Topic
MYF5
About: MYF5 is a research topic. Over the lifetime, 933 publications have been published within this topic receiving 69231 citations. The topic is also known as: bHLHc2 & myogenic factor 5.
Papers published on a yearly basis
Papers
More filters
TL;DR: In this article, the major open reading frame encoded by this cDNA contains a short protein segment similar to a sequence present in the myc protein family, and the expression of one of these cDNAs transfected into C3H10T1/2 fibroblasts, where it is not normally expressed, is sufficient to convert them to stable myoblasts.
3,162 citations
TL;DR: The paired box transcription factor Pax7 was isolated by representational difference analysis as a gene specifically expressed in cultured satellite cell-derived myoblasts and it was demonstrated that satellite cells and muscle-derived stem cells represent distinct cell populations.
2,148 citations
TL;DR: It is shown by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5, a gene previously thought to be expressed only in the myogenic lineage.
Abstract: Brown fat can increase energy expenditure and protect against obesity through a specialized program of uncoupled respiration. Here we show by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5, a gene previously thought to be expressed only in the myogenic lineage. We also demonstrate that the transcriptional regulator PRDM16 (PRD1-BF1-RIZ1 homologous domain containing 16) controls a bidirectional cell fate switch between skeletal myoblasts and brown fat cells. Loss of PRDM16 from brown fat precursors causes a loss of brown fat characteristics and promotes muscle differentiation. Conversely, ectopic expression of PRDM16 in myoblasts induces their differentiation into brown fat cells. PRDM16 stimulates brown adipogenesis by binding to PPAR-gamma (peroxisome-proliferator-activated receptor-gamma) and activating its transcriptional function. Finally, Prdm16-deficient brown fat displays an abnormal morphology, reduced thermogenic gene expression and elevated expression of muscle-specific genes. Taken together, these data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myoblast markers and is not involved in white adipogenesis.
2,116 citations
TL;DR: Observations suggest that either Myf-5 or MyoD is required for the determination of skeletal myoblasts, their propagation, or both during embryonic development and indicate that these factors play, at least in part, functionally redundant roles in myogenesis.
1,686 citations
TL;DR: To test Myogenin's role in vivo, mice homozygous for a targeted mutation in the myogenin gene were generated and these mice survive fetal development but die immediately after birth and show a severe reduction of all skeletal muscle.
Abstract: Myogenin is a muscle-specific transcription factor that can induce myogenesis in a variety of cell types in tissue culture. To test myogenin's role in vivo, mice homozygous for a targeted mutation in the myogenin gene were generated. These mice survive fetal development but die immediately after birth and show a severe reduction of all skeletal muscle. Myogenin-mutant mice differ from mice carrying mutations in genes for the related myogenic factors Myf5 and MyoD, which have no muscle defects. Myogenin is therefore essential for the development of functional skeletal muscle.
1,316 citations