ArticleHuman molecular genetics2011
Impaired motoneuronal retrograde transport in two models of SBMA implicates two sites of androgen action.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Mid1 is associated with androgen-dependent axonal vulnerability of motor neurons in spinal and bulbar muscular atrophy.Cell death & disease · 2022Article
- Neuromuscular junction pathology is correlated with differential motor unit vulnerability in spinal and bulbar muscular atrophy.Acta neuropathologica communications · 2022Article
- Disease AffectsInternational journal of molecular sciences · 2019Article
- Polyglutamine Repeats in Neurodegenerative Diseases.Annual review of pathology · 2019Review
- Androgen receptor polyglutamine expansion drives age-dependent quality control defects and muscle dysfunction.The Journal of clinical investigation · 2018Article
- Pre-clinical symptoms of SBMA may not be androgen-dependent: implications from two SBMA mouse models.Human molecular genetics · 2018Article
- Beta-agonist stimulation ameliorates the phenotype of spinal and bulbar muscular atrophy mice and patient-derived myotubes.Scientific reports · 2017Article
- Non-autonomous Cellular Responses to Ototoxic Drug-Induced Stress and Death.Frontiers in cellular neuroscience · 2017Review
- The Ubiquitination, Disaggregation and Proteasomal Degradation Machineries in Polyglutamine Disease.Frontiers in molecular neuroscience · 2017Review
- Rescue of Metabolic Alterations in AR113Q Skeletal Muscle by Peripheral Androgen Receptor Gene Silencing.Cell reports · 2016Article
- Neuromuscular junctions are pathological but not denervated in two mouse models of spinal bulbar muscular atrophy.Human molecular genetics · 2016Article
- Glycolytic-to-oxidative fiber-type switch and mTOR signaling activation are early-onset features of SBMA muscle modified by high-fat diet.Acta neuropathologica · 2016Article
- The polyglutamine-expanded androgen receptor responsible for spinal and bulbar muscular atrophy inhibits the APC/C(Cdh1) ubiquitin ligase complex.Scientific reports · 2016Article
- Defects in Neuromuscular Transmission May Underlie Motor Dysfunction in Spinal and Bulbar Muscular Atrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Androgen-dependent loss of muscle BDNF mRNA in two mouse models of SBMA.Experimental neurology · 2015Article
- Contractile dysfunction in muscle may underlie androgen-dependent motor dysfunction in spinal bulbar muscular atrophy.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Disrupting SUMOylation enhances transcriptional function and ameliorates polyglutamine androgen receptor-mediated disease.The Journal of clinical investigation · 2015Article
- Article
- Antiandrogen flutamide protects male mice from androgen-dependent toxicity in three models of spinal bulbar muscular atrophy.Endocrinology · 2014Article
- Peripheral androgen receptor gene suppression rescues disease in mouse models of spinal and bulbar muscular atrophy.Cell reports · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal and bulbar muscular atrophy (SBMA) impairs motor function in men and is linked to a CAG repeat mutation in the androgen receptor (AR) gene. Defects in motoneuronal retrograde axonal transport may critically mediate motor dysfunction in SBMA, but the site(s) where AR disrupts transport is unknown. We find deficits in retrograde labeling of spinal motoneurons in both a knock-in (KI) and a myogenic transgenic (TG) mouse model of SBMA. Likewise, live imaging of endosomal trafficking in sciatic nerve axons reveals disease-induced deficits in the flux and run length of retrogradely transported endosomes in both KI and TG males, demonstrating that disease triggered in muscle can impair retrograde transport of cargo in motoneuron axons, possibly via defective retrograde signaling. Supporting the idea of impaired retrograde signaling, we find that vascular endothelial growth factor treatment of diseased muscles reverses the transport/trafficking deficit. Transport velocity is also affected in KI males, suggesting a neurogenic component. These results demonstrate that androgens could act via both cell autonomous and non-cell autonomous mechanisms to disrupt axonal transport in motoneurons affected by SBMA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.