Anti - Mouse, MyoD1 Clone 5.8A
- Known as:
- Anti - Mouse, MyoD1 Clone 5.8A
- Catalog number:
- 60-0101-7
- Product Quantity:
- 7mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse MyoD1 Clone 5.8A
Related genes to: Anti - Mouse, MyoD1 Clone 5.8A
- Gene:
- CCNQ NIH gene
- Name:
- cyclin Q
- Previous symbol:
- FAM58A
- Synonyms:
- -
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-19
- Date modifiied:
- 2017-07-14
- Gene:
- CCNQP2 NIH gene
- Name:
- CCNQ pseudogene 2
- Previous symbol:
- FAM58AP1, FAM58CP
- Synonyms:
- FAM58Y
- Chromosome:
- Yq12
- Locus Type:
- pseudogene
- Date approved:
- 2010-05-11
- Date modifiied:
- 2018-02-20
- Gene:
- EMC9 NIH gene
- Name:
- ER membrane protein complex subunit 9
- Previous symbol:
- C14orf122, FAM158A
- Synonyms:
- CGI-112
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-17
- Date modifiied:
- 2014-11-19
- Gene:
- KIR2DL1 NIH gene
- Name:
- killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 1
- Previous symbol:
- -
- Synonyms:
- cl-42, nkat1, 47.11, p58.1, CD158A
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-14
- Date modifiied:
- 2016-11-09
- Gene:
- MYOD1 NIH gene
- Name:
- myogenic differentiation 1
- Previous symbol:
- MYF3
- Synonyms:
- PUM, MYOD, bHLHc1
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2015-07-22
Related products to: Anti - Mouse, MyoD1 Clone 5.8A
Related articles to: Anti - Mouse, MyoD1 Clone 5.8A
- MicroRNAs are important regulators of skeletal muscle development and regeneration; however, the molecular basis by which exercise-induced miRNAs preserve middle-aged muscle function remains to be elucidated. This study aimed to investigate how aerobic exercise delays skeletal muscle attenuation by reversing age-related miRNAs dysregulation in male mice. Twelve-month-old male C57BL/6J mice (MC) ( = 8/group) were randomly assigned to a sedentary control group (OC) or an aerobic exercise group (OE) (12 m/min, 40 min/session, three sessions/week, for 12 weeks). miRNA sequencing identified differentially expressed miRNAs (DEmiRNAs), followed by miRNA-mRNA network construction. The results demonstrated that aerobic exercise improved muscle strength and mass while attenuating early atrophy and fibrosis. Four atrophy-associated DEmiRNAs (miR-150-5p, miR-199a-5p, miR-3535, and miR-329-5p) were reversed after aerobic exercise intervention. GO and KEGG profiling demonstrated that target genes were predominantly involved in protein binding and the Wnt signaling pathway. miR-199a-5p and miR-150-5p, with the most predicted targets, were selected as candidate mechanistic contributors, and FZD4 was confirmed as a common downstream target. Further analysis confirmed that miR-199a-5p and miR-150-5p inhibition attenuated D-galactose-induced C2C12 myotube atrophy, reducing Atrogin-1 and increasing MyoD1, FZD4, and β-catenin expression. These findings suggest that the exercise-induced miR-150-5p/miR-199a-5p axis may alleviate muscle aging in middle age via the restoration of key proteins in Wnt signaling and contribute preliminary observational evidence relevant to the understanding of aerobic exercise intervention in sarcopenia. - Source: PubMed
Publication date: 2026/06/25
Zhang LeHe JingziWang LiZhang Huan - Adult sinonasal rhabdomyosarcoma (RMS) is an exceptionally rare and aggressive malignancy originating from mesenchymal cells. It poses a significant diagnostic challenge due to its morphological and immunohistochemical overlap with other small round blue cell tumors, such as neuroendocrine carcinoma and olfactory neuroblastoma. Accurate diagnosis requires a high index of suspicion, advanced imaging, and comprehensive histopathology aided with immunohistochemistry (IHC) for specific myogenic markers like Myogenin and MyoD1. - Source: PubMed
Publication date: 2026/07/13
Khademi BijanYousefi AlirezaBagheri MiladYousufzai ShayanFatehi Negar - 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 - Dedifferentiated liposarcoma (DDLPS) is the most common retroperitoneal soft tissue sarcoma, characterized by and gene co-amplification. However, DDLPS with heterologous myogenic differentiation is extremely rare and poses a significant diagnostic challenge due to its expression of myogenic markers such as desmin, myogenin, and MyoD1, which can easily lead to misclassification as primary rhabdomyosarcoma. Testicular metastasis of DDLPS is even rarer, with only isolated case reports documented in the literature. We report a case of a 46-year-old male who presented with a large retroperitoneal mass without testicular involvement on initial imaging. He underwent en bloc resection of the retroperitoneal tumor including right nephrectomy and right hemicolectomy. Ten days postoperatively, he developed a right scrotal mass, prompting radical orchiectomy. Initial pathological evaluation suggested rhabdomyosarcoma based on desmin and MyoD1 positivity. However, subsequent expert pathological consultation with fluorescence hybridization (FISH) analysis revealed and gene amplification in both specimens, establishing the final diagnosis of DDLPS with prominent heterologous myogenic differentiation. Postoperative chest CT demonstrated early pulmonary metastases, underscoring the aggressive nature of this tumor. This case highlights the critical importance of / FISH testing in accurately diagnosing DDLPS with heterologous differentiation, particularly when myogenic markers are expressed, to avoid misdiagnosis and guide appropriate management. - Source: PubMed
Publication date: 2026/06/22
Ma HaosongFeng RunlinZi GuorunLi YiqingXu QuanlvKe Changxing - Cultured fish meat requires efficient expansion of piscine satellite cells (PSCs). However, prolonged culture impairs proliferation and differentiation. Here, astaxanthin (Ast) and naringin (Nar) were evaluated as food-grade alternatives to synthetic modulators such as MHY1485. The combination of Ast and Nar promoted proliferation by accelerating cell-cycle progression and reducing apoptosis. Synergy analysis (Bliss, HAS, and ZIP) indicated a synergistic effect between Ast and Nar. Ast combined with Nar also improved mitochondrial function and redox homeostasis, as evidenced by increased mitochondrial membrane potential, decreased mitochondrial superoxide, and decreased intracellular ROS levels. Furthermore, co-treatment upregulated the expression of myogenic markers, including MyoD1, MyoG, and MyHC, and promoted myotube formation. Mechanistically, these effects of Ast and Nar were associated with mTOR activation, as indicated by phosphorylation levels, while inhibition of mTOR with rapamycin (Rap) attenuated these effects. Collectively, these results highlighted that Ast combined with Nar was an excellent supplement for large-scale expansion and differentiation of PSCs. - Source: PubMed
Publication date: 2026/07/06
Jiang NingningBao HanYin RuiChen Qihe