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John McAnally

Researcher at University of Texas Southwestern Medical Center

Publications -  46
Citations -  11171

John McAnally is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Skeletal muscle & Regulation of gene expression. The author has an hindex of 33, co-authored 38 publications receiving 10141 citations.

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The Endothelial-Specific MicroRNA miR-126 Governs Vascular Integrity and Angiogenesis

TL;DR: It is shown that an endothelial cell-restricted microRNA (miR-126) mediates developmental angiogenesis in vivo and enhances the proangiogenic actions of VEGF and FGF and promotes blood vessel formation by repressing the expression of Spred-1, an intracellular inhibitor of angiogenic signaling.
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Histone Deacetylase 4 Controls Chondrocyte Hypertrophy during Skeletogenesis

TL;DR: It is reported that HDAC4, which is expressed in prehypertrophic chondrocytes, regulates chONDrocyte hypertrophy and endochondral bone formation by interacting with and inhibiting the activity of Runx2, a transcription factor necessary for chondrosclerosis.
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Hippo pathway effector Yap promotes cardiac regeneration

TL;DR: It is reported that mice bearing mutant alleles of Yap and its paralog WW domain containing transcription regulator 1 (Taz) exhibit gene dosage-dependent cardiac phenotypes, suggesting redundant roles of these Hippo pathway effectors in establishing proper myocyte number and maintaining cardiac function.
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MicroRNA-206 Delays ALS Progression and Promotes Regeneration of Neuromuscular Synapses in Mice

TL;DR: It is shown that a small noncoding RNA that is selectively expressed in skeletal muscle, miR-206, senses motor neuron injury or loss and helps ameliorate resultant muscle damage by promoting regeneration of neuromuscular synapses and slows disease progression in ALS.
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MicroRNAs miR-143 and miR-145 modulate cytoskeletal dynamics and responsiveness of smooth muscle cells to injury.

TL;DR: MiR-143 and miR-145 act as integral components of the regulatory network whereby SRF controls cytoskeletal remodeling and phenotypic switching of SMCs during vascular disease.