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Tripartite motif containing 55

MuRF2, tripartite motif-containing 55, TRIM55
The protein encoded by this gene contains a RING zinc finger, a motif known to be involved in protein-protein interactions. This protein associates transiently with microtubules, myosin, and titin during muscle sarcomere assembly. It may act as a transient adaptor and plays a regulatory role in the assembly of sarcomeres. Four alternatively spliced transcript variants encoding distinct isoforms have been described. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: IRF, MURF3, Ubiquitin, HAD, titin
Papers on MuRF2
Kinetoplast adaptations in American strains from Trypanosoma vivax.
Alvarez-Valin et al., Montevideo, Uruguay. In Mutat Res, Mar 2015
Moreover, all but three genes (A6-ATPase, RPS12 and MURF2) are not edited in the American strains, whereas editing takes place normally in all (editable) genes from the African strain.
Induction of Ankrd1 in Dilated Cardiomyopathy Correlates with the Heart Failure Progression.
Labeit et al., Mannheim, Germany. In Biomed Res Int, 2014
Expression patterns of 8 mechanoptotic machinery-associated titin ligands (ANKRD1, ANKRD2, TRIM63, TRIM55, NBR1, MLP, FHL2, and TCAP) were quantitated in endomyocardial biopsies from 25 patients with advanced IDCM.
MuRF2 regulates PPARγ1 activity to protect against diabetic cardiomyopathy and enhance weight gain induced by a high fat diet.
Willis et al., Chapel Hill, United States. In Cardiovasc Diabetol, 2014
Recent studies have implicated the muscle-specific ubiquitin ligase muscle ring finger-2 (MuRF2) in inhibiting the nuclear transcription factor SRF. Initial studies of MuRF2-/- hearts revealed enhanced PPAR activity, leading to the hypothesis that MuRF2 regulates PPAR activity by post-translational ubiquitination.
Muscle ring finger-3 protects against diabetic cardiomyopathy induced by a high fat diet.
Willis et al., Chapel Hill, United States. In Bmc Endocr Disord, 2014
We recently identified that muscle ring finger-1 (MuRF1) and MuRF2 differentially inhibit PPAR activities by mono-ubiquitination, leading to the hypothesis that MuRF3 may regulate PPAR activity in vivo to regulate DCM.
Disuse deterioration of human skeletal muscle challenged by resistive exercise superimposed with vibration: evidence from structural and proteomic analysis.
Blottner et al., Milano, Italy. In Faseb J, 2014
The aim was to analyze by confocal and electron microscopy the effects of vibration on myofibril and filament integrity in soleus (Sol) and vastus lateralis (VL) muscle; differential proteomics of contractile, cytoskeletal, and costameric proteins (TN-C, ROCK1, and FAK); and expression of PGC1α and atrophy-related master genes MuRF1 and MuRF2.
Dietary methionine availability affects the main factors involved in muscle protein turnover in rainbow trout (Oncorhynchus mykiss).
Seiliez et al., France. In Br J Nutr, 2014
Similarly, the mRNA levels of several proteasome-related genes (Fbx32, MuRF2, MuRF3, ZNF216 and Trim32) were significantly up-regulated by methionine limitation.
MuRF1 activity is present in cardiac mitochondria and regulates reactive oxygen species production in vivo.
Willis et al., Greenville, United States. In J Bioenerg Biomembr, 2014
The lack of mitochondrial function phenotype identified in MuRF1-/- hearts may be due to the overlapping interactions of MuRF1 and MuRF2 with energy regulating proteins found by yeast two-hybrid studies reported here, implying a duplicity in MuRF1 and MuRF2's regulation of mitochondrial function.
Titin kinase is an inactive pseudokinase scaffold that supports MuRF1 recruitment to the sarcomeric M-line.
Mayans et al., Mannheim, Germany. In Open Biol, 2014
Given previous evidence of MuRF2 interaction, we propose that the cellular role of TK is to act as a conformationally regulated scaffold that functionally couples the ubiquitin ligases MuRF1 and MuRF2, thereby coordinating muscle-specific ubiquitination pathways and myofibril trophicity.
Deletion of atrophy enhancing genes fails to ameliorate the phenotype in a mouse model of spinal muscular atrophy.
Burghes et al., Columbus, United States. In Neuromuscul Disord, 2014
In skeletal and cardiac tissue MAFbx and MuRF1 transcripts were upregulated whereas MuRF2 and MuRF3 levels were unchanged in Δ7 SMA mice.
Rare variants in genes encoding MuRF1 and MuRF2 are modifiers of hypertrophic cardiomyopathy.
Song et al., Beijing, China. In Int J Mol Sci, 2013
In this study we screened all the three members of the MuRF family, MuRF1, MuRF2 and MuRF3, in 594 unrelated HCM patients and 307 healthy controls by targeted resequencing.
MURF2B, a novel LC3-binding protein, participates with MURF2A in the switch between autophagy and ubiquitin proteasome system during differentiation of C2C12 muscle cells.
Karsenti et al., Paris, France. In Plos One, 2012
In skeletal muscles, the MURF2 proteins display E3 ubiquitin ligase structure suggesting that they may covalently attach ubiquitin polypeptides to still unknown target proteins.
Cardiac systolic dysfunction in doxorubicin-challenged rats is associated with upregulation of MuRF2 and MuRF3 E3 ligases.
Kurtenbach et al., São Carlos, Brazil. In Exp Clin Cardiol, 2012
MuRF2 and MuRF3 were also upregulated in the high-dose group but not in the low-dose group.
Developmental regulation of MURF E3 ubiquitin ligases in skeletal muscle.
Gautel et al., London, United Kingdom. In J Muscle Res Cell Motil, 2012
MURF2 isoforms undergo pre- and postnatal switching and overall downregulation in developing skeletal muscle.
Developmental regulation of MURF ubiquitin ligases and autophagy proteins nbr1, p62/SQSTM1 and LC3 during cardiac myofibril assembly and turnover.
Gautel et al., London, United Kingdom. In Dev Biol, 2011
MURF2 expression parallels that of the autophagy-associated proteins LC3, p62/SQSTM1 and nbr1
MuRF1 is a muscle fiber-type II associated factor and together with MuRF2 regulates type-II fiber trophicity and maintenance.
Labeit et al., São Paulo, Brazil. In J Struct Biol, 2010
Data suggest that expression of MuRF1 is required for remodeling of type-II fibers under pathophysiological stress states, whereas MuRF1 and MuRF2 together are required for maintenance of type-II fibers, possibly via the regulation of myozenin-1.
Cooperative control of striated muscle mass and metabolism by MuRF1 and MuRF2.
Labeit et al., Mannheim, Germany. In Embo J, 2008
Double knockout (dKO) mice obtained by the inactivation of all four MuRF1 and MuRF2 alleles developed extreme cardiac and milder skeletal muscle hypertrophy.
The kinase domain of titin controls muscle gene expression and protein turnover.
Gautel et al., London, United Kingdom. In Science, 2005
Nbr1 targets the ubiquitin-associated p62/SQSTM1 to sarcomeres, and p62 in turn interacts with MuRF2, a muscle-specific RING-B-box E3 ligase and ligand of the transactivation domain of the serum response transcription factor (SRF).
Guide RNAs in kinetoplastid mitochondria have a nonencoded 3' oligo(U) tail involved in recognition of the preedited region.
Simpson et al., Los Angeles, United States. In Cell, 1990
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.
Editing of kinetoplastid mitochondrial mRNAs by uridine addition and deletion generates conserved amino acid sequences and AUG initiation codons.
Simpson et al., Los Angeles, United States. In Cell, 1988
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.
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