with changes in MuRF1 mRNA [15].
  • Finally, administration of the glucocorticoid receptor antagonist RU-486 did not prevent burn-induced atrophy of the gastrocnemius or the associated elevation in atrogin-1, MuRF-1, or polyUb [16].
  • Insulin and insulin-like growth factor-1 act through the phosphoinositide 3-kinase/AKT pathway to suppress the expression of two of these enzymes, MuRF1 and MAFbx/atrogin-1 [17].
  • Thus, under in vivo conditions in mature adult rats, the sepsis-induced increase in muscle atrogin-1 and MuRF1 mRNA appears both glucocorticoid and TNF independent and is unresponsive to leucine [4].
  • The aim of this study was to examine the effect of polyethylene glycol linked to soluble TNFRI (PEG-sTNFRI) on gene expression of the atrogens MuRF-1 and MAFbx in skeletal muscle of arthritic rats [18].

Regulatory relationships of TRIM63

  • Four hours after administration of the anabolic agent insulin-like growth factor (IGF)-I to burned rats, the mRNA content of atrogin-1 and polyUb in gastrocnemius had returned to control values and the elevation in MuRF-1 was reduced 50% [16].

Other interactions of TRIM63

  • Cell culture studies suggest that MURF-1 specifically has a role in maintaining titin M-line integrity and yeast two-hybrid studies point toward its participation in muscle stress response pathways and gene expression [2].
  • Therefore, IGF-1/Akt and TNFalpha represent potential mediators implicated in the regulation of MuRF1 and atrogin-1 genes during aging [19].
  • This response occurred despite fully blunting the increases in the mRNA for of atrogin-1, MURF-1, and myostatin, e.g., sensitive gene markers of an activated catabolic state [20].
  • The gene expression and activity of calpains and the muscle wasting-associated ubiquitin ligases, atrogin-1 and MuRF1, are not altered in patients with primary hyperparathyroidism [21].
  • Genes, found in this region, include 12S and 9S ribosomal RNAs, subunits 7, 8 and 9 of NADH dehydrogenase (ND7, ND8 and ND9) and subunit 6 of ATPase (A6 or MURF4), as well as the genes (MURF1, MURF5 and G3) with unknown function [22].

Analytical, diagnostic and therapeutic context of TRIM63

  • Northern blots demonstrated that SMRZ is expressed exclusively in striated muscle [13].
  • 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 [23].
  • After 48 h of burn injury (40% total body surface area full-thickness scald burn) gastrocnemius weight was reduced, and this change was associated with an increased mRNA abundance for atrogin-1 and MuRF-1 (3.1- to 8-fold, respectively) [16].
  • A biopsy was obtained from the sternohyoid muscle in patients undergoing surgery for primary HPT (n=8) and in normocalcemic control patients undergoing thyroid surgery (n=11). mRNA levels for atrogin-1, MuRF1 and the calcium-regulated proteases, mu- and m-calpain, were determined by real-time PCR [21].
  • The expression of MAFbx/Murf-1 and troponin I was analyzed by RT-PCR and Western blotting in the non-infarcted area of the left ventricle [24].


  1. Akt signalling through GSK-3{beta}, mTOR and Foxo1 is involved in human skeletal muscle hypertrophy and atrophy. L??ger, B., Cartoni, R., Praz, M., Lamon, S., D??riaz, O., Crettenand, A., Gobelet, C., Rohmer, P., Konzelmann, M., Luthi, F., Russell, A.P. J. Physiol. (Lond.) (2006) [Pubmed]
  2. Functional properties of the titin/connectin-associated proteins, the muscle-specific RING finger proteins (MURFs), in striated muscle. Gregorio, C.C., Perry, C.N., McElhinny, A.S. J. Muscle Res. Cell. Motil. (2005) [Pubmed]
  3. Into the heart: The emerging role of the ubiquitin-proteasome system. Willis, M.S., Patterson, C. J. Mol. Cell. Cardiol. (2006) [Pubmed]
  4. 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]
  5. Viral interferon regulatory factor 1 of Kaposi's sarcoma-associated herpesvirus interacts with a cell death regulator, GRIM19, and inhibits interferon/retinoic acid-induced cell death. Seo, T., Lee, D., Shim, Y.S., Angell, J.E., Chidambaram, N.V., Kalvakolanu, D.V., Choe, J. J. Virol. (2002) [Pubmed]
  6. The utility of an improved readability short form of the MMPI with elderly male patients. Ward, L.C., Meyers, R. Journal of clinical psychology. (1984) [Pubmed]
  7. IKKbeta/NF-kappaB activation causes severe muscle wasting in mice. Cai, D., Frantz, J.D., Tawa, N.E., Melendez, P.A., Oh, B.C., Lidov, H.G., Hasselgren, P.O., Frontera, W.R., Lee, J., Glass, D.J., Shoelson, S.E. Cell (2004) [Pubmed]
  8. Guide RNAs in kinetoplastid mitochondria have a nonencoded 3' oligo(U) tail involved in recognition of the preedited region. Blum, B., Simpson, L. Cell (1990) [Pubmed]
  9. Editing of kinetoplastid mitochondrial mRNAs by uridine addition and deletion generates conserved amino acid sequences and AUG initiation codons. Shaw, J.M., Feagin, J.E., Stuart, K., Simpson, L. Cell (1988) [Pubmed]
  10. Identification of ubiquitin ligases required for skeletal muscle atrophy. Bodine, S.C., Latres, E., Baumhueter, S., Lai, V.K., Nunez, L., Clarke, B.A., Poueymirou, W.T., Panaro, F.J., Na, E., Dharmarajan, K., Pan, Z.Q., Valenzuela, D.M., DeChiara, T.M., Stitt, T.N., Yancopoulos, G.D., Glass, D.J. Science (2001) [Pubmed]
  11. Signalling pathways that mediate skeletal muscle hypertrophy and atrophy. Glass, D.J. Nat. Cell Biol. (2003) [Pubmed]
  12. Muscle-specific RING finger-1 interacts with titin to regulate sarcomeric M-line and thick filament structure and may have nuclear functions via its interaction with glucocorticoid modulatory element binding protein-1. McElhinny, A.S., Kakinuma, K., Sorimachi, H., Labeit, S., Gregorio, C.C. J. Cell Biol. (2002) [Pubmed]
  13. A novel human striated muscle RING zinc finger protein, SMRZ, interacts with SMT3b via its RING domain. Dai, K.S., Liew, C.C. J. Biol. Chem. (2001) [Pubmed]
  14. Muscle-specific RING finger 1 is a bona fide ubiquitin ligase that degrades cardiac troponin I. Kedar, V., McDonough, H., Arya, R., Li, H.H., Rockman, H.A., Patterson, C. Proc. Natl. Acad. Sci. U.S.A. (2004) [Pubmed]
  15. IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1. Sacheck, J.M., Ohtsuka, A., McLary, S.C., Goldberg, A.L. Am. J. Physiol. Endocrinol. Metab. (2004) [Pubmed]
  16. Burn-induced increase in atrogin-1 and MuRF-1 in skeletal muscle is glucocorticoid independent but downregulated by IGF-I. Lang, C.H., Huber, D., Frost, R.A. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2007) [Pubmed]
  17. Molecular signaling pathways regulating muscle proteolysis during atrophy. Franch, H.A., Price, S.R. Current opinion in clinical nutrition and metabolic care. (2005) [Pubmed]
  18. Tumour necrosis factor blockade did not prevent the increase of muscular muscle RING finger-1 and muscle atrophy F-box in arthritic rats. Granado, M., Mart??n, A.I., Priego, T., L??pez-Calder??n, A., Villan??a, M.A. J. Endocrinol. (2006) [Pubmed]
  19. Atrophy-related ubiquitin ligases, atrogin-1 and MuRF1 are up-regulated in aged rat Tibialis Anterior muscle. Clavel, S., Coldefy, A.S., Kurkdjian, E., Salles, J., Margaritis, I., Derijard, B. Mech. Ageing Dev. (2006) [Pubmed]
  20. Isometric resistance exercise fails to counteract skeletal muscle atrophy processes during the initial stages of unloading. Haddad, F., Adams, G.R., Bodell, P.W., Baldwin, K.M. J. Appl. Physiol. (2006) [Pubmed]
  21. The gene expression and activity of calpains and the muscle wasting-associated ubiquitin ligases, atrogin-1 and MuRF1, are not altered in patients with primary hyperparathyroidism. Evenson, A., Mitchell, J., Wei, W., Poylin, V., Parangi, S., Hasselgren, P.O. Int. J. Mol. Med. (2006) [Pubmed]
  22. Partial kinetoplast-mitochondrial gene organization and expression in the respiratory deficient plant trypanosomatid Phytomonas serpens. Maslov, D.A., Nawathean, P., Scheel, J. Mol. Biochem. Parasitol. (1999) [Pubmed]
  23. 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]
  24. Myocardial expression of Murf-1 and MAFbx after induction of chronic heart failure: Effect on myocardial contractility. Adams, V., Linke, A., Wisloff, U., D??ring, C., Erbs, S., Kr??nkel, N., Witt, C.C., Labeit, S., M??ller-Werdan, U., Schuler, G., Hambrecht, R. Cardiovasc. Res. (2007) [Pubmed]
WikiGenes - Universities