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lncMUMA promoted myogenic differentiation by functioning as a miR-762 sponge to regulate the core myogenic regulator MyoD in vitro. The enforced expression of lncMUMA relieved the decreases in MyoD protein and muscle mass in miR-762 knockin mice
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Ablation of the Hes1 oscillator in stem cells interfered with stable MyoD oscillations and led to prolonged periods of sustained MyoD expression, resulting in increased differentiation propensity
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MyoD upstream noncoding RNA (MUNC) overexpression in MYOD (-/-) C2C12 cells induces many myogenic transcripts in the complete absence of MyoD protein. Genomewide analysis showed that, while many genes are regulated by MUNC in a MyoD-dependent manner, there is a set of genes that are regulated by MUNC, both upward and downward, independently of MyoD.
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By comparative genomic analysis of single nucleotide polymorphism (SNPs) across publicly available data from 17 strains of laboratory mice, the authors show that variant sequences within the MyoD-bound motifs, but not their genome-wide counterparts, are under selection.
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Expression patterns of the joint marker Gdf5, tendon and ligament marker Scleraxis, early muscle marker MyoD1, and blood vessel marker Cadherin5 (Cdh5) are presented during the most active phases of embryonic mouse limb patterning.
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An absolute requirement for either MyoD or Myf5 in muscle regeneration.
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MyoD signaling during myogenesis is regulated by HDAC1.
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Linc-RAM regulates expression of myogenic genes by directly binding MyoD, which in turn promotes the assembly of the MyoD-Baf60c-Brg1 complex on the regulatory elements of target genes.
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ACL regulates the net amount of acetyl groups available, leading to alterations in acetylation of H3(K9/14) and H3(K27) at the MYOD locus, thus increasing MYOD expression.
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Studies indicate MyoD displays function to regulate determination of skeletal muscle progenitors [Review].
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Muscle regulatory transcription factor MyoD regulates the expression of the pro-apoptotic Bcl2 family member PUMA by binding to the promoter region of PUMA. The increase in MyoD binding to the PUMA promoter as a consequence of culture in differentiation media (DM) is diminished in myoblasts silenced for MyoD expression. In myoblasts silenced for MyoD expression, p53 binding to the PUMA promoter is diminished in response
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our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.
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The data showed that Mettl3 is required for MyoD mRNA expression in proliferative myoblasts.
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Gm7325, as a novel MyoD-target gene, is specifically induced in activated satellite cells, and may have an important role in skeletal myogenesis.
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The ELF-EMFs did not affect C2C12 myoblast viability or proliferation rate. Conversely, at ELF-EMF intensity in the mT range, the myogenic process was accelerated, through increased expression of MyoD, myogenin, and connexin 43
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In this study, we identified ubiquitin-specific protease 4 (USP4), one of deubiquitinating enzymes, as a suppressor of MRFs by demonstrating that a knockdown of USP4 enhances myogenesis by controlling MyoD and the level of myogenesis marker proteins in C2C12 cells... we propose that USP4 is a key player in myogenic differentiation; it controls myogenic regulatory factors in a catalytic-independent manner
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MyoD regulates the oxidative metabolic capacity of adult skeletal muscle;ChIP-seq analysis identified MyoD binding on the PGC-1b, but not PGC-1a, gene locus;MyoD cooperates with alternative NF-kappaB to regulate PGC-1b transcription; MyoD and RelB co-occupy many other genes involved in aerobic respiration
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LSD1 is required for the timely expression of MyoD in limb buds.
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bn1 expression is induced during myoblast differentiation, in a p38 MAP kinase- and MyoD- dependent manner. RNAi-mediated depletion of drebrin, or treatment with a chemical drebrin inhibitor, resulted in a similar phenotype in myoblasts: defective differentiation, with low levels of early and late differentiation markers and inefficient production of myofibers.
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Data show that MyoD and myogenin associate with distinct chromatin states.