MyoG EMSA Kit
- Known as:
- MyoG EMSA Kit
- Catalog number:
- AY1214
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- MyoG EMSA Kit
Related genes to: MyoG EMSA Kit
- Gene:
- MYOG NIH gene
- Name:
- myogenin
- Previous symbol:
- MYF4
- Synonyms:
- bHLHc3
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-11-20
- Date modifiied:
- 2016-10-05
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- Studies examining the paracrine effect of fibroblasts on the myogenesis of bovine muscle satellite cells (MuSCs) have confirmed their stimulating effect on proliferation and early differentiation. However, traditional two-dimensional (2D) cell culture models fail to accurately represent the complexity of in vivo muscle tissue. This study aims to investigate the paracrine effect of fibroblasts on myogenesis in a three-dimensional (3D) cell culture model. Cells were cultured in monoculture and co-culture with fibroblasts in a spinner flask using gelatin microcarriers, Cultishper, which maximizes the growth surface area for adherent cells. Then, muscle cells from the co-culture were sorted by the FACS method based on negative expression of CD90, a fibroblast-associated marker. The progress of myogenesis was assessed based on qPCR analysis for selected muscle markers and at the protein level for skeletal myosin. Fluorescent staining and luminescent metabolic assays were performed to control culture conditions. The obtained results revealed up-regulation of genes involved in cell activation and proliferation (PAX7, MYF5, and MYOD) and differentiation (MYOG, EGR1, and MYH). Metabolism analyses did not show changes between mono- and co-culture conditions. To summarize, fibroblasts through paracrine signaling promote early differentiation of MuSCs and potentially proliferation, which provides valuable insights for the advancement of cultured meat production. - Source: PubMed
Publication date: 2026/05/11
Zygmunt KarolinaPiórkowska KatarzynaAdamiak JuliaWitarski Wojciech - Distant hybridization combines beneficial genes from different species to create high-quality germplasm with altered phenotypes and genotypes. In our previous study, two fast-growing hybrid breams (BTBB and BBTB) were developed through a multi-step breeding strategy involving distant hybridization between blunt snout bream (Megalobrama amblycephala, 2n = 48, BSB, ♀) and topmouth culter (Culter alburnus, 2n = 48, TC, ♂), followed by two rounds of backcrossing. To elucidate the mechanisms of muscle development and rapid growth, we compared growth performance, muscle texture, antioxidant enzyme activities, and the expression of myogenic regulatory factor (MRF) genes between the hybrids and their parents. The results showed that both BBTB and BTBB had significantly greater body weight and body length than BSB (p < 0.05). Histological analysis showed that the two hybrid breams had significantly lower muscle fiber density (p < 0.05) and significantly larger muscle fiber diameter than BSB (p < 0.05). Muscle texture analysis indicated that BBTB had higher adhesiveness than BSB, whereas BTBB exhibited significantly greater springiness than BSB. Antioxidant analysis showed that, compared with BSB, MDA levels were significantly lower in BBTB and BTBB (p < 0.05), whereas CAT, SOD, and GSH levels were higher. Sequence analysis showed that the full-length cDNA sequences of myod, myog, myf5, and myf6 were highly conserved between the hybrid offspring and their parents. RT-qPCR analysis revealed that the expression levels of MRFs and mstn were relatively high in the muscle tissues of both BTBB and BSB, whereas mstn expression was lower in BTBB than in BSB, suggesting that MRFs and mstn may act coordinately in the regulation of rapid growth in BTBB. In contrast, the expression levels of MRFs and mstn in BBTB were significantly lower than those in BSB, suggesting that MRF expression may increase transiently during rapid growth and then decline. Overall, the two hybrid breams exhibited distinct molecular regulatory patterns, and their superior muscle phenotypes may be associated with muscle fiber development, enhanced antioxidant capacity, and the balance between positive myogenic regulation and mstn-mediated negative regulation. These findings indicate that BBTB and BTBB are promising germplasm resources for aquaculture breeding. - Source: PubMed
Publication date: 2026/05/08
Zhou ZhifengYang XiangqiongOuyang XingeChen XinHuang YujieChen KuoFan SiyuYu XinxinLi ShengnanTao Min - Skeletal muscle injury is prevalent in clinical practice and sports medicine, and efficient regeneration is crucial for restoring motor function. Niacin (vitamin B3, NIA), a water-soluble essential nutrient and key precursor of nicotinamide adenine dinucleotide (NAD + ), regulates muscle metabolism and mitochondrial function, but its role and underlying mechanisms in skeletal muscle injury repair remain unclear. In this study, a mouse model of acute skeletal muscle injury was established via intramuscular injection of bupivacaine hydrochloride, and C2C12 myoblasts were used as an in vitro model to explore NIA's effects on muscle regeneration and myogenic differentiation. In vivo experiments showed that oral NIA supplementation (73 m g/kg/day for 8 weeks) significantly promoted repair of the injured tibialis anterior (TA) muscle: compared with the NC group, NIA-treated mice had increased TA muscle mass, larger myofiber cross-sectional area, a higher proportion of centrally nucleated fibers, and improved muscle function. Western blot analysis revealed that NIA upregulated the expression of myogenic regulatory factors (MRFs) including Pax7, MyoD, and MyoG in injured tissues. In vitro assays demonstrated that NIA promoted C2C12 myoblast differentiation dose-dependently, with 1 mM as the optimal concentration, confirmed by increased MyoD and MyoG expression and a higher myotube fusion index. Bioinformatics analyses predicted the PI3K/Akt signaling pathway as a potential downstream target. Mechanistically, NIA increased Akt phosphorylation (p-Akt) in C2C12 cells, while PI3K inhibition by LY294002 eliminated NIA-induced p-Akt upregulation, MRFs expression, and myotube fusion. In conclusion, NIA accelerates skeletal muscle regeneration and enhances C2C12 myoblast differentiation by activating the PI3K/Akt signaling pathway. This study clarifies NIA's molecular mechanism in muscle regeneration and provides a theoretical basis for its clinical application in treating skeletal muscle injury. - Source: PubMed
Publication date: 2026/05/02
Dai LizhiWang JingxuanCao ZheyuanYu TongLiu JiaLi YouchongZhang YuhaoXiao Jianhua - Chronic massive rotator cuff tears (MRCTs) pose a major clinical challenge due to irreversible muscle degeneration, including atrophy, fatty infiltration, and fibrosis, which persists even after surgical repair. Existing strategies fail to modulate the pathological microenvironment and essential electrical signaling. This study presents a self-reinforcing electroactive fibrous patch, designated polyethylene@polyethylene terephthalate/reduced graphene oxide (PE@PET/rGO), which integrates graphene-mediated electrical stimulation with mechanical reinforcement. Through mussel-inspired modification and hot-pressing, rGO nanosheets are uniformly embedded into a PE@PET nonwoven fabric scaffold, achieving a synergistic enhancement in electrical conductivity (3.54 × 10 S/cm), tensile strength (15.99 MPa), and Young's modulus (40.58 MPa). It enables programmable adhesion via molten PE "self-glue" for stable deployment. In vitro evaluations demonstrate that the patch promotes myoblast alignment, elongation (myotube length: 176.80 ± 7.08 μm vs. 105.64 ± 8.63 μm in controls), and fusion index (51.80 ± 5.85% vs. 26.68 ± 1.48%), while suppressing adipogenesis (lipid droplet area: 85.42 ± 1.28 μm/cell vs. 296.74 ± 6.26 μm/cell in adipogenic media). Mechanistically, graphene-mediated electrical stimulation activates Ca signaling, upregulates myogenic markers (MHC, MyoG, MyoD) and inhibits adipogenic factors (PPARγ, C/EBPα). This work establishes a robust bioelectronic platform combining mechanical, electrical, and biological functionality, offering a promising strategy for treating chronic muscle degeneration. - Source: PubMed
Publication date: 2026/04/28
Wu XueqinLiu ZichunSha ZhouSong YuhengGe YiranJue HaoHua YinghuiFei XiangZhu Meifang - The progressive skeletal muscle degeneration observed in Duchenne Muscular Dystrophy (DMD) patients requires multiple cycles of satellite cells (SCs) activation to promote tissue regeneration. Dystrophic SCs present intrinsic defects, and the disrupting fibrotic niche hinders appropriate muscle recovery. Traditional 2D culture systems face challenges in modeling the DMD muscle niche and SCs behavior. Our aim was to validate a 3D culture of skeletal muscle spheroids (iSMS) for DMD modeling, as compared to the traditional 2D culture, while investigating the pathophysiological mechanisms of dystrophin deficiency in vitro. - Source: PubMed
Publication date: 2026/05/02
Esposito Joycede Souza Leite FelipeBarbosa Igor Nevesda Mata Martins Thaís Mariade Oliveira Olberg Giovanna GonçalvesAl Tanoury ZiadTelles-Silva Kayque Alvesda Silva Pardo Mayana CristinaJazedje TatianaBortolin Raul HernandesHirata Mario HiroyukiPourquié OlivierZatz Mayana