Long non-coding RNAs (lncRNAs) are potent transcriptional and posttranscriptional regulators of mammalian gene expression programs. By interacting with different molecular partners, particularly proteins and other RNAs, lncRNAs serve diverse roles in biological processes. One such process is myogenesis, wherein mononucleated, undifferentiated myoblasts proliferate and further differentiate into multinucleated, mature muscle fibers capable of contractile activity. Through myogenesis, muscle is created during development and is regenerated in adult life. As myogenesis is impaired with advancing age and in certain pathologies, understanding it in molecular detail can uncover therapeutic targets. However, the specific molecular mechanisms by which lncRNAs regulate human myogenesis are poorly understood. In this thesis, we have uncovered a novel muscle-specific lncRNA, lncFAM71E1-2:2 (lncFAM), which increased robustly during early human myogenesis. Silencing lncFAM attenuated differentiation of human myoblasts into myotubes, while overexpression of lncFAM promoted this process. As lncFAM resides in the nucleus, chromatin isolation by RNA purification followed by mass spectrometry (ChIRP-MS) analysis was employed to identify the molecular mechanisms whereby it might promote myogenesis. Analysis of lncFAM-interacting proteins revealed that lncFAM recruited the RNA-binding protein HNRNPL to the promoter of MYBPC2, in turn increasing MYBPC2 mRNA transcription and enhancing production of the myogenic protein MYBPC2. These results highlight a mechanism whereby a novel ribonucleoprotein complex, lncFAM-HNRNPL, promotes MYBPC2 expression transcriptionally to increase myogenesis.