MYF5 antibody - N-terminal region (ARP32134_P050)
- Known as:
- MYF5 (anti-) - N-terminal region (ARP32134_P050)
- Catalog number:
- arp32134_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MYF5 antibody - N-terminal region (ARP32134_P050)
Related genes to: MYF5 antibody - N-terminal region (ARP32134_P050)
- Gene:
- MYF5 NIH gene
- Name:
- myogenic factor 5
- Previous symbol:
- -
- Synonyms:
- bHLHc2
- Chromosome:
- 12q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2016-10-05
Related products to: MYF5 antibody - N-terminal region (ARP32134_P050)
Related articles to: MYF5 antibody - N-terminal region (ARP32134_P050)
- Myogenesis is a tightly regulated process by a cascade of well-coordinated events and pathways. Other than the known myogenic regulator factor (MRF) family including Myf5, MyoD, Myogenin and MRF4, our previous study identified BAMBI is involved in muscle regeneration and siRNA-mediated BAMBI knockdown impairs C2C12 myoblast differentiation. However, the potential role of BAMBI in determining cell linage and fate specification in C2C12 myoblast remains unexplored. In this study, we analyzed the RNA-seq data and discovered that BAMBI expression was dynamically regulated during proliferation and differentiation period of C2C12 myoblasts. By establishing cell line with the loss of function and gain of function of BAMBI in C2C12 myoblasts, we demonstrated that BAMBI deletion totally abrogated myogenic differentiation of C2C12 myoblast cells. In addition, loss of BAMBI converts C2C12 myoblasts to brown adipocytes through downregulation MyoD and upregulation of Prdm16. Conversely, BAMBI overexpression strikingly enhanced myogenic differentiation of C2C12 myoblasts by upregulating MyoD expression. Taken together, our results establish that BAMBI is a vital myogenic factor involved in myoblasts differentiation and as a key regulator governing the balance between myogenic and adipogenic lineage in C2C12 myoblast cells. - Source: PubMed
Publication date: 2026/08/06
Yao XiangpingXie Liwei - Age-related sarcopenia is characterized by a progressive decline in skeletal muscle mass and function, with satellite cell dysfunction representing a central pathogenic mechanism. Diosgenin, a steroidal saponin derived from plants of the Dioscorea genus, has demonstrated potential anti-aging properties; however, its role in sarcopenia remains unclear. In this study, naturally aged C57BL/6J mice and a D-galactose (D-gal)-induced senescent C2C12 cell model were employed to systematically investigate the effects of diosgenin on muscle function, satellite cell dynamics, and the sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) signaling pathway. Diosgenin treatment significantly improved forelimb grip strength and exercise endurance, increased the gastrocnemius muscle index, and enlarged muscle fiber cross-sectional area in aged mice. Mechanistically, diosgenin upregulated the expression of myokines meteorin-like protein (METRNL) and insulin-like growth factor 1 (IGF-1) at both mRNA and protein levels, increased the number of proliferative satellite cells positive for paired box 7 (Pax7) and Ki67, and enhanced the expression of myogenic markers, including myogenic factor 5 (Myf5), Pax7, and myosin heavy chain II (MyHC II). These effects were mediated by direct activation of SIRT1, leading to deacetylation of PGC-1α. Notably, pharmacological inhibition of SIRT1 with EX527 markedly abrogated the diosgenin-induced effects. Molecular docking and cellular thermal shift assays further confirmed the direct interaction between diosgenin and SIRT1. Collectively, these findings demonstrate that diosgenin alleviates age-related sarcopenia by activating the SIRT1/PGC-1α signaling pathway to promote satellite cell proliferation and myogenic differentiation, highlighting its potential as a promising therapeutic candidate for sarcopenia. - Source: PubMed
Zeng XinDing HanLi ZiyeWang QianGuan PeiyaoWang TingtingWang JiayunFu YansongChen LizhangQin Hong - Skeletal muscle regeneration is a dynamic biological process that requires metabolic remodeling, satellite cell activation, inflammatory responses, and tissue remodeling. Although biological sex is recognized as an important determinant of skeletal muscle regeneration, whether males and females utilize distinct metabolic programs during regeneration remains poorly understood. In the present study, we investigated sex-dependent differences in metabolic remodeling and regenerative responses following cardiotoxin (CTX)-induced skeletal muscle injury in mice. Targeted metabolomic analysis performed at 7 days post-injury (DPI) revealed clear sex-dependent metabolic remodeling. Principal component analysis and pathway enrichment analysis identified glycolysis/gluconeogenesis as the most significantly altered metabolic pathway following injury. Male mice exhibited higher levels of several glycolytic, tricarboxylic acid (TCA) cycle, and amino acid metabolites than female mice. In contrast, female mice showed greater expression of Pax7, Myf5, and Myod1, together with increased Pax7-positive cells, greater Cyclin D1 staining, and higher expression of Ccne1, Cdc2, and Cdk4. Local inflammatory responses also differed between sexes, with distinct temporal patterns of MCP-1, IL-6, TNF-α, and CD45 during regeneration. Histological analyses demonstrated greater lipid accumulation in female muscle at 7 DPI, whereas both sexes exhibited comparable percentages of centrally nucleated fibers and similar restoration of muscle architecture by 21 DPI. Together, these findings indicate that biological sex is associated with differences in metabolism, satellite cell-associated responses, inflammatory responses, and tissue remodeling during skeletal muscle regeneration. Although males and females ultimately achieved comparable structural recovery, the regenerative process differed substantially during the early phase after injury. These findings provide additional insight into the biological processes underlying sex-dependent skeletal muscle regeneration and establish a foundation for future studies investigating the mechanisms linking metabolism to regeneration. - Source: PubMed
Publication date: 2026/07/13
Jin Jong BeomSoukup ToriRobinson AngeliqueBlack EmberWilliams AddisonPranay AtulHumphries KennethKim Dong YeonKim YooLucas EdralinHammer Shane MBae Jiyoung - This study explored the effects of dietary riboflavin supplementation on breast meat quality, muscle fiber characteristics, metabonomics, transcriptomics, and phosphoproteomics of Pekin ducks. A total of 96 14-day-old ducks were randomly allotted to two treatment groups, each with 8 replicates of 6 birds, and were fed diets supplemented with 0 or 10 mg/kg riboflavin for 28 days. Compared to the control group without riboflavin supplementation, dietary riboflavin supplementation significantly increased breast muscle shear force, myofiber diameter, perimeter, and cross-sectional area, as well as myofibril diameter. Dietary riboflavin supplementation increased gene expression involved in myogenic differentiation of breast muscle in Pekin ducks, including MYOD, MRF4, and MYF5. Breast muscle metabolomics revealed that riboflavin stimulated fatty acid beta oxidation, as most carnitine-related metabolites were upregulated. Transcriptomics analysis revealed that riboflavin upregulated seven genes involved in muscle contraction (MYO3A, MYO5B, MYH11, MYBPC1, TNNI1, TNNT2, A2M), and ten genes involved in fatty acid synthesis, oxidation, and transport processes, which may contribute to enhanced intramuscular fat content. Furthermore, phosphoproteomics analysis indicated dietary riboflavin supplementation altered the phosphorylation levels of proteins involved in muscle contraction and glycolysis (PGM1, ENO1, and TPI1), which may lead to an increase in pH. In conclusion, riboflavin supplementation in the diet improved the breast meat quality and fiber development of ducks probably by activating fatty acid beta oxidation, synthesis, and transport, as well as muscle contraction, while simultaneously depressing glycolysis process. - Source: PubMed
Publication date: 2026/06/22
Wu QingyiShao QingZhou WeiZhuang LeiJin YongyanZhou ZhengkuiXie MingHou ShuishengTang Jing - Recent reports indicate that stem cell spheres might offer enhanced therapeutic benefits by promoting cell engraftment ability, stemness, angiogenesis, and chemotaxis. Hence, we investigated whether amniotic fluid stem cells (AFSC) spheres could provide therapeutic benefits in stress urinary incontinence (SUI) due to their urethral sphincter-specific commitment. The isolated human AFSCs were characterized by flow-cytometry-based immunophenotyping and their multidifferentiation potential (osteo-, adipo-, and chondrogenic lineages). Time-dependent (>12, 16∼20, and 48 hours) culture conditions for AFSCsphere formation were optimized. Urodynamic parameters, including leak point pressure (LPP) and intercontraction interval (ICI), were determined. hAFSCsphere with ∼150 m diameter with minimal core necrosis at 16∼20 hours was found optimal for therapeutic application in the pudendal nerve injury-induced SUI rat model. The AFSCs demonstrated mesenchymal stem cell characteristics and multi-differentiation capabilities with retained levels of pluripotency and neural progenitor markers, SOX2 and nestin, respectively. Compared to AFSC, the AFSCsphere group showed superior LPP and ICI in rats; however, with either modest, relatively low, or unchanged levels of myogenic-lineage genes (, myoD, myogenin, and desmin) between them. Bladder and external urethral sphincter histologic architecture were also improved. Notably, AFSCsphere showed the elevated levels of secetome (VEGF, IL-6, IL-8, IL-9, and MIP-1) than AFSC, when compared to control. This could be attributed to non-myogenic pathways, such as paracrine dominance, including anti-inflammatory, angiogenic, or neurotrophic. Conclusively, our study revealed that AFSCsphere may improve urodynamics despite a significant increase in myogenic regulatory factor expression. Therefore, future studies should quantify AFSCsphere-specific properties, like stemness and cell-cell interactions, in reaching enhanced therapeutic outcomes. - Source: PubMed
Publication date: 2026/07/09
Lu Shing-HwaHwang Shiaw-MinDubey Navneet KumarTsai Ming-SongYun Tien-FuLiao Jiunn-Wang