Anti - Mouse, MyoD1 Clone 5.8A
- Known as:
- Anti - Mouse, MyoD1 Clone 5.8A
- Catalog number:
- 60-0101
- Product Quantity:
- 6 mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse MyoD1 Clone 5.8A
Ask about this productRelated 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
- Although Mettl3-mediated N6-methyladenosine (mA) modification has confirmed to regulate mammalian development, the precise mechanisms by which it controls myoblast differentiation and fusion remain unclear. Here, we found that Mettl3 expression and global mA levels decreased during myogenic differentiation. Mettl3 knockdown inhibited myoblast proliferation, promoted myoblast differentiation and fusion, and reduced protein degradation in myotubes, whereas its overexpression had the opposite effects. High-throughput sequencing identified forkhead box O1 (FOXO1) as a potential target of Mettl3-mediated myogenesis. Mechanically, Mettl3-mediated methylation of FOXO1 3'untranslated region (3'UTR) promotes its translation in a Ythdf3-dependent manner, thereby suppressing the MyoD1-Myomaker/Myomixer axis and activating the ubiquitin-proteasome system (UPS). Furthermore, FOXO1 knockdown alleviates the impaired myoblast differentiation and fusion induced by Mettl3 overexpression by upregulating the MyoD1-Myomaker/Myomixer axis and suppressing the UPS. Collectively, these findings indicate that Mettl3 inhibits myoblast differentiation and fusion via the FOXO1-mediated MyoD1-Myomaker/Myomixer axis and UPS in an mA-Ythdf3-dependent manner. - Source: PubMed
Publication date: 2026/07/03
Deng KaipingSu YalongLiu ZhipengWu JinxingHu SiluZhang ZhenRen CaifangLiu ZhilinWang LiqinFan YixuanZhang YanliWang Feng - Grass carp (Ctenopharyngodon idella) is a major aquaculture species, yet production efficiency is often constrained by growth performance and metabolic disorders such as hepatic lipid deposition. Conventional selective breeding faces challenges in further improving these complex traits, necessitating precision genetic interventions. In this study, we combined comparative transcriptomics with CRISPR/Cas9 mediated gene disruption to investigate the regulatory role of Pik3r1. Comparative RNA-seq of fast- and slow-growing individuals together with protein-protein interaction network analysis identified Pik3r1 as a candidate negative regulator of growth. To validate its function, we generated Pik3r1 mosaic F0 mutants by targeting the SH3 domain of Pik3r1. Disruption of Pik3r1 conferred a profound growth advantage, increasing body weight by 51.8% and body length by 13.5% compared to wild-type controls. Histological analyses revealed that enhanced muscle accretion was driven by both hypertrophy with a 22.50% increase in myofiber cross-sectional area and hyperplasia characterized by an 18.90% rise in fiber density, coupled with a 67.7% reduction in hepatic lipid accumulation. At the molecular level, Pik3r1 disruption relieved the inhibitory effect on the PI3K/AKT/mTOR cascade, with upregulation of PI3K, AKT, mTOR, S6K1, Myod1, and Mybpc1 and downregulation of 4ebp1 and Pik3ca in muscle, accompanied by upregulation of PPARα and CPT1a and downregulation of FASN and ACC1 in the liver. Furthermore, a clear genotype phenotype correlation was observed: fish carrying confirmed premature termination codons exhibited substantially greater growth enhancement (77.6% increase in body weight) than those with in-frame mutations. Collectively, our results support Pik3r1 as a key regulator linking somatic growth and lipid metabolism in grass carp, and highlight its potential as a target for molecular breeding aimed at improving yield and carcass quality. - Source: PubMed
Publication date: 2026/06/30
Lv WenyaoMeng XinzhanSun TianyangChen YuxuanLi WeizhongSheng TaoCong QianYu QiaozhenHe RuitaoHe RuicongShen YubangRen JianfengQiu JunqiangGui LangLi JialeXu Xiaoyan - Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder primarily affecting male children and resulting in progressive degeneration and attempted regeneration of muscle with replacement of myofibers by adipose and fibrotic tissue. DMD patients have mutations in the gene encoding for the large cytoskeletal protein dystrophin, which plays an essential role in the dystrophin-glycoprotein complex (DGC) as a structural connector within cardiac and skeletal muscle. The absence of dystrophin and DGC proteins leads to increased membrane fragility, dysregulation of calcium homeostasis, oxidative damage in muscle cells, and finally, premature death of the patients. Rhabdomyosarcoma (RMS), a soft tissue sarcoma arising from subpopulations of muscle cells and their precursors, has previously been reported in DMD patients and mouse models of DMD. Here, we report a case series of RMS arising from skeletal muscles in a -mutated () rat model developed using transcription activator-like effector nucleases targeting exon 23 of the gene on a Sprague Dawley background. Subcutaneous firm masses were noted grossly in 8 male rats aged 6 to 17 months. The histologic findings were consistent with a sarcoma of skeletal muscle, with a population of small round cells in addition to spindle-shaped cells and occasional large multinucleated cells. The neoplasms were immunoreactive for myogenin, MyoD1, and desmin. Histology and immunohistochemistry supported the diagnosis of RMS. This represents a potentially novel animal model of DMD-associated RMS. - Source: PubMed
Publication date: 2026/06/30
Moore Rachel HLuo SiWeiLafoux AudeLe Guiner CarolineHuchet CorinneKuo Shanny HTerceve OliviaMack David LSheppard HeatherLarcher ThibautSnyder Jessica M - Junmu No.1 is a commercially important Chinese pig breed, yet stable in vitro models for investigating its muscle development mechanisms and genetic regulation remain lacking; this study aimed to establish an immortalized porcine satellite cell line from Junmu No.1 pigs to address this gap. Primary porcine satellite cells (PSCs) were isolated from a 2-day-old Junmu No.1 piglet and immortalized via lentiviral transduction using the pHAGE-EF1α-eGFP-SV40LT-BleoR vector. The resulting cell line (imPSC-JM) was characterized for morphology, satellite cell marker expression, karyotype stability, myogenic differentiation capacity, and long-term proliferative potential, and RNA sequencing combined with Gene Set Enrichment Analysis (GSEA) was performed to assess transcriptomic fidelity relative to primary PSCs. The imPSC-JM line retained characteristic spindle-shaped satellite cell morphology, consistently expressed PAX7, maintained a normal diploid karyotype (2 = 38, XY), and showed stable SV40 large T antigen expression, enabling sustained proliferation exceeding 100 cumulative population doublings while preserving myogenic differentiation and the formation of multinucleated myotubes expressing Desmin, MYHC, and DMD. Transcriptomic profiles were highly concordant with primary PSCs (Pearson r ≥ 0.95; R = 0.9188; 83.8% of expressed genes unchanged), with key satellite-cell and myogenic regulator genes (PAX7, MYOD1, MYF5, MYOG, MYF6) unaltered, while GSEA revealed upregulation of autophagy and inflammatory signaling and downregulation of ribosome biogenesis. The imPSC-JM line thus provides a reliable experimental platform with high transcriptomic fidelity for studying muscle development and genetic regulation in Junmu No.1 pigs. - Source: PubMed
Publication date: 2026/06/04
Li JingHe YuZhang XiaoranNing JiayiWang DaliBai ChunyanSun BoxingZhang ShaoxuanLiang ShuangSun Hao - Sarcopenia is an age-related disorder characterized by loss of muscle mass, strength, and function, driven by oxidative stress, chronic inflammation, and protein imbalance. Broccoli-derived peptides (BDP) exert anti-inflammatory and myofiber-protective effects, while leucine regulates energy metabolism and redox balance. - Source: PubMed
Publication date: 2026/06/19
Yuan KexinWu WenbinSu NingCui MingyangQi JingyiZhang YangZhang ZhengyangAn PengLuo JunjieLuo Yongting