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John M. Shelton

Researcher at University of Texas Southwestern Medical Center

Publications -  160
Citations -  26014

John M. Shelton is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Skeletal muscle & Myocyte. The author has an hindex of 75, co-authored 152 publications receiving 23041 citations. Previous affiliations of John M. Shelton include Children's Medical Center of Dallas & University of Texas at Dallas.

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Reeler/Disabled-like disruption of neuronal migration in knockout mice lacking the VLDL receptor and ApoE receptor 2.

TL;DR: It is suggested that VLDLR and ApoER2 participate in transmitting the extracellular Reelin signal to intracellular signaling processes initiated by mDab1, a cytosolic protein that activates tyrosine kinases.
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A calcineurin-dependent transcriptional pathway controls skeletal muscle fiber type

TL;DR: These results identify a molecular mechanism by which different patterns of motor nerve activity promote selective changes in gene expression to establish the specialized characteristics of slow and fast myofibers.
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Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor.

TL;DR: Findings reveal a central role for FXR in protecting the distal small intestine from bacterial invasion and suggest that FXR agonists may prevent epithelial deterioration and bacterial translocation in patients with impaired bile flow.
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A Micropeptide Encoded by a Putative Long Noncoding RNA Regulates Muscle Performance

TL;DR: Findings identify myoregulin (MLN) as an important regulator of skeletal muscle physiology and highlight the possibility that additional micropeptides are encoded in the many RNAs currently annotated as noncoding.
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Postnatal genome editing partially restores dystrophin expression in a mouse model of muscular dystrophy.

TL;DR: To correct DMD by skipping mutant dystrophin exons in postnatal muscle tissue in vivo, adeno-associated virus–9 (AAV9) is used to deliver gene-editing components to postnatal mdx mice, a model of DMD and other monogenic disorders after birth.