Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD

Goode, Alice; Butler, Kevin; Long, Jed; Cavey, James; Scott, Daniel; Shaw, Barry; Sollenberger, Jill; Gell, Christopher; Johansen, Terje; Oldham, Neil J.; Searle, Mark; Layfield, Robert

doi:10.1080/15548627.2016.1170257

All Outputs (4)

Carbene footprinting accurately maps binding sites in protein–ligand and protein–protein interactions (2016)
Journal Article

Specific interactions between proteins and their binding partners are fundamental to life processes. The ability to detect protein complexes, and map their sites of binding, is crucial to understanding basic biology at the molecular level. Methods th... Read More about Carbene footprinting accurately maps binding sites in protein–ligand and protein–protein interactions.

ALS-FTLD associated mutations of SQSTM1 impact on Keap1-Nrf2 signalling (2016)
Journal Article

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.

Mass spectrometry insights into a tandem ubiquitin-binding domain hybrid engineered for the selective recognition of unanchored polyubiquitin (2016)
Journal Article

Unanchored polyubiquitin chains are emerging as importanregulators of cellular physiology with diverse roles paralleling those of substrate-conjugated polyubiquitin. However tools able to discriminate unanchored polyubiquitin chains of different isop... Read More about Mass spectrometry insights into a tandem ubiquitin-binding domain hybrid engineered for the selective recognition of unanchored polyubiquitin.

Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD (2016)
Journal Article

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.