Mutant superoxide dismutase 1 (SOD1), a cause of amyotrophic lateral sclerosis, disrupts the recruitment of SMN, the spinal muscular atrophy protein to nuclear Cajal bodies

Nuclear Localization of Human SOD1 and Mutant SOD1-Specific Disruption of Survival Motor Neuron Protein Complex in Transgenic Amyotrophic Lateral Sclerosis Mice

(2012) Barry Gertz et al.   JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY

SMN1 gene duplications are associated with sporadic ALS

(2012) H. M. Blauw et al.   NEUROLOGY

Spinal Muscular Atrophy

(2011) Stephen J. Kolb   ARCHIVES OF NEUROLOGY

Temporal requirement for high SMN expression in SMA mice

(2011) T. T. Le et al.   HUMAN MOLECULAR GENETICS

Postsymptomatic restoration of SMN rescues the disease phenotype in a mouse model of severe spinal muscular atrophy

(2011) Cathleen M. Lutz et al.   JOURNAL OF CLINICAL INVESTIGATION

Molecular pathways of motor neuron injury in amyotrophic lateral sclerosis

(2011) Laura Ferraiuolo et al.   Nature Reviews Neurology

WRAP53 Is Essential for Cajal Body Formation and for Targeting the Survival of Motor Neuron Complex to Cajal Bodies

(2010) Salah Mahmoudi et al.   PLOS BIOLOGY

Survival motor neuron deficiency enhances progression in an amyotrophic lateral sclerosis mouse model

(2009) Bradley J. Turner et al.   NEUROBIOLOGY OF DISEASE

The Cajal body

(2008) Glenn E. Morris   BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH

Reduced SMN protein impairs maturation of the neuromuscular junctions in mouse models of spinal muscular atrophy

(2008) Shingo Kariya et al.   HUMAN MOLECULAR GENETICS

Astrocytes as determinants of disease progression in inherited amyotrophic lateral sclerosis

(2008) Koji Yamanaka et al.   NATURE NEUROSCIENCE

The Threat of Instability: Neurodegeneration Predicted by Protein Destabilization and Aggregation Propensity

(2008) Elizabeth M Meiering   PLOS BIOLOGY