Thomas M. Wishart

Progressive abnormalities in skeletal muscle and neuromuscular junctions of transgenic mice expressing the Huntington's disease mutation.

The slow Wallerian degeneration protein, WldS, binds directly to VCP/p97 and partially redistributes it within the nucleus.

The neuroprotective WldS gene regulates expression of PTTG1 and erythroid differentiation regulator 1-like gene in mice and human cells.

Delayed synaptic degeneration in the CNS of Wlds mice after cortical lesion.

Synaptic vulnerability in neurodegenerative disease.

Differential proteomics analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wlds) gene.

Design of a novel quantitative PCR (QPCR)-based protocol for genotyping mice carrying the neuroprotective Wallerian degeneration slow (Wlds) gene.

VCP binding influences intracellular distribution of the slow Wallerian degeneration protein, Wld(S).

Modified cell cycle status in a mouse model of altered neuronal vulnerability (slow Wallerian degeneration; Wlds).

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

Protein product of CLN6 gene responsible for variant late-onset infantile neuronal ceroid lipofuscinosis interacts with CRMP-2.

Molecular correlates of axonal and synaptic pathology in mouse models of Batten disease.

Expression of the neuroprotective slow Wallerian degeneration (WldS) gene in non-neuronal tissues.

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

Synaptic protection in the brain of WldS mice occurs independently of age but is sensitive to gene-dose.

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

ApoE isoform-specific regulation of regeneration in the peripheral nervous system.

Reversible molecular pathology of skeletal muscle in spinal muscular atrophy.

Using induced pluripotent stem cells (iPSC) to model human neuromuscular connectivity: promise or reality?

WldS prevents axon degeneration through increased mitochondrial flux and enhanced mitochondrial Ca2+ buffering.

Combining comparative proteomics and molecular genetics uncovers regulators of synaptic and axonal stability and degeneration in vivo.

Total protein analysis as a reliable loading control for quantitative fluorescent Western blotting.

Label-free proteomics identifies Calreticulin and GRP75/Mortalin as peripherally accessible protein biomarkers for spinal muscular atrophy.

Dysregulation of ubiquitin homeostasis and β-catenin signaling promote spinal muscular atrophy.

A novel mouse model of Warburg Micro Syndrome reveals roles for RAB18 in eye development and organisation of the neuronal cytoskeleton.

The rat striatum responds to nigro-striatal degeneration via the increased expression of proteins associated with growth and regeneration of neuronal circuitry.

Increased levels of UCHL1 are a compensatory response to disrupted ubiquitin homeostasis in spinal muscular atrophy and do not represent a viable therapeutic target.

Label-free quantitative proteomic profiling identifies disruption of ubiquitin homeostasis as a key driver of schwann cell defects in spinal muscular atrophy.

Loss of glial neurofascin155 delays developmental synapse elimination at the neuromuscular junction.