We are analyzing https://link.springer.com/article/10.1186/s13395-018-0182-x.

Title:
Dystrophin R16/17-syntrophin PDZ fusion protein restores sarcolemmal nNOSμ | Skeletal Muscle
Description:
Background Loss of sarcolemmal nNOSμ is a common manifestation in a wide variety of muscle diseases and contributes to the dysregulation of multiple muscle activities. Given the critical role sarcolemmal nNOSμ plays in muscle, restoration of sarcolemmal nNOSμ should be considered as an important therapeutic goal. Methods nNOSμ is anchored to the sarcolemma by dystrophin spectrin-like repeats 16 and 17 (R16/17) and the syntrophin PDZ domain (Syn PDZ). To develop a strategy that can independently restore sarcolemmal nNOSμ, we engineered an R16/17-Syn PDZ fusion construct and tested whether this construct alone is sufficient to anchor nNOSμ to the sarcolemma in three different mouse models of Duchenne muscular dystrophy (DMD). Results Membrane-associated nNOSμ is completely lost in DMD. Adeno-associated virus (AAV)-mediated delivery of the R16/17-Syn PDZ fusion construct successfully restored sarcolemmal nNOSμ in all three models. Further, nNOS restoration was independent of the dystrophin-associated protein complex. Conclusions Our results suggest that the R16/17-Syn PDZ fusion construct is sufficient to restore sarcolemmal nNOSμ in the dystrophin-null muscle.
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Keywords {🔍}

muscle, nnosμ, article, google, scholar, pdz, cas, sarcolemmal, protein, fusion, domain, mice, dystrophin, nnos, syntrophin, muscular, nitric, oxide, mdx, skeletal, dystrophy, expression, sarcolemma, fig, restoration, aav, mouse, rsyn, duchenne, cell, synthase, neuronal, construct, mol, yue, antibody, duan, localization, dapc, gfp, loss, restore, restored, studies, dba, cmahmdx, activity, gene, biol, models,

Topics {✒️}

neuronal-type nitric-oxide synthase nitric-oxide synthase types r16/17-inclusive micro-dystrophin dba/2 j-mdx congenic mice exercise-stimulated glucose transport dystrophin-deficient skeletal muscle mouse anti-pan-syntrophin antibody nitric oxide release-transient severe dba/2j-mdx model nitric oxide-mediated activation nnosmu-deficient skeletal muscle suspension-induced muscle atrophy rabbit anti-c-terminus involves triple-plasmid transfection received research support mouse anti-β-sarcoglycan antibody mouse anti-β-dystroglycan antibody short-term mechanical unloading alpha-syntrophin pdz domain insulin-resistant skeletal muscle 7-kb mini-dystrophin gene dystrophin cooh-terminal domain 16 mg/ml nitroblue tetrazolium zucker fa/fa rats dystrophin r16/17-syntrophin pdz cardiac excitation-contraction coupling membrane-directed {alpha}-dystrobrevin nitric oxide synthases nitric oxide synthase exercise-induced mitochondrial biogenesis skeletal muscle regeneration aging-related muscle atrophy skeletal muscle fatigue pcr-based cloning method article download pdf mouse anti-dystrobrevin antibody membrane-enriched microsomal fraction membrane-bound r16/17 dystrophin-deficient mdx muscles restored sarcolemmal nnosμ dba/2 j-mdx mice membrane-bound nnosμ mouse anti-r17 antibody mouse skeletal muscle wild-type bl10 mice full-length dystrophin x-ray crystallography studies homozygous cmah/mdx mice full access r16/17-syn pdz

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         headline:Dystrophin R16/17-syntrophin PDZ fusion protein restores sarcolemmal nNOSμ
         description:Loss of sarcolemmal nNOSμ is a common manifestation in a wide variety of muscle diseases and contributes to the dysregulation of multiple muscle activities. Given the critical role sarcolemmal nNOSμ plays in muscle, restoration of sarcolemmal nNOSμ should be considered as an important therapeutic goal. nNOSμ is anchored to the sarcolemma by dystrophin spectrin-like repeats 16 and 17 (R16/17) and the syntrophin PDZ domain (Syn PDZ). To develop a strategy that can independently restore sarcolemmal nNOSμ, we engineered an R16/17-Syn PDZ fusion construct and tested whether this construct alone is sufficient to anchor nNOSμ to the sarcolemma in three different mouse models of Duchenne muscular dystrophy (DMD). Membrane-associated nNOSμ is completely lost in DMD. Adeno-associated virus (AAV)-mediated delivery of the R16/17-Syn PDZ fusion construct successfully restored sarcolemmal nNOSμ in all three models. Further, nNOS restoration was independent of the dystrophin-associated protein complex. Our results suggest that the R16/17-Syn PDZ fusion construct is sufficient to restore sarcolemmal nNOSμ in the dystrophin-null muscle.
         datePublished:2018-11-22T00:00:00Z
         dateModified:2018-11-22T00:00:00Z
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            Neuronal nitric oxide synthase
            Sarcolemma
            Skeletal muscle
            Dystrophin
            Syntrophin
            Fusion protein
            Cell Biology
            Developmental Biology
            Biochemistry
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      headline:Dystrophin R16/17-syntrophin PDZ fusion protein restores sarcolemmal nNOSμ
      description:Loss of sarcolemmal nNOSμ is a common manifestation in a wide variety of muscle diseases and contributes to the dysregulation of multiple muscle activities. Given the critical role sarcolemmal nNOSμ plays in muscle, restoration of sarcolemmal nNOSμ should be considered as an important therapeutic goal. nNOSμ is anchored to the sarcolemma by dystrophin spectrin-like repeats 16 and 17 (R16/17) and the syntrophin PDZ domain (Syn PDZ). To develop a strategy that can independently restore sarcolemmal nNOSμ, we engineered an R16/17-Syn PDZ fusion construct and tested whether this construct alone is sufficient to anchor nNOSμ to the sarcolemma in three different mouse models of Duchenne muscular dystrophy (DMD). Membrane-associated nNOSμ is completely lost in DMD. Adeno-associated virus (AAV)-mediated delivery of the R16/17-Syn PDZ fusion construct successfully restored sarcolemmal nNOSμ in all three models. Further, nNOS restoration was independent of the dystrophin-associated protein complex. Our results suggest that the R16/17-Syn PDZ fusion construct is sufficient to restore sarcolemmal nNOSμ in the dystrophin-null muscle.
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      dateModified:2018-11-22T00:00:00Z
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         Neuronal nitric oxide synthase
         Sarcolemma
         Skeletal muscle
         Dystrophin
         Syntrophin
         Fusion protein
         Cell Biology
         Developmental Biology
         Biochemistry
         general
         Systems Biology
         Biotechnology
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      name:Department of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, USA
      name:Department of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, USA
      name:Department of Neurology, School of Medicine, University of Missouri, Columbia, USA
      name:Department of Bioengineering, University of Missouri, Columbia, USA
      name:Department of Molecular Microbiology and Immunology, School of Medicine, University of Missouri, Columbia, USA

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