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)
- Skeletal muscle growth in poultry depends on the proliferation and differentiation of skeletal muscle satellite cells (SMSCs), yet the regulatory landscape governing these processes in quail remains poorly defined. In this study, primary SMSCs were isolated from embryonic day 15 quail pectoral muscle and validated by PAX7 immunostaining and MYHC immunostaining following induction of differentiation. rRNA-depleted RNA-seq was performed at three developmental stages: satellite cells after differential adhesion (DA), proliferating myoblasts (GM), and differentiated myotubes after 4 d (DM4). Transcriptome profiling identified 9,728 common genes expressed in three group, with 1,254 genes differentially expressed across all pairwise comparisons. Functional enrichment analyses indicated a coordinated shift from cell cycle progression in proliferating cells to muscle contraction, oxidative phosphorylation, and calcium signaling during differentiation. Short time-series expression miner (STEM) analysis revealed distinct temporal expression patterns, highlighting proliferation-associated regulators (e.g., KDR, PIK3R1, MYF5, MYF6, NOTCH1, and WNT2) and myotube-related genes (e.g., ALDH18A1, HOXC8, TBX5, and EN1) as central nodes within stage-specific networks. In addition, 935 lncRNAs and 13,588 circRNAs were detected, many displaying stage-specific expression patterns. Predicted lncRNA-mRNA interactions and circRNA host gene enrichment implicated these noncoding RNAs in muscle development and metabolic remodeling. A competing endogenous RNA network highlighted miR-466-x and novel-m0255-5p as potential post-transcriptional regulators of muscle-related genes, including VEGFA, HDAC4, MYLK4, and NOX4. These findings provide a comprehensive transcriptomic resource for quail myogenesis and identify candidate coding and noncoding regulators relevant to muscle growth in poultry. - Source: PubMed
Publication date: 2026/08/03
Liu JingJiang HongxiaXiao XiaoyunLiao ZurongWang YuxiangDing ZhenxvanChai XuewenLiu HaodongHuang XvwenWei WenhuaXie YunongLiu LuoyangWang ZikunHu XiaolongLiu SanfengChen BiaoMao Huirong - 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