PLASTIC MINI COLUMNS
- Known as:
- PLASTIC MINI COLUMNS
- Catalog number:
- MC-100
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Agarose Bead
- Gene target:
- PLASTIC MINI COLUMNS
Related genes to: PLASTIC MINI COLUMNS
- Gene:
- MYMX NIH gene
- Name:
- myomixer, myoblast fusion factor
- Previous symbol:
- -
- Synonyms:
- MINION
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2017-05-11
- Date modifiied:
- 2017-07-19
Related products to: PLASTIC MINI COLUMNS
Related articles to: PLASTIC MINI COLUMNS
- Duchenne muscular dystrophy (DMD), caused by mutations of the DMD gene, is a lethal degenerative disease with no cure. Stimulating myogenesis of muscle stem cells (MuSCs) represents a promising strategy to ameliorate muscle pathology in DMD patients. Although previous work has revealed a role of N-terminal methyltransferase 1 (NTMT1) in myogenesis, its potential as a therapeutic target to ameliorate muscular dystrophy remains unexplored. - Source: PubMed
Publication date: 2026/04/15
Zhang HaoyuanHe MingAsif MuhammadDeng YouchaoHuang RongKuang Shihuan - Myoblast fusion is essential for skeletal muscle growth and repair, yet the upstream signals regulating this process remain incompletely understood. Here, we show that the cytokine TWEAK promotes myotube formation through activation of alternative NF-κB signaling. Transcriptomic profiling of TWEAK-treated myotubes reveals upregulation of Myomixer (Mymx) and the chemokine CXCL10, both critical for fusion. Mechanistically, the NF-κB member RelB directly binds the Mymx and Cxcl10 gene promoters, enhancing their transcription. Genetic or pharmacological disruption of this pathway impairs myoblast fusion in both C2C12 and primary mouse myoblasts, while Mymx overexpression rescues fusion in TWEAK-deficient myoblasts. In mouse models, TWEAK treatment enhances myotube formation during muscle regeneration, whereas loss of TWEAK reduces fusion efficiency. These findings identify TWEAK-alternative NF-κB signaling as a key regulator of muscle cell fusion through direct transcriptional control of Mymx and Cxcl10 and defines targetable pathways to enhance repair in muscle disease. - Source: PubMed
Publication date: 2026/04/02
Lala-Tabbert NeenaHumphrey AllanRatsun DianaEarl NathalieSt-Jean MartineLaCasse Eric CKorneluk Robert G - This study presents the first characterization of a primary cell culture from white skeletal muscle of European sea bass (Dicentrarchus labrax). Using immunofluorescence and gene expression analyses over 12 days, cell activation, proliferation, differentiation, fusion, and maturation phases were described. During culture development, myogenic regulatory factors (myf5, myod1, myod2, myog, mrf4) were sequentially expressed. Proliferation peaked at days 4-6, with high Pcna and Myod immunodetection and gene expression of pax7, c-met, and pcna. Early downregulation of cell cycle regulators, cdkn1a and cdkn1cb, and mstnb may have contributed to proliferation, while cdkn1bb progressively increased, likely to promote differentiation. The Gh/Igf axis showed differential regulation, igf-1 decreasing early and igf-2, igf-1ra, igf-1rb, and igfbp-1a gradually rising. Differentiation, myotube formation, and maturation were marked by higher Myhc staining, sarcomere development, and upregulation of cdh15, cav3, mef2, mymk, mymx, myhcb, and wnt4. Anabolic (akt2, mtor, eif4ebp1) and proteolytic-related genes (foxo1a, murf1, mafbx, capn1, capn3b, atg12, map1lc3b) increased in later stages. Comparison with other vertebrates revealed both conserved and species-specific regulatory mechanisms of myogenesis. These findings provide a comprehensive molecular framework of skeletal muscle development in European sea bass and establish a valuable in vitro model for studying fish muscle biology and potential aquaculture and biotechnology applications. - Source: PubMed
Publication date: 2025/12/10
García-Pérez IsabelRodríguez InmaculadaRubio AlbertDíaz-Serrano CarlaCapilla EncarnaciónNavarro IsabelBlasco JosefinaGutiérrez Joaquim - Skeletal muscle formation involves the fusion of myocytes into precisely aligned, multinucleated myofibres. These fibres continue to grow through reiterative rounds of myocyte fusion, incorporating new myonuclei and supporting muscle growth, repair and regeneration over organismal life span. The vertebrate-specific myocyte fusogens, Myomaker (Mymk) and Myomixer (Mymx), are crucial for generating multinucleated skeletal muscles. Here, using quantitative imaging and a mymx knockout strain, we explored the impact on myogenesis at different life stages of the zebrafish. We demonstrate that during the initial phase of muscle formation, mymx has a spatiotemporally varied expression across all axes of the developing myotome, not just along the anterior-posterior axis. On Mymx loss, myotome morphogenesis is disrupted, with both cell and tissue structure impacted. In particular, the shape of the resulting myotome segments is altered. Moreover, we show differential effects of Mymk versus Mymx loss on myocyte fusion and muscle growth. Finally, we report that perturbation to adult muscle multinucleation and size impacted bone development, again with different phenotypic severities among the two fusogen mutants. Together, our work provides insights into the interplay between myocyte fusion, myotome morphogenesis and acquisition of final adult form. - Source: PubMed
Publication date: 2025/12/18
Dhar SunandanThomas SerenaYeo Hui LiSaunders Timothy ERoy Sudipto - Muscle RING finger (MuRF) proteins are striated muscle-specific E3 ubiquitin ligases essential for muscle homeostasis. Whereas MuRF1 is well known for its role in muscle atrophy, MuRF2 and MuRF3 contribute to microtubule stabilization, influencing muscle differentiation and function. Their cooperative functions in regulating myogenesis are unclear. This study aimed to identify novel MuRF2 and MuRF3 interaction partners and investigate their function in myogenic differentiation. - Source: PubMed
Li NingHamati JidaLi YiBrinschwitz BjörnGhait MohamedMartin ElisaLodka DörteHammer ElkeFielitz BrittaVölker UweDittmar GunnarSommer ThomasLuft Friedrich CFielitz Jens