Abstract：
:Mutations in the human MYH7 gene, encoding a slow skeletal muscle/β-cardiac myosin heavy chain, cause different types of myopathies. The nematode model Caenorhabditis elegans has frequently been employed to study the molecular and physiological consequences of MYH7 mutations in muscle function by introducing mutations into the unc-54 gene, the worm MYH7 ortholog. We report here that the C. elegans model is not appropriate for such studies if they involve expression of the UNC-54 protein (wild-type or fused to green fluorescent protein) above endogenous levels.
journal_name
Biotechniquesjournal_title
BioTechniquesauthors
Gil-Gálvez A,Carbonell-Corvillo P,Paradas C,Miranda-Vizuete Adoi
10.2144/btn-2020-0012subject
Has Abstractpub_date
2020-06-01 00:00:00pages
296-299issue
6eissn
0736-6205issn
1940-9818journal_volume
68pub_type
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