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    Fbxo32 F-box protein 32 [ Mus musculus (house mouse) ]

    Gene ID: 67731, updated on 20-Jul-2021

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    MAFbx plays an important role in the mediation of excessive inflammation, including neutrophil infiltration, inflammasome formation, and production of proinflammatory cytokines.

    Endogenous muscle atrophy F-box is involved in the development of cardiac rupture after myocardial infarction.
    Usui S, Chikata A, Takatori O, Takashima SI, Inoue O, Kato T, Murai H, Furusho H, Nomura A, Zablocki D, Kaneko S, Sadoshima J, Takamura M.

    atrogin-1+/- and atrogin-1-/- mice had attenuated muscle dysfunction following influenza infection

    Influenza A Virus Infection Induces Muscle Wasting via IL-6 Regulation of the E3 Ubiquitin Ligase Atrogin-1.
    Radigan KA, Nicholson TT, Welch LC, Chi M, Amarelle L, Angulo M, Shigemura M, Shigemura A, Runyan CE, Morales-Nebreda L, Perlman H, Ceco E, Lecuona E, Dada LA, Misharin AV, Mutlu GM, Sznajder JI, Budinger GRS., Free PMC Article

    The results indicate that FBXO-32 contributes to SK2 down-regulation and that the F-box domain is essential for FBXO-32 function.

    F-box protein-32 down-regulates small-conductance calcium-activated potassium channel 2 in diabetic mouse atria.
    Ling TY, Yi F, Lu T, Wang XL, Sun X, Willis MS, Wu LQ, Shen WK, Adelman JP, Lee HC., Free PMC Article

    These findings suggest that the circadian clock controls the day-night oscillation of Atrogin1 expression and the therapeutic effects of weight-bearing are dependent on its timing.

    Day-Night Oscillation of Atrogin1 and Timing-Dependent Preventive Effect of Weight-Bearing on Muscle Atrophy.
    Aoyama S, Kojima S, Sasaki K, Ishikawa R, Tanaka M, Shimoda T, Hattori Y, Aoki N, Takahashi K, Hirooka R, Takizawa M, Haraguchi A, Shibata S., Free PMC Article

    Oligonol-mediated downregulation of Atrogin-1 and MuRF1 gene expression alleviates muscle loss and improves the impaired myotube formation, indicating that oligonol supplementation may be useful for the attenuation of myotube loss.

    Oligonol, a Low-Molecular Weight Polyphenol Derived from Lychee, Alleviates Muscle Loss in Diabetes by Suppressing Atrogin-1 and MuRF1.
    Liu HW, Chen YJ, Chang YC, Chang SJ., Free PMC Article

    Indoxyl sulfate enhanced the production of atrogin-1 by enhancing oxidative stress in skeletal muscle, leading to muscle atrophy.

    Indoxyl sulfate potentiates skeletal muscle atrophy by inducing the oxidative stress-mediated expression of myostatin and atrogin-1.
    Enoki Y, Watanabe H, Arake R, Sugimoto R, Imafuku T, Tominaga Y, Ishima Y, Kotani S, Nakajima M, Tanaka M, Matsushita K, Fukagawa M, Otagiri M, Maruyama T., Free PMC Article

    Transcriptional analysis of endophilin-A mutant mice, complemented by proteomics, highlighted ataxia- and protein-homeostasis-related genes and revealed upregulation of the E3-ubiquitin ligase FBXO32/atrogin-1 and its transcription factor FOXO3A.

    Endophilin-A Deficiency Induces the Foxo3a-Fbxo32 Network in the Brain and Causes Dysregulation of Autophagy and the Ubiquitin-Proteasome System.
    Murdoch JD, Rostosky CM, Gowrisankaran S, Arora AS, Soukup SF, Vidal R, Capece V, Freytag S, Fischer A, Verstreken P, Bonn S, Raimundo N, Milosevic I., Free PMC Article

    Valproic acid attenuated muscle wasting and myotube atrophy and reduced C/EBPbeta binding to atrogin1 promoter locus in the myotubes.

    Valproic acid attenuates skeletal muscle wasting by inhibiting C/EBPβ-regulated atrogin1 expression in cancer cachexia.
    Sun R, Zhang S, Hu W, Lu X, Lou N, Yang Z, Chen S, Zhang X, Yang H.

    These results have revealed the roles for atrogin-1 in the regulation of smooth muscle contractility through enhancement of myocardin ubiquitylation/degradation and its transcriptional activity.

    Atrogin-1 Increases Smooth Muscle Contractility Through Myocardin Degradation.
    Singh P, Li D, Gui Y, Zheng XL.

    educed PABPN1 levels caused a consistent decline in distal PAS utilization in the 3'-UTR of a subset of OPMD-dysregulated genes. This alternative PAS utilization led to up-regulation of Atrogin-1, a key muscle atrophy regulator, but down regulation of proteasomal genes. Additionally reduced PABPN1 levels caused a reduction in proteasomal activity, and transition in MyHC isotope expression pattern in myofibers.

    PABPN1-Dependent mRNA Processing Induces Muscle Wasting.
    Riaz M, Raz Y, van Putten M, Paniagua-Soriano G, Krom YD, Florea BI, Raz V., Free PMC Article

    Iron-induced skeletal muscle atrophy is suggested to involve the E3 ubiquitin ligase mediated by the reduction of Akt-FOXO3a signaling by oxidative stress.

    Iron-induced skeletal muscle atrophy involves an Akt-forkhead box O3-E3 ubiquitin ligase-dependent pathway.
    Ikeda Y, Imao M, Satoh A, Watanabe H, Hamano H, Horinouchi Y, Izawa-Ishizawa Y, Kihira Y, Miyamoto L, Ishizawa K, Tsuchiya K, Tamaki T.

    MAFbx mRNA expression was decreased in old mice relative to adult mice, whereas MuRF1 mRNA expression was less affected by ageing

    Effects of ageing on expression of the muscle-specific E3 ubiquitin ligases and Akt-dependent regulation of Foxo transcription factors in skeletal muscle.
    Wagatsuma A, Shiozuka M, Takayama Y, Hoshino T, Mabuchi K, Matsuda R.

    Suggest role for atrogin-1 up-regulation in simvastatin-induced heart mitochondria dysfunction.

    Simvastatin induces mitochondrial dysfunction and increased atrogin-1 expression in H9c2 cardiomyocytes and mice in vivo.
    Bonifacio A, Mullen PJ, Mityko IS, Navegantes LC, Bouitbir J, Krähenbühl S.

    Atrogin1 was upregulated in cancer cachexia mice. Atrogin1 knockdown protected skeletal muscle cells from TNF-alpha induced atrophy.

    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.

    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.

    MAFbx not only regulates protein degradation, but also reduces protein synthesis, exerting a dual role in regulating cardiac mass and preventing from cardiac hypertrophy.

    MAFbx/Atrogin-1 is required for atrophic remodeling of the unloaded heart.
    Baskin KK, Rodriguez MR, Kansara S, Chen W, Carranza S, Frazier OH, Glass DJ, Taegtmeyer H., Free PMC Article

    mechanical vibration strongly down-regulates atrophy genes myostatin and atrogin-1 both in vivo and in vitro.

    Low-amplitude high frequency vibration down-regulates myostatin and atrogin-1 expression, two components of the atrophy pathway in muscle cells.
    Ceccarelli G, Benedetti L, Galli D, Prè D, Silvani G, Crosetto N, Magenes G, Cusella De Angelis MG.

    mTORC1 promotes denervation-induced muscle atrophy through a mechanism involving the activation of FoxO and E3 ubiquitin ligases.

    mTORC1 promotes denervation-induced muscle atrophy through a mechanism involving the activation of FoxO and E3 ubiquitin ligases.
    Tang H, Inoki K, Lee M, Wright E, Khuong A, Khuong A, Sugiarto S, Garner M, Paik J, DePinho RA, Goldman D, Guan KL, Shrager JB.

    atrogin-1 promotes cardiomyocyte health through mediating the interplay between the ubiquitin/proteasome system and autophagy/lysosome system and its alteration promotes development of cardiomyopathies

    Atrogin-1 deficiency promotes cardiomyopathy and premature death via impaired autophagy.
    Zaglia T, Milan G, Ruhs A, Franzoso M, Bertaggia E, Pianca N, Carpi A, Carullo P, Pesce P, Sacerdoti D, Sarais C, Catalucci D, Krüger M, Mongillo M, Sandri M., Free PMC Article

    Smad3 expression is sufficient to stimulate atrogin-1 promoter activity, inhibit Akt/mTOR signaling and protein synthesis, and induce muscle fiber atrophy.

    Smad3 induces atrogin-1, inhibits mTOR and protein synthesis, and promotes muscle atrophy in vivo.
    Goodman CA, McNally RM, Hoffmann FM, Hornberger TA., Free PMC Article

    Loss of SPARC not only upregulates atrogin 1 expression but also enhances transforming growth factor (TGF)beta signaling, which may in turn cause muscle atrophy.

    Loss of SPARC in mouse skeletal muscle causes myofiber atrophy.
    Nakamura K, Nakano S, Miyoshi T, Yamanouchi K, Nishihara M.

    The muscle wasting effects of the myostatin-atrogin-1 axis are not only limited to the degradation of MyoD and eukaryotic translation initiation factor 3 subunit f, but also encompass several other muscle proteins.

    Identification of atrogin-1-targeted proteins during the myostatin-induced skeletal muscle wasting.
    Lokireddy S, Wijesoma IW, Sze SK, McFarlane C, Kambadur R, Sharma M.

    Expression of MAFbx/Atrogin-1 and MuRF1 was significantly greater in the plantaris muscle than in the soleus muscle during the early stage of atrophy.

    Differential gene expression of muscle-specific ubiquitin ligase MAFbx/Atrogin-1 and MuRF1 in response to immobilization-induced atrophy of slow-twitch and fast-twitch muscles.
    Okamoto T, Torii S, Machida S.

    C/EBPbeta-/- mice were resistant to Lewis lung cancer-induced atrogin1 upregulation and muscle wasting. Activation of the p38beta MAPK-C/EBPbeta signalling pathway appears to be a key component of cachexia.

    C/EBPβ mediates tumour-induced ubiquitin ligase atrogin1/MAFbx upregulation and muscle wasting.
    Zhang G, Jin B, Li YP., Free PMC Article

    Downregulation of MAFbx inhibits cardiac hypertrophy in part through stabilization of IkappaB-alpha and inactivation of nuclear factor-kappaB

    Endogenous muscle atrophy F-box mediates pressure overload-induced cardiac hypertrophy through regulation of nuclear factor-kappaB.
    Usui S, Maejima Y, Pain J, Hong C, Cho J, Park JY, Zablocki D, Tian B, Glass DJ, Sadoshima J., Free PMC Article

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