Cholesterol availability modulates myoblast fusion.

Cholesterol availability modulates myoblast fusion

The requirement of cholesterol for myoblast fusion has been linked to the primary step in the fusion process, calcium-dependent aggregation (recognition). Inhibition of cholesterol synthesis with 25-hydroxycholesterol or compactin in the absence of exogenous lipid dramatically inhibits calcium-mediated aggregation and concomitant fusion within several hours. Restimulating cholesterol synthesis ...

NO induces myoblast fusion

T elomere association with nuclear pores is critical not only for transcriptional silencing but also for effi cient repair of double-stranded breaks in the subtelomeric region of budding yeast chromosomes, according to Therizols et al. (page 189). As in many organisms, yeast telomeres localize to the nuclear periphery. To determine whether nuclear pore proteins are involved in telomere tetherin...

c-Myb Inhibits Myoblast Fusion

Satellite cells represent a heterogeneous population of stem and progenitor cells responsible for muscle growth, repair and regeneration. We investigated whether c-Myb could play a role in satellite cell biology because our previous results using satellite cell-derived mouse myoblast cell line C2C12 showed that c-Myb was expressed in growing cells and downregulated during differentiation. We de...

Normal myoblast fusion requires myoferlin.

Muscle growth occurs during embryonic development and continues in adult life as regeneration. During embryonic muscle growth and regeneration in mature muscle, singly nucleated myoblasts fuse to each other to form myotubes. In muscle growth, singly nucleated myoblasts can also fuse to existing large, syncytial myofibers as a mechanism of increasing muscle mass without increasing myofiber numbe...

Invasive podosomes and myoblast fusion.