June 23, 2007Human Molecular Genetics

Functional capacity of dystrophins carrying deletions in the N-terminal actin-binding domain

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Population

2-day-old dystrophin-deficient mdx mice

Comparison

Microdystrophins lacking ABS2 and 3 or ABS3… vs Microdystrophin with an intact ABD1

Design

Preclinical

Follow-up

4 months

Authors

GBGlen B. BanksSeattle Pacific University PGPaul GregorevicThe University of Melbourne JAJames M. AllenUniversity of the Free State

Discussion

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Implication

Preserving intact ABD1 in microdystrophins may be required for DMD therapy; animal data leaves open human translation.

Structured PICO

Population

2-day-old dystrophin-deficient mdx mice

Intervention

Microdystrophins lacking ABS2 and 3 or ABS3 alone delivered via recombinant adeno-associated viral vectors into the tibialis anterior muscles

Comparator

Microdystrophin with an intact ABD1

Outcome

Specific force generation and susceptibility to contraction-induced injury at 4 months of agesurrogate

An intact N-terminal actin-binding domain (ABD1) is required to support normal contractile properties of skeletal muscle and protect against myofiber necrosis in dystrophin-deficient models.

Cite This Study

Banks et al. (2007) studied this question.

synapsesocial.com/papers/6a7cb46b8a7077a9e43f7330 https://doi.org/10.1093/hmg/ddm158

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Functional capacity of dystrophins carrying deletions in the N-terminal actin-binding domain

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Functional capacity of dystrophins carrying deletions in the N-terminal actin-binding domain

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider