MyoG EMSA Probe Set
- Known as:
- MyoG EMSA Probe Set
- Catalog number:
- AY1214P
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- MyoG EMSA Probe Set
Ask about this productRelated genes to: MyoG EMSA Probe Set
- 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
Related products to: MyoG EMSA Probe Set
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated0.2 mm, 30 cm Spacer Set
0.2 mm, 30 cm Spacer Set0.35 mm, 30 cm Spacer Set
0.35 mm, 30 cm Spacer Set0.5 mm, 30 cm Spacer Set
0.5 mm, 30 cm Spacer Set0.75 mm Dual Gel Cast Set
0.75 mm Dual Gel Cast Set0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
0.75 mm Plate Set, RM
Related articles to: MyoG EMSA Probe Set
- Sarcopenic obesity (SO) is well-characterized in older adults, but its impact on muscle development in children remains poorly understood. This study investigated the effects of childhood obesity on musculoskeletal health and the underlying mechanisms. - Source: PubMed
Wang SenjieZhang WeiQin ZhewenZhou XuelianXue ChuqingWang DanLiang XinyiZhang ZixinZhan ShuminWang ShanWu WeiFu JunfenUllah Rahim - 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 - This study investigated the synergistic effects of liquid fermentation of rapeseed meal (RSM) on feed microbiota, growth performance, and muscle development in growing pigs. RSM was fermented using four compound probiotics and eleven enzyme preparations, and microbial changes were analyzed using 16S rRNA sequencing. Seventy-two Duroc × Jingfen White pigs were randomly assigned to three groups: soybean meal (Ctrl), RSM, and fermented RSM (FRSM). FRSM showed higher trichloroacetic acid-soluble protein (TCA-sp) content and significantly lower neutral detergent fiber (NDF), acid detergent fiber (ADF), anti-nutritional factors (ANFs), and toxins (TS) ( < 0.01). Fermentation increased microbial diversity, with higher abundances of and . Compared with Ctrl and RSM, the feed-to-gain ratio (F/G) decreased in the FRSM group ( < 0.01). FRSM also improved serum antioxidant capacity, enhanced intestinal villus height (VH)and villus height/crypt depth ratio (VH/CD), and upregulated the expression of tight junction proteins (ZO-1, occludin) and the anti-inflammatory factor IL-10 ( < 0.01). FRSM group also increased myofiber diameter and cross-sectional area in the and elevated , and expression ( < 0.01). RNA-seq revealed 2094 differentially expressed genes enriched in metabolic pathways. Overall, FRSM improved growth performance, intestinal health, and muscle development in growing pigs, which may guide the development of protein resource utilization technologies. - Source: PubMed
Publication date: 2026/04/02
Liu JingchaoZhang TingLi YunkaiZhang JingyiZhao XiaoleiLi MengCao GuoqingLi BugaoGuo XiaohongYang Yang - Aging significantly alters cellular mechanics and mitochondrial physiology, with chronic low-grade inflammation (inflammaging). However, its role in skeletal muscle atrophy and fibrosis is poorly understood. This study addressed the unresolved mechanism using a 2.5D coculture model of RAW264.7 macrophages and C2C12 myoblasts, exposed to lipopolysaccharide (LPS, a fibrosis inducer), with a focus on myogenesis, fibrogenesis, cellular stiffness, and mitochondrial metabolism. Paracrine signals from LPS-stimulated macrophages decreased myogenic markers MyHC and MyoG, increased fibrosis markers, and elevated fibrotic cell stiffness. Mitochondrial metabolism was disrupted, indicated by lowered maximal respiration and increased proton leak, demonstrating impaired energy production. To explore the alleviation of muscle atrophy and promote regeneration, a biomaterial-based therapeutic approach involving the use of pirfenidone (PFD, pulmonary antifibrotic drug)-loaded hydrogels composed of silk fibroin and agarose was investigated. Treatment reduced fibrotic stiffness by ∼40%, increased myotube formation by 33%, improved mitochondrial function, and restored mitochondrial structure, with a 20% increase in maximal respiration and a 50% decrease in proton leak in the seahorse assay. Sustained release of PFD from tissue-mimicking hydrogels effectively suppressed the expression of fibrotic markers such as α-SMA and COL1 while simultaneously increasing the expression of myogenic genes. RNA transcriptomics further corroborated the upregulation of myogenic pathways and the downregulation of fibrogenic signaling. This study highlights the potential of PFD-loaded hydrogels as a novel therapeutic strategy to target inflammation-induced muscle fibrosis and promote skeletal muscle regeneration, demonstrating both the prevention of fibrotic progression and reversal of the established inflammation-induced fibrosis in vitro, with promising translational potential for treating sarcopenia. - Source: PubMed
Publication date: 2026/03/16
Gopinath VarshinyPatel NiravChitteti RamamurthyBalakrishnan NidhishPanner Selvam Manesh KumarPatel Hemal HLal RatneshMuthuvijayan VigneshRajasekaran Mahadevan - Although intravenous lipid emulsions are routinely administered to preterm infants, their specific effects on skeletal muscle development remain unclear. In this study, a soybean oil-based lipid emulsion (Intralipid 20) was administered via intravenous infusion to fetal sheep (gestational day 88-90) at a dose rising from 1 g/kg/day (day 0) to 3 g/kg/day (days 2-8). Intralipid infusion did not alter overall fetal body weight, tibialis anterior (TA) muscle mass or serum testosterone levels. Histological analyses revealed no significant differences in muscle fibre diameter or collagen content in TA muscles between groups. However, Intralipid significantly upregulated the expression of key myogenic regulatory genes, including Myog (myogenin) and Myod (myogenic differentiation 1), while downregulating the expression of several genes associated with fibrogenesis: Col1a1 (collagen type I α1 chain), Col3a1 (collagen type III α1 chain), Lh2b (lysyl hydroxylase 2b) and P4ha (prolyl 4-hydroxylase α). In contrast, Intralipid had no significant effect on the expression of genes associated with intramuscular adipogenesis, including Pparg (peroxisome proliferator-activated receptor γ), Pdgfra (platelet-derived growth factor receptor α), Zfp423 (zinc finger protein 423), Slc27a1 (solute carrier family 27 member 1), C/ebpa (CCAAT/enhancer-binding protein α) and Fasn (fatty acid synthase). Similarly, genes related to inflammation, such as Tnfa (tumour necrosis factor α), Il-6 (interleukin 6), Tlr4 (Toll-like receptor 4) and Tlr2 (Toll-like receptor 2), were unaffected. In conclusion, these findings indicate that short-term lipid exposure alters gene expression patterns without measurable structural changes, suggesting that transcriptional responses may precede overt morphological remodelling in fetal skeletal muscle. - Source: PubMed
Publication date: 2026/04/09
Li XinruiAlaniz Sarah MLouey SamanthaDeavila Jeanene MarieJonker Sonnet SDu Min