Overexpression of IGF-1 in Muscle Attenuates Disease in a Mouse Model of Spinal and Bulbar Muscular Atrophy
Open Access
- 13 August 2009
- journal article
- research article
- Published by Elsevier BV in Neuron
- Vol. 63 (3), 316-328
- https://doi.org/10.1016/j.neuron.2009.07.019
Abstract
No abstract availableThis publication has 54 references indexed in Scilit:
- In vivo suppression of polyglutamine neurotoxicity by C-terminus of Hsp70-interacting protein (CHIP) supports an aggregation model of pathogenesisNeurobiology of Disease, 2009
- Spinal and bulbar muscular atrophy: a motoneuron or muscle disease?Current Opinion in Pharmacology, 2008
- Subcutaneous IGF-1 is not beneficial in 2-year ALS trialNeurology, 2008
- Ablation of the UPR-Mediator CHOP Restores Motor Function and Reduces Demyelination in Charcot-Marie-Tooth 1B MiceNeuron, 2008
- Overexpression of wild-type androgen receptor in muscle recapitulates polyglutamine diseaseProceedings of the National Academy of Sciences of the United States of America, 2007
- Androgen-dependent pathology demonstrates myopathic contribution to the Kennedy disease phenotype in a mouse knock-in modelJCI Insight, 2006
- Androgen-dependent pathology demonstrates myopathic contribution to the Kennedy disease phenotype in a mouse knock-in modelJCI Insight, 2006
- Pathogenesis, animal models and therapeutics in Spinal and bulbar muscular atrophy (SBMA)Experimental Neurology, 2006
- Protein aggregation and neurodegenerative diseaseNature Medicine, 2004
- The IGF-1/PI3K/Akt Pathway Prevents Expression of Muscle Atrophy-Induced Ubiquitin Ligases by Inhibiting FOXO Transcription FactorsMolecular Cell, 2004