| pubmed-article:18435820 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18435820 | lifeskim:mentions | umls-concept:C0042567 | lld:lifeskim |
| pubmed-article:18435820 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:18435820 | lifeskim:mentions | umls-concept:C0012578 | lld:lifeskim |
| pubmed-article:18435820 | lifeskim:mentions | umls-concept:C1160320 | lld:lifeskim |
| pubmed-article:18435820 | lifeskim:mentions | umls-concept:C1522240 | lld:lifeskim |
| pubmed-article:18435820 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18435820 | pubmed:dateCreated | 2008-7-9 | lld:pubmed |
| pubmed-article:18435820 | pubmed:abstractText | Muscle formation and repair depends critically on the fusion of myoblasts. Despite the importance of this process, little is known about the cellular and molecular mechanisms regulating fusion. Forward genetic screens in Drosophila melanogaster have uncovered genes that, when mutated, prevent myoblast fusion. Analyses of these gene products have indicated that the actin cytoskeleton and its regulation play a central role in the fusion process. In this review, we discuss recent advances in the field, including new imaging approaches to analyze fusion as well as a description of novel genes required for fusion. In particular, we highlight what has been learned about the requirement of a specific actin structure at the site of fusion. We also place these findings from Drosophila within the context of myoblast fusion in vertebrates. | lld:pubmed |
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