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In addition, the structural and biochemical analysis of five Bcl-xl substitution mutants will provide structural insights into the design and development of anti-cancer drugs.

Since production of multiple dystrophin isoforms due to alternative splicing or exon skipping is totally prevented in the DMD-null mouse, these new mutants will provide an improved model system for functional studies of dystrophin and its isoforms.

Further studies with these mutants will provide additional insight into the mechanisms of muscular dystrophies and will help in the development of useful drugs for WWS patients.

Further identification of the regulatory process and metabolic pathway in mutants will provide insights into the impaired miRNA biogenesis and abnormal trichome cell differentiation.

Maternal-zygotic zebrafish lkb1 mutants will provide a system to address whether and how Lkb1 functions in the first cleavage stages in vertebrates.

We anticipate that these mouse mutants will provide useful tools for others to perform further studies on eIF3h function in the cell.

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We speculate that the STX11 Arg78Cys mutant will provide further insight into the pathobiology of STX11 in PTCL and will reveal novel roles of STX11 in normal T-cells.

We agree with the reviewers that rescuing the ERAD phenotype with a Ubl4AK48R mutant will provide valuable information on whether ubiquitination of Ubl4A on Lys48 is the only USP13 depletion-associated deficiency that causes ERAD defects.

The analysis of the orientational correlations (see Materials and methods) of the residue fluctuations among the mutant and the coevolved mutant structures will provide a dynamic mechanistic perspective for the role of mutations.

Such behavioral phenotypes were quite unique, and further analysis of the mutant mice will provide a novel insight into the circadian regulation of the behavioral activities.

Microarray analysis in slk1, slk2 and luh mutant plants will provide additional insight into the abiotic stress response genes regulated by SLK1, SLK2 and LUH.

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