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)
- The antibiotic toxicity and risks associated with their residues pose a serious threat to food safety. - Source: PubMed
Publication date: 2026/09/19
Yu ZheDing Qian-WenHao QiangYao Yuan-YuanRan ChaoYang Ya-LinZhang ZhenZhou Zhi-Gang - Copper is an essential trace element for beef cattle, yet its muscle developmental regulatory mechanism remains unclear. This study investigated the effects of copper sulfate (CuSO₄) on myogenic differentiation of bovine skeletal muscle-derived cells (BSMC) and the underlying molecular mechanisms. BSMC were isolated from the longissimus thoracis muscle of three 30-month-old crossbred steers, with each steer defined as an independent experimental unit corresponding to a separate biological replicate (n = 3). Based on cell viability, CuSO₄ was used at 0, 0.1, 1, and 10 µM. All cell samples were harvested at differentiation day 6 (D6). The 0.1 µM CuSO₄ treatment during cell growth significantly promoted D6 myotube formation (P = 0.049), and upregulated mRNA and protein expression of myogenic differentiation 1 (MyoD) (P = 0.044, P = 0.030), as well as protein expression of hypoxia-inducible factor-1α (HIF-1α) (P = 0.037) and β-catenin (P = 0.050). During differentiation, 1 µM CuSO₄ significantly facilitated D6 myotube formation (P = 0.0004), increased myogenic factor 5(Myf5) mRNA and protein expression (P = 0.030, P = 0.006), and elevated HIF-1α (P = 0.025) and β-catenin (P = 0.004) protein levels, whereas Wnt10b protein expression remained unaltered (P = 0.930). Single or combined pharmacological inhibition of HIF-1α and β-catenin markedly reversed copper's pro-myogenic effect on BSMC. In conclusion, copper modulates BSMC myogenic differentiation via the HIF-1α/β-catenin axis by enhancing β-catenin protein stability independent of Wnt10b transcription. HIF-1α acts upstream to drive β-catenin, and a reciprocal regulatory relationship may exist in which β-catenin in turn helps sustain HIF-1α abundance, thereby supporting cascade signaling and downstream myogenic transcription. This study elucidates copper's molecular mechanism governing muscle development and provides theoretical support for precise copper supplementation to improve beef production performance. - Source: PubMed
Publication date: 2026/09/16
Liu Bai HanZhang Jin GePeng Dong QiaoJin Yong Cheng - Cancer cachexia is a complex metabolic syndrome characterized by progressive skeletal muscle wasting and poor clinical outcomes. Previous studies have mainly focused on the association between cancer-derived extracellular vesicles and atrophy of differentiated myotubes, whereas their effects on myoblast differentiation markers have not been sufficiently elucidated. In this exploratory in vitro study, vesicle fractions isolated from MC38, CT26, MCA205, and B16F10 cancer cell lines under serum-deprived conditions were referred to as small extracellular vesicles (sEVs) and used to treat C2C12 myoblasts during differentiation. Compared with the control group, the sEV-treated groups showed reduced myotube diameter and differentiation area on day 6, while the mRNA expression patterns of , (), , , , and several MHC isoforms showed time-dependent changes. GO/KEGG analysis of commonly identified proteins revealed enrichment of terms related to mRNA metabolism, the cell cycle, and the proteasome. These findings suggest that treatment with cancer cell-derived sEVs may be associated with impaired in vitro differentiation of C2C12 myoblasts. - Source: PubMed
Publication date: 2026/09/04
Lee WoojinYang SeongjaeYu HyeonseoKim YeongminCho SeongminKim Hyeong YunKim UijooKong HyunseokKim Sang Bum - Rapid muscle growth suppresses intramuscular fat deposition in chickens, leading to decreased meat quality; however, the underlying mechanism remains unclear. Here, we compared differences in myogenic and adipogenic properties in the breast muscle of Ross 308 (RS) and Xueshan (XS) broilers during growth, and analyzed the contribution of hormone levels and vascular density to these differences. Our results showed that body weight, breast muscle ratio, and myofiber size were significantly greater in RS broilers from embryonic day 12 (E12), and these differences became more pronounced after day 21 (D21), which was accompanied by marked increases in the abundance of PAX7⁺ satellite cells (SCs) and enhanced expression of PAX7, MYF5, MYOD, and MYOG. In addition, higher levels of T, T, and IGF-1 were found in both yolk and serum of RS broilers from E12 to D42. In contrast, XS broilers exhibited greater intramuscular fat deposition before hatching, which was accompanied by greater number of TCF4⁺ fibro/adipogenic progenitors (FAPs) and enhanced expression of PDGFRA and ZNF423. Consistently, the number of CD31⁺ endothelial cells and expression of CD31 and VEGFA were also higher in XS broilers from E12 to D1, suggesting that enhanced angiogenesis supported FAPs proliferation. Therefore, the rapid muscle growth and enhanced myogenic capacity of SCs suppressed the proliferation and adipogenic differentiation of FAPs in broilers, with hormone levels and angiogenesis playing regulatory roles. These findings provide valuable insights into the competing mechanism of myogenesis and intramuscular adipogenesis in broilers. - Source: PubMed
Publication date: 2026/08/16
Sun XuanLiu JianliangZhang XiuzeLiu YingXing TongZhang LinGao FengZhao Liang - Dysferlinopathy is a rare muscular dystrophy characterized by chronic muscle damage and ineffective regeneration. While late-stage morphological changes, such as fibroadipose replacement, are well described, the early molecular mechanisms driving muscle fiber loss and regenerative failure at the onset of the disease remain largely uncharacterized. To address this gap, we investigated the skeletal muscles of dysferlin-deficient Bla/J mice during the early manifestation stage (3 months of age). This exploratory study aimed to identify primary pathomorphogenetic events by correlating the transcriptomic profile of the tissue with its specific histopathological and ultrastructural alterations. We performed a comparative analysis of the m. gastrocnemius in 3-month-old Bla/J mice versus wild-type controls using RNA sequencing, RT-qPCR, histomorphometry and transmission electron microscopy. The results revealed atrophy and muscle fiber necrosis without the expected induction of Fbxo32 and Trim63 ubiquitin ligases, suggesting ubiquitin-proteasome system-independent muscle mass loss. Furthermore, the absence of Casp3, Bak1, and Bad induction, confirmed by the lack of active caspase-3, excluded apoptosis as the primary death mechanism. A differentiation block in satellite cells was confirmed by the lack of Myf5, Myod1, and Myog induction and a trend toward Tead4 suppression, pointing to an early failure of the reparative program. Exploratory RNA sequencing also identified a suppression of Prkn expression accompanied by LC3B-II-positive autophagosome accumulation. Immunohistochemical and immunofluorescent evaluation of the mitochondrial network (TOMM20) revealed abnormal accumulations and dense clumping, indicating impaired organelle clearance. Furthermore, ultrastructural analysis demonstrated internal organelle damage and the presence of myelin-like structures, consistent with a state of stalled mitophagy. Collectively, this exploratory study demonstrates that early muscle atrophy and myofiber necrosis in dysferlinopathy occur independently of canonical ubiquitin-proteasome and apoptotic pathways. Instead, the disease manifestation stage is structurally characterized by stalled mitochondrial clearance and a delayed regenerative response. - Source: PubMed
Publication date: 2026/09/10
Limaev Igor SGladyshev Nikita SYakovlev Ivan AShigapova Leila KhShagimardanova Elena IChekmareva Irina AZolkin Alexey GGusev Oleg ADeev Roman V