Search results for "myotube"

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Differentiation of Murine C2C12 Myoblasts Strongly Reduces the Effects of Myostatin on Intracellular Signaling

2020

Alongside in vivo models, a simpler and more mechanistic approach is required to study the effects of myostatin on skeletal muscle because myostatin is an important negative regulator of muscle size. In this study, myostatin was administered to murine (C2C12) and human (CHQ) myoblasts and myotubes. Canonical and noncanonical signaling downstream to myostatin, related ligands, and their receptor were analyzed. The effects of tumorkines were analyzed after coculture of C2C12 and colon cancer-C26 cells. The effects of myostatin on canonical and noncanonical signaling were strongly reduced in C2C12 cells after differentiation. This may be explained by increased follistatin, an endogenous blocke…

Muscle Fibers Skeletallcsh:QR1-502lihaksetlcsh:MicrobiologyArticleTGF-BETA SUPERFAMILYCell LineMyoblastsMicetumorkineCell Line TumorfollistatinAnimalsHumansCANCER CACHEXIAskeletal muscleMUSCLE ATROPHYlihassolutSmadsoluviestintäRECEPTORCell DifferentiationIN-VITROMyostatinmusculoskeletal systemMAPKActivinsLEUKEMIA INHIBITORY FACTORACTIVIN-AinflammationCulture Media ConditionedCELLSPROTEIN-SYNTHESISmyotubeGROWTH1182 Biochemistry cell and molecular biologyproteiinit3111 BiomedicinecocultureSignal Transduction
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Musashi-2 contributes to myotonic dystrophy muscle dysfunction by promoting excessive autophagy through miR-7 biogenesis repression

2021

Skeletal muscle symptoms strongly contribute to mortality of myotonic dystrophy type 1 (DM1) patients. DM1 is a neuromuscular genetic disease caused by CTG repeat expansions that, upon transcription, sequester the Muscleblind-like family of proteins and dysregulate alternative splicing of hundreds of genes. However, mis-splicing does not satisfactorily explain muscle atrophy and wasting, and several other contributing factors have been suggested, including hyperactivated autophagy leading to excessive catabolism. MicroRNA ( miR ) -7 has been demonstrated to be necessary and sufficient to repress the autophagy pathway in cell models of the disease, but the origin of its low levels in DM1 was…

autophagyMSI2 antisense oligonucleotides autophagy miR-7 muscle atrophy muscle dysfunction myotonic dystrophy myotubesRM1-950BiologyMyotonic dystrophyMSI2chemistry.chemical_compoundDrug DiscoverymedicineMyocyteGene silencingMBNL1muscle dysfunctionmyotonic dystrophyMyogenesisAutophagymiR-7Skeletal musclemedicine.diseaseMuscle atrophyCell biologymedicine.anatomical_structurechemistryMolecular MedicineTherapeutics. Pharmacologyantisense oligonucleotidesmedicine.symptomMolecular Therapy - Nucleic Acids
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