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Pharmacological and exercise‐induced activation of AMPK as emerging therapies for myotonic dystrophy type 1 patients

The Journal of physiology, 2022-07, Vol.600 (14), p.3249-3264

2022

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Sex‐dependent role of Pannexin 1 in regulating skeletal muscle and satellite cell function

Journal of cellular physiology, 2022-10, Vol.237 (10), p.3944-3959

2022

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Expression of Pannexin 1 and Pannexin 3 during skeletal muscle development, regeneration, and Duchenne muscular dystrophy

Journal of cellular physiology, 2018-10, Vol.233 (10), p.7057-7070

2018

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Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation

Nature communications, 2022-11, Vol.13 (1), p.7108-7108, Article 7108

2022

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Postsynaptic chromatin is under neural control at the neuromuscular junction

The EMBO journal, 2007-02, Vol.26 (4), p.1117-1128

2007

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Misregulation of calcium-handling proteins promotes hyperactivation of calcineurin-NFAT signaling in skeletal muscle of DM1 mice

Human molecular genetics, 2017-06, Vol.26 (12), p.2192-2206

2017

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Vorinostat Improves Myotonic Dystrophy Type 1 Splicing Abnormalities in DM1 Muscle Cell Lines and Skeletal Muscle from a DM1 Mouse Model

International journal of molecular sciences, 2023-02, Vol.24 (4), p.3794

2023

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Staufen1 Regulates Multiple Alternative Splicing Events either Positively or Negatively in DM1 Indicating Its Role as a Disease Modifier

PLoS genetics, 2016-01, Vol.12 (1), p.e1005827-e1005827

2016

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Muscle-specific expression of the RNA-binding protein Staufen1 induces progressive skeletal muscle atrophy via regulation of phosphatase tensin homolog

Human molecular genetics, 2017-05, Vol.26 (10), p.1821-1838

2017

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Differential regulation of autophagy by STAU1 in alveolar rhabdomyosarcoma and non‐transformed skeletal muscle cells

Cellular oncology (Dordrecht), 2021-08, Vol.44 (4), p.851-870

2021

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AChR β-Subunit mRNAs Are Stabilized by HuR in a Mouse Model of Congenital Myasthenic Syndrome With Acetylcholinesterase Deficiency

Frontiers in molecular neuroscience, 2020-12, Vol.13, p.568171-568171

2020

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MUSK, a new target for mutations causing congenital myasthenic syndrome

Human molecular genetics, 2004-12, Vol.13 (24), p.3229-3240

2004

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Maintenance of CCL5 mRNA stores by post‐effector and memory CD8 T cells is dependent on transcription and is coupled to increased mRNA stability

European Journal of Immunology, 2006-10, Vol.36 (10), p.2745-2754

2006

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Synapse-Specific Gene Expression at the Neuromuscular Junction

Annals of the New York Academy of Sciences, 2003-09, Vol.998 (1), p.53-65

2003

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Combinatorial therapies for rescuing myotonic dystrophy type 1 skeletal muscle defects

Trends in molecular medicine, 2022-06, Vol.28 (6), p.439-442

2022

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HDAC6 regulates microtubule stability and clustering of AChRs at neuromuscular junctions

The Journal of cell biology, 2020-08, Vol.219 (8)

2020

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Combinatorial treatment with exercise and AICAR potentiates the rescue of myotonic dystrophy type 1 mouse muscles in a sex-specific manner

Human molecular genetics, 2023-01, Vol.32 (4), p.551-566

2023

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Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles

Human molecular genetics, 2018-10, Vol.27 (19), p.3361-3376

2018

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Expression of mutant Ets protein at the neuromuscular synapse causes alterations in morphology and gene expression

EMBO reports, 2002-11, Vol.3 (11), p.1075-1081

2002

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A novel CARM1–HuR axis involved in muscle differentiation and plasticity misregulated in spinal muscular atrophy

Human molecular genetics, 2022-05, Vol.31 (9), p.1453-1470

2022

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Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation

Nature communications, 2022-11, Vol.13

2022

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Thrombin reduces MuSK and acetylcholine receptor expression along with neuromuscular contact size in vitro

The European journal of neuroscience, 2004-04, Vol.19 (8), p.2099-2108

2004

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Thrombin downregulates muscle acetylcholine receptors via an IP3 signaling pathway by activating its G-protein-coupled protease-activated receptor-1

Journal of cellular physiology, 2003-07, Vol.196 (1), p.105-112

2003

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The RNA-binding protein Staufen1 is increased in DM1 skeletal muscle and promotes alternative pre-mRNA splicing

The Journal of cell biology, 2012-03, Vol.196 (6), p.699-712

2012

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Overexpression of Staufen1 in DM1 mouse skeletal muscle exacerbates dystrophic and atrophic features

Human molecular genetics, 2020-08, Vol.29 (13), p.2185-2199

2020

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Pharmacological and exercise‐induced activation of AMPK as emerging therapies for myotonic dystrophy type 1 patients

Sex‐dependent role of Pannexin 1 in regulating skeletal muscle and satellite cell function

Expression of Pannexin 1 and Pannexin 3 during skeletal muscle development, regeneration, and Duchenne muscular dystrophy

Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation

Postsynaptic chromatin is under neural control at the neuromuscular junction

Misregulation of calcium-handling proteins promotes hyperactivation of calcineurin-NFAT signaling in skeletal muscle of DM1 mice

Vorinostat Improves Myotonic Dystrophy Type 1 Splicing Abnormalities in DM1 Muscle Cell Lines and Skeletal Muscle from a DM1 Mouse Model

Staufen1 Regulates Multiple Alternative Splicing Events either Positively or Negatively in DM1 Indicating Its Role as a Disease Modifier

Muscle-specific expression of the RNA-binding protein Staufen1 induces progressive skeletal muscle atrophy via regulation of phosphatase tensin homolog

Differential regulation of autophagy by STAU1 in alveolar rhabdomyosarcoma and non‐transformed skeletal muscle cells

AChR β-Subunit mRNAs Are Stabilized by HuR in a Mouse Model of Congenital Myasthenic Syndrome With Acetylcholinesterase Deficiency

MUSK, a new target for mutations causing congenital myasthenic syndrome

Maintenance of CCL5 mRNA stores by post‐effector and memory CD8 T cells is dependent on transcription and is coupled to increased mRNA stability

Synapse-Specific Gene Expression at the Neuromuscular Junction

Combinatorial therapies for rescuing myotonic dystrophy type 1 skeletal muscle defects

HDAC6 regulates microtubule stability and clustering of AChRs at neuromuscular junctions

Combinatorial treatment with exercise and AICAR potentiates the rescue of myotonic dystrophy type 1 mouse muscles in a sex-specific manner

Pharmacological and physiological activation of AMPK improves the spliceopathy in DM1 mouse muscles

Expression of mutant Ets protein at the neuromuscular synapse causes alterations in morphology and gene expression

A novel CARM1–HuR axis involved in muscle differentiation and plasticity misregulated in spinal muscular atrophy

Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation

Thrombin reduces MuSK and acetylcholine receptor expression along with neuromuscular contact size in vitro

Thrombin downregulates muscle acetylcholine receptors via an IP3 signaling pathway by activating its G-protein-coupled protease-activated receptor-1

The RNA-binding protein Staufen1 is increased in DM1 skeletal muscle and promotes alternative pre-mRNA splicing

Overexpression of Staufen1 in DM1 mouse skeletal muscle exacerbates dystrophic and atrophic features

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