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elegans, mice or fish. ‘To understand the mechanism, it is important to know that in DMD, various mutations in the dystrophin gene prevent the production of a functional gene product, i.e. a protein.
The deletion of residues 239-272 from the hamster beta-adrenergic receptor resulted in a loss of the ability of the receptor, expressed in mouse L cells, to stimulate adenylate cyclase (Dixon, R. A. F ...