Murray G. Blackmore

This study shows that chronic activation of corticospinal tract neurons after spinal injury does not improve axonal sprouting or behavioral recovery.

This study delivers hyper-IL-6 to spinal cord neurons using retrograde AAV, activating Stat3 but causing severe tremors and weight loss in mice.

This study shows that Sox11 overexpression in mature corticospinal tract neurons reactivates embryonic growth-related gene expression, suggesting its potential to promote axon regeneration.

This study profiles the transcriptional response of supraspinal cell types to spinal injury in mice, finding that CST neurons respond more strongly to injuries closer to the brain than to distant spinal injuries.

The paper uses single nuclei RNA sequencing to identify transcriptional profiles and marker genes for supraspinal neurons projecting to the lumbar spinal cord in mice.

The paper quantifies the supraspinal connectome in mice to identify anatomical correlates of functional recovery after spinal injury.

The paper identifies novel transcription factor synergies that enhance axon growth by analyzing co-occupancy patterns and validating them through experimental screens and animal models.

This paper demonstrates that combining KLF6 gene therapy with neural progenitor cell grafts can restore corticospinal tract function after spinal injury in mice.

This study uses retrograde viral vectors and 3D microscopy to map supraspinal connectivity in the spinal cord and demonstrate their therapeutic potential.

This study shows KLF6 promotes axon growth in CNS neurons by co-occupying regulatory DNA with STAT3, leading to synergistic gene expression changes.

The paper develops a bioinformatic pipeline to analyze chromatin accessibility and gene networks in cortical neurons, finding that developmental chromatin restriction limits axon regeneration and identifies potential pioneer factors to overcome this barrier.