All Outputs (2)

ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling (2016)
Journal Article
Goode, A., Rea, S., Sultana, M., Shaw, B., Searle, M. S., & Layfield, R. (2016). ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling. Molecular and Cellular Neuroscience, 76, https://doi.org/10.1016/j.mcn.2016.08.004

The transcription factor Nrf2 and its repressor protein Keap1 play key roles in the regulation of antioxidant stress responses and both Keap1-Nrf2 signalling and oxidative stress have been implicated in the pathogenesis of the ALS-FTLD spectrum of ne... Read More about ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling.

Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD (2016)
Journal Article
Goode, A., Butler, K., Long, J., Cavey, J., Scott, D., Shaw, B., …Layfield, R. (2016). Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD. Autophagy, 12(7), 1094-1104. https://doi.org/10.1080/15548627.2016.1170257

Growing evidence implicates impairment of autophagy as a candidate pathogenic mechanism in the spectrum of neurodegenerative disorders which includes amyotrophic lateral sclerosis and frontotemporal lobar degeneration (ALS-FTLD). SQSTM1, which encode... Read More about Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD.