https://www.selleckchem.com/pr....oducts/acalabrutinib
These alternate transcripts were expressed at very low levels in the wild-type mice and were significantly upregulated in the mutant mice, indicating that pre-translational splicing defects may be a critical component of the disease mechanism associated with the mutation. Evidence of reduced expression of the full-length CFL2 transcript was also observed in the muscle biopsy sample of the patient with p.A35T mutation. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email jou
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