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    TRIM63 tripartite motif containing 63 [ Homo sapiens (human) ]

    Gene ID: 84676, updated on 28-Oct-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Evaluation of TRIM63 RNA in situ hybridization (RNA-ISH) as a potential biomarker for alveolar soft-part sarcoma (ASPS).

    Evaluation of TRIM63 RNA in situ hybridization (RNA-ISH) as a potential biomarker for alveolar soft-part sarcoma (ASPS).
    Taylor AS, Mannan R, Pantanowitz L, Chinnaiyan AM, Dhanasekaran SM, Hrycaj S, Cao X, Chan MP, Lucas D, Wang XM, Mehra R., Free PMC Article

    04/3/2024
    Myeloma cells shift osteoblastogenesis to adipogenesis by inhibiting the ubiquitin ligase MURF1 in mesenchymal stem cells.

    Myeloma cells shift osteoblastogenesis to adipogenesis by inhibiting the ubiquitin ligase MURF1 in mesenchymal stem cells.
    Liu Z, Liu H, He J, Lin P, Tong Q, Yang J., Free PMC Article

    11/6/2021
    Mutations in TRIM63 cause an autosomal-recessive form of hypertrophic cardiomyopathy.

    Mutations in TRIM63 cause an autosomal-recessive form of hypertrophic cardiomyopathy.
    Salazar-Mendiguchía J, Ochoa JP, Palomino-Doza J, Domínguez F, Díez-López C, Akhtar M, Ramiro-León S, Clemente MM, Pérez-Cejas A, Robledo M, Gómez-Díaz I, Peña-Peña ML, Climent V, Salmerón-Martínez F, Hernández C, García-Granja PE, Mogollón MV, Cárdenas-Reyes I, Cicerchia M, García-Giustiniani D, Lamounier A Jr, Gil-Fournier B, Díaz-Flores F, Salguero R, Santomé L, Syrris P, Olivé M, García-Pavía P, Ortiz-Genga M, Elliott PM, Monserrat L, GENESCOPIC Research Group., Free PMC Article

    07/3/2021
    Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1.

    Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1.
    Xia P, Chen J, Liu Y, Fletcher M, Jensen BC, Cheng Z., Free PMC Article

    12/12/2020
    MuRF1 turned out to be also a target for a new post-translational modification arbitrated by conjugation of SUMO1 and it is mediated by the SUMO ligases E2 UBC9 and the E3 PIASgamma/4. SUMOylation takes place at lysine 238 localized at the second coiled-coil protein domain that is required for efficient substrate interaction for polyubiquitination.

    Muscle RING-finger protein-1 (MuRF1) functions and cellular localization are regulated by SUMO1 post-translational modification.
    Heras G, Namuduri AV, Traini L, Shevchenko G, Falk A, Bergström Lind S, Jia M, Tian G, Gastaldello S., Free PMC Article

    07/25/2020
    Using a combination of electron paramagnetic resonance, on spin-labeled protein, and disulfide crosslinking, the study shows that TRIM63 follows the structural conservation of the TRIM dimerization domain, observed in other proteins. the COS-box motif folds back onto the dimerization coiled-coil motif, predictably forming a four-helical bundle at the center of the protein and emulating the architecture of canonical TRIMs.

    Exploration of the TRIM Fold of MuRF1 Using EPR Reveals a Canonical Antiparallel Structure and Extended COS-Box.
    Stevens M, Franke B, Skorupka KA, Cafiso DS, Pornillos O, Mayans O, Norman DG., Free PMC Article

    06/20/2020
    an impaired interaction between titin and MURF1 as a novel mechanism underlying the pathogenesis ofHypertrophic cardiomyopathy (HCM).

    Perturbation of the titin/MURF1 signaling complex is associated with hypertrophic cardiomyopathy in a fish model and in human patients.
    Higashikuse Y, Mittal N, Arimura T, Yoon SH, Oda M, Enomoto H, Kaneda R, Hattori F, Suzuki T, Kawakami A, Gasch A, Furukawa T, Labeit S, Fukuda K, Kimura A, Makino S., Free PMC Article

    05/30/2020
    Our study revealed that TRIM63, acting as an oncogene, is involved in breast cancer progression by activating the Wnt/beta-catenin signaling pathway

    A novel oncogene TRIM63 promotes cell proliferation and migration via activating Wnt/β-catenin signaling pathway in breast cancer.
    Li K, Pan W, Ma Y, Xu X, Gao Y, He Y, Wei L, Zhang J.

    02/29/2020
    missense single nucleotide polymorphism (A>G, rs2275950 ) within the TRIM63 gene (encoding MuRF-1 and potentially affecting titin mechanical properties) was associated with the variable response to unaccustomed eccentric exercise.

    TRIM63 (MuRF-1) gene polymorphism is associated with biomarkers of exercise-induced muscle damage.
    Baumert P, G-REX Consortium, Lake MJ, Drust B, Stewart CE, Erskine RM., Free PMC Article

    02/9/2019
    role of the muscle specific E3s MuRF-1 and MAFbx in skeletal muscle wasting during various pathologies, as well as their regulation by modifiable lifestyle factors, were explored (review)

    The role of E3 ubiquitin-ligases MuRF-1 and MAFbx in loss of skeletal muscle mass.
    Rom O, Reznick AZ.

    12/23/2017
    the involvement of oxidative stress in the atrophy of COPD peripheral muscle cells in vitro, via the FoxO1/MuRF1/atrogin-1 signaling pathway of the ubiquitin/proteasome system

    Involvement of the FoxO1/MuRF1/Atrogin-1 Signaling Pathway in the Oxidative Stress-Induced Atrophy of Cultured Chronic Obstructive Pulmonary Disease Myotubes.
    Pomiès P, Blaquière M, Maury J, Mercier J, Gouzi F, Hayot M., Free PMC Article

    08/5/2017
    The mitochondrial damage-cGAS-STING-IRF3 pathway is critically involved in metabolic stress-induced endothelial inflammation.

    STING-IRF3 Triggers Endothelial Inflammation in Response to Free Fatty Acid-Induced Mitochondrial Damage in Diet-Induced Obesity.
    Mao Y, Luo W, Zhang L, Wu W, Yuan L, Xu H, Song J, Fujiwara K, Abe JI, LeMaire SA, Wang XL, Shen YH., Free PMC Article

    06/24/2017
    Altogether, these results suggest a novel function for p63 as a contributor to muscular atrophic processes via the regulation of multiple genes, including the muscle atrophy gene Trim63.

    Transcriptional activator TAp63 is upregulated in muscular atrophy during ALS and induces the pro-atrophic ubiquitin ligase Trim63.
    von Grabowiecki Y, Abreu P, Blanchard O, Palamiuc L, Benosman S, Mériaux S, Devignot V, Gross I, Mellitzer G, Gonzalez de Aguilar JL, Gaiddon C., Free PMC Article

    11/12/2016
    A novel protein aggregate myopathies and cardiomyopathy resulting from combined homozygous MuRF1 null mutation and heterozygous MuRF3 missense mutation.

    New cardiac and skeletal protein aggregate myopathy associated with combined MuRF1 and MuRF3 mutations.
    Olivé M, Abdul-Hussein S, Oldfors A, González-Costello J, van der Ven PF, Fürst DO, González L, Moreno D, Torrejón-Escribano B, Alió J, Pou A, Ferrer I, Tajsharghi H.

    04/30/2016
    Vitamin D3 might have an inhibitory effect on the expression of MAFbx and MuRF1 in skeletal muscle.

    1α,25(OH)2D3 downregulates gene expression levels of muscle ubiquitin ligases MAFbx and MuRF1 in human myotubes.
    Hayakawa N, Fukumura J, Yasuno H, Fujimoto-Ouchi K, Kitamura H.

    01/16/2016
    MURF1 expression intended to be increased in the skeletal muscle of patients with malignant disease even before cancer related cachexia weight loss.

    Muscle-specific E3 ubiquitin ligases are involved in muscle atrophy of cancer cachexia: an in vitro and in vivo study.
    Yuan L, Han J, Meng Q, Xi Q, Zhuang Q, Jiang Y, Han Y, Zhang B, Fang J, Wu G.

    01/2/2016
    TRIM63 gene expression involved in skin hyperpigmentation.

    Identification of Genes Expressed in Hyperpigmented Skin Using Meta-Analysis of Microarray Data Sets.
    Yin L, Coelho SG, Valencia JC, Ebsen D, Mahns A, Smuda C, Miller SA, Beer JZ, Kolbe L, Hearing VJ., Free PMC Article

    12/19/2015
    Expression of USP19 correlates with that of MuRF1 and MAFbx/atrogin-1 in skeletal muscles

    Inactivation of the ubiquitin-specific protease 19 deubiquitinating enzyme protects against muscle wasting.
    Bédard N, Jammoul S, Moore T, Wykes L, Hallauer PL, Hastings KE, Stretch C, Baracos V, Chevalier S, Plourde M, Coyne E, Wing SS.

    11/28/2015
    Skeletal muscle atrophy induced by Angiotensin II involves activation of MuRF1 expression.

    Angiotensin II Induces Skeletal Muscle Atrophy by Activating TFEB-Mediated MuRF1 Expression.
    Du Bois P, Pablo Tortola C, Lodka D, Kny M, Schmidt F, Song K, Schmidt S, Bassel-Duby R, Olson EN, Fielitz J., Free PMC Article

    10/31/2015
    These data strongly supported that rare variants in MuRF1 and MuRF2 are associated with higher penetrance and more severe clinical manifestations of hypertrophic cardiomyopathy.

    Rare variants in genes encoding MuRF1 and MuRF2 are modifiers of hypertrophic cardiomyopathy.
    Su M, Wang J, Kang L, Wang Y, Zou Y, Feng X, Wang D, Ahmad F, Zhou X, Hui R, Song L., Free PMC Article

    01/31/2015
    In conclusion, atrogin-1, MuRF1, FOXO1/3A, and eIF3-f mRNA, and protein levels, are differentially regulated by exercise contraction mode but not WPH supplementation combined with hypertrophy-inducing training.

    Influence of divergent exercise contraction mode and whey protein supplementation on atrogin-1, MuRF1, and FOXO1/3A in human skeletal muscle.
    Stefanetti RJ, Lamon S, Rahbek SK, Farup J, Zacharewicz E, Wallace MA, Vendelbo MH, Russell AP, Vissing K.

    01/24/2015
    Data reveal that Titin protein is a pseudokinase with non-detectable catalytic output but is a high-affinity binding locus for MuRF1.

    Titin kinase is an inactive pseudokinase scaffold that supports MuRF1 recruitment to the sarcomeric M-line.
    Bogomolovas J, Gasch A, Simkovic F, Rigden DJ, Labeit S, Mayans O., Free PMC Article

    01/10/2015
    both MuRF1 and MAFbx are enriched in skeletal, cardiac, and smooth muscle--REVIEW

    Skeletal muscle atrophy and the E3 ubiquitin ligases MuRF1 and MAFbx/atrogin-1.
    Bodine SC, Baehr LM., Free PMC Article

    11/8/2014
    SMAD3 regulates transcription of MuRF-1 by increasing FoxO3 binding at a conserved FRE-SBE motif within the proximal promoter region, and by increasing FoxO3 protein content and transcriptional activity.

    SMAD3 augments FoxO3-induced MuRF-1 promoter activity in a DNA-binding-dependent manner.
    Bollinger LM, Witczak CA, Houmard JA, Brault JJ., Free PMC Article

    10/11/2014
    In MuRF1 the COS-box mediates the in vivo targeting of sarcoskeletal structures and points to the pharmacological relevance of the COS domain for treating MuRF1-mediated muscle atrophy.

    Molecular basis for the fold organization and sarcomeric targeting of the muscle atrogin MuRF1.
    Franke B, Gasch A, Rodriguez D, Chami M, Khan MM, Rudolf R, Bibby J, Hanashima A, Bogomolovas J, von Castelmur E, Rigden DJ, Uson I, Labeit S, Mayans O., Free PMC Article

    09/13/2014
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