Lyndsay Murray

Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy.

Loss of translation elongation factor (eEF1A2) expression in vivo differentiates between Wallerian degeneration and dying-back neuronal pathology.

Transcriptional regulation of the AP-1 and Nrf2 target gene sulfiredoxin.

Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy.

Alternative splicing events are a late feature of pathology in a mouse model of spinal muscular atrophy.

Smoking cessation interventions in cancer care: opportunities for oncology nurses and nurse scientists.

SMN deficiency disrupts brain development in a mouse model of severe spinal muscular atrophy.

The response of neuromuscular junctions to injury is developmentally regulated.

Induction of cell stress in neurons from transgenic mice expressing yellow fluorescent protein: implications for neurodegeneration research.

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy.

A critical Smn threshold in mice dictates onset of an intermediate spinal muscular atrophy phenotype associated with a distinct neuromuscular junction pathology.

Fasudil improves survival and promotes skeletal muscle development in a mouse model of spinal muscular atrophy.

Defects in neuromuscular junction remodelling in the Smn(2B/-) mouse model of spinal muscular atrophy.

A novel function for the survival motoneuron protein as a translational regulator.

Early onset muscle weakness and disruption of muscle proteins in mouse models of spinal muscular atrophy.